首页 > 最新文献

Oncology reports最新文献

英文 中文
[Corrigendum] Long non‑coding RNA H19 regulates LASP1 expression in osteosarcoma by competitively binding to miR‑29a‑3p. [更正] 长非编码 RNA H19 通过与 miR-29a-3p 竞争性结合调节骨肉瘤中 LASP1 的表达。
IF 4.2 3区 医学 Q1 Medicine Pub Date : 2024-04-19 DOI: 10.3892/or.2024.8737
Hao Jin, Huan Wang, Xin Jin, Wenbo Wang
Following the publication of the above article, an interested reader drew to the authors' attention that, for the cell invasion assay experiments shown in Fig. 2D on p. 5, there appeared to be an overlapping section of data comparing between the Sao‑2/Control and MG‑63/siH19 panels, such that these data had been derived from the same original source where the panels were intended to portray the results from differently performed epxeriments. Upon examining their original data, the authors have realized that, in Fig. 2D, an inadvertent error was made in the copying and pasting of the two groups of pictures, resulting in the image belonging to the Saos‑2 cell experiment being mistakenly pasted as the image for the MG‑63 cell experiment. The authors carefully checked the original pictures and the experimental record, and found that the two groups of cells were close to the same morphology. The corrected version of Fig. 2, containing data from an alternatively performed experiment for Fig. 2D, is shown on the next page. Note that the error did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this. They also apologize to the readership for any inconvenience caused. [Oncology Reports 46: 207, 2021; DOI: 10.3892/or.2021.8158].
在上述文章发表后,一位感兴趣的读者提请作者注意,在第 5 页图 2D 所示的细胞侵袭实验 中,Sao-2/对照组和 MG-63/siH19 组之间的数据似乎有重叠部分,而这些数据来自同一原始数据 源,这两组数据旨在反映不同实验的结果。作者在检查原始数据时发现,在图 2D 中,两组图片的复制和粘贴出现了疏忽,导致属于 Saos-2 细胞实验的图片被误粘贴为 MG-63 细胞实验的图片。作者仔细核对了原始图片和实验记录,发现两组细胞的形态接近一致。更正后的图 2 显示在下一页,其中包含了图 2D 替代实验的数据。请注意,该错误并不影响论文中报告的总体结论。所有作者均同意发表本更正,并感谢《肿瘤学报告》编辑允许他们有机会发表本更正。他们还对给读者带来的不便表示歉意。[肿瘤学报告 46: 207, 2021; DOI: 10.3892/or.2021.8158]。
{"title":"[Corrigendum] Long non‑coding RNA H19 regulates LASP1 expression in osteosarcoma by competitively binding to miR‑29a‑3p.","authors":"Hao Jin, Huan Wang, Xin Jin, Wenbo Wang","doi":"10.3892/or.2024.8737","DOIUrl":"https://doi.org/10.3892/or.2024.8737","url":null,"abstract":"Following the publication of the above article, an interested reader drew to the authors' attention that, for the cell invasion assay experiments shown in Fig. 2D on p. 5, there appeared to be an overlapping section of data comparing between the Sao‑2/Control and MG‑63/siH19 panels, such that these data had been derived from the same original source where the panels were intended to portray the results from differently performed epxeriments. Upon examining their original data, the authors have realized that, in Fig. 2D, an inadvertent error was made in the copying and pasting of the two groups of pictures, resulting in the image belonging to the Saos‑2 cell experiment being mistakenly pasted as the image for the MG‑63 cell experiment. The authors carefully checked the original pictures and the experimental record, and found that the two groups of cells were close to the same morphology. The corrected version of Fig. 2, containing data from an alternatively performed experiment for Fig. 2D, is shown on the next page. Note that the error did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of <i>Oncology Reports</i> for allowing them the opportunity to publish this. They also apologize to the readership for any inconvenience caused. [Oncology Reports 46: 207, 2021; DOI: 10.3892/or.2021.8158].","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140629681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The role of ferroptosis in radiotherapy and combination therapy for head and neck squamous cell carcinoma (Review). 头颈部鳞状细胞癌的放疗和综合疗法中铁细胞增多症的作用(综述)。
IF 4.2 3区 医学 Q1 Medicine Pub Date : 2024-04-19 DOI: 10.3892/or.2024.8738
Yu Feng, Xiulei Li, Bingwu Yang, Maocai Li, Yongya Du, Jing Wang, Siyu Liu, Lili Gong, Lianqing Li, Lei Gao
Head and neck squamous cell carcinoma (HNSCC) is a highly aggressive, heterogeneous tumour usually caused by alcohol and tobacco consumption, making it one of the most common malignancies worldwide. Despite the fact that various therapeutic approaches such as surgery, radiation therapy (RT), chemotherapy (CT) and targeted therapy have been widely used for HNSCC in recent years, its recurrence rate and mortality rate remain high. RT is the standard treatment choice for HNSCC, which induces reactive oxygen species production and causes oxidative stress, ultimately leading to tumour cell death. CT is a widely recognized form of cancer treatment that treats a variety of cancers by eliminating cancer cells and preventing them from reproducing. Immune checkpoint inhibitor and epidermal growth factor receptor are important in the treatment of recurrent or metastatic HNSCC. Iron death, a type of cell death regulated by peroxidative damage to phospholipids containing polyunsaturated fatty acids in cell membranes, has been found to be a relevant death response triggered by tumour RT in recent years. In the present review, an overview of the current knowledge on RT and combination therapy and iron death in HNSCC was provided, the mechanisms by which RT induces iron death in tumour cells were summarized, and therapeutic strategies to target iron death in HNSCC were explored. The current review provided important information for future studies of iron death in the treatment of HNSCC.
头颈部鳞状细胞癌(HNSCC)是一种侵袭性极强的异质性肿瘤,通常由饮酒和吸烟引起,是全球最常见的恶性肿瘤之一。尽管近年来手术、放射治疗(RT)、化疗(CT)和靶向治疗等各种治疗方法已广泛应用于 HNSCC,但其复发率和死亡率仍然居高不下。RT 是 HNSCC 的标准治疗选择,它会诱导活性氧的产生并导致氧化应激,最终导致肿瘤细胞死亡。CT 是一种被广泛认可的癌症治疗方式,它通过消除癌细胞并阻止其繁殖来治疗各种癌症。免疫检查点抑制剂和表皮生长因子受体是治疗复发性或转移性 HNSCC 的重要药物。铁死是一种由细胞膜中含有多不饱和脂肪酸的磷脂过氧化损伤调控的细胞死亡,近年来已被发现是由肿瘤RT引发的一种相关死亡反应。本综述概述了目前有关 RT 和联合疗法以及 HNSCC 中铁死亡的知识,总结了 RT 诱导肿瘤细胞铁死亡的机制,并探讨了针对 HNSCC 中铁死亡的治疗策略。本综述为今后研究治疗 HNSCC 中的铁死亡提供了重要信息。
{"title":"The role of ferroptosis in radiotherapy and combination therapy for head and neck squamous cell carcinoma (Review).","authors":"Yu Feng, Xiulei Li, Bingwu Yang, Maocai Li, Yongya Du, Jing Wang, Siyu Liu, Lili Gong, Lianqing Li, Lei Gao","doi":"10.3892/or.2024.8738","DOIUrl":"https://doi.org/10.3892/or.2024.8738","url":null,"abstract":"Head and neck squamous cell carcinoma (HNSCC) is a highly aggressive, heterogeneous tumour usually caused by alcohol and tobacco consumption, making it one of the most common malignancies worldwide. Despite the fact that various therapeutic approaches such as surgery, radiation therapy (RT), chemotherapy (CT) and targeted therapy have been widely used for HNSCC in recent years, its recurrence rate and mortality rate remain high. RT is the standard treatment choice for HNSCC, which induces reactive oxygen species production and causes oxidative stress, ultimately leading to tumour cell death. CT is a widely recognized form of cancer treatment that treats a variety of cancers by eliminating cancer cells and preventing them from reproducing. Immune checkpoint inhibitor and epidermal growth factor receptor are important in the treatment of recurrent or metastatic HNSCC. Iron death, a type of cell death regulated by peroxidative damage to phospholipids containing polyunsaturated fatty acids in cell membranes, has been found to be a relevant death response triggered by tumour RT in recent years. In the present review, an overview of the current knowledge on RT and combination therapy and iron death in HNSCC was provided, the mechanisms by which RT induces iron death in tumour cells were summarized, and therapeutic strategies to target iron death in HNSCC were explored. The current review provided important information for future studies of iron death in the treatment of HNSCC.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140623974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Lidocaine attenuates TMZ resistance and inhibits cell migration by modulating the MET pathway in glioblastoma cells. 利多卡因通过调节胶质母细胞瘤细胞的MET通路,减轻TMZ耐药性并抑制细胞迁移。
IF 4.2 3区 医学 Q1 Medicine Pub Date : 2024-04-12 DOI: 10.3892/or.2024.8731
Ming-Shan Chen, Zhi-Yong Chong, Cheng Huang, Hsiu-Chen Huang, Pin-Hsuan Su, Jui-Chieh Chen
Glioblastoma multiforme (GBM) is the most aggressive type of malignant brain tumor. Currently, the predominant clinical treatment is the combination of surgical resection with concurrent radiotherapy and chemotherapy, using temozolomide (TMZ) as the primary chemotherapy drug. Lidocaine, a widely used amide‑based local anesthetic, has been found to have a significant anticancer effect. It has been reported that aberrant hepatocyte growth factor (HGF)/mesenchymal‑epithelial transition factor (MET) signaling plays a role in the progression of brain tumors. However, it remains unclear whether lidocaine can regulate the MET pathway in GBM. In the present study, the clinical importance of the HGF/MET pathway was analyzed using bioinformatics. By establishing TMZ‑resistant cell lines, the impact of combined treatment with lidocaine and TMZ was investigated. Additionally, the effects of lidocaine on cellular function were also examined and confirmed using knockdown techniques. The current findings revealed that the HGF/MET pathway played a key role in brain cancer, and its activation in GBM was associated with increased malignancy and poorer patient outcomes. Elevated HGF levels and activation of its receptor were found to be associated with TMZ resistance in GBM cells. Lidocaine effectively suppressed the HGF/MET pathway, thereby restoring TMZ sensitivity in TMZ‑resistant cells. Furthermore, lidocaine also inhibited cell migration. Overall, these results indicated that inhibiting the HGF/MET pathway using lidocaine can enhance the sensitivity of GBM cells to TMZ and reduce cell migration, providing a potential basis for developing novel therapeutic strategies for GBM.
多形性胶质母细胞瘤(GBM)是侵袭性最强的恶性脑肿瘤。目前,主要的临床治疗方法是手术切除与同期放化疗相结合,以替莫唑胺(TMZ)作为主要化疗药物。利多卡因是一种广泛使用的酰胺类局麻药,具有显著的抗癌作用。有报道称,肝细胞生长因子(HGF)/间充质上皮转化因子(MET)信号传导异常在脑肿瘤的进展中起作用。然而,利多卡因能否调节 GBM 中的 MET 通路仍不清楚。本研究利用生物信息学分析了HGF/MET通路的临床重要性。通过建立TMZ耐药细胞系,研究了利多卡因和TMZ联合治疗的影响。此外,还利用基因敲除技术研究并证实了利多卡因对细胞功能的影响。目前的研究结果表明,HGF/MET通路在脑癌中起着关键作用,它在GBM中的激活与恶性程度增加和患者预后较差有关。研究发现,HGF水平的升高及其受体的激活与GBM细胞对TMZ的耐药性有关。利多卡因能有效抑制 HGF/MET 通路,从而恢复 TMZ 耐药细胞对 TMZ 的敏感性。此外,利多卡因还能抑制细胞迁移。总之,这些结果表明,使用利多卡因抑制 HGF/MET 通路可以提高 GBM 细胞对 TMZ 的敏感性并减少细胞迁移,为开发 GBM 的新型治疗策略提供了潜在的基础。
{"title":"Lidocaine attenuates TMZ resistance and inhibits cell migration by modulating the MET pathway in glioblastoma cells.","authors":"Ming-Shan Chen, Zhi-Yong Chong, Cheng Huang, Hsiu-Chen Huang, Pin-Hsuan Su, Jui-Chieh Chen","doi":"10.3892/or.2024.8731","DOIUrl":"https://doi.org/10.3892/or.2024.8731","url":null,"abstract":"Glioblastoma multiforme (GBM) is the most aggressive type of malignant brain tumor. Currently, the predominant clinical treatment is the combination of surgical resection with concurrent radiotherapy and chemotherapy, using temozolomide (TMZ) as the primary chemotherapy drug. Lidocaine, a widely used amide‑based local anesthetic, has been found to have a significant anticancer effect. It has been reported that aberrant hepatocyte growth factor (HGF)/mesenchymal‑epithelial transition factor (MET) signaling plays a role in the progression of brain tumors. However, it remains unclear whether lidocaine can regulate the MET pathway in GBM. In the present study, the clinical importance of the HGF/MET pathway was analyzed using bioinformatics. By establishing TMZ‑resistant cell lines, the impact of combined treatment with lidocaine and TMZ was investigated. Additionally, the effects of lidocaine on cellular function were also examined and confirmed using knockdown techniques. The current findings revealed that the HGF/MET pathway played a key role in brain cancer, and its activation in GBM was associated with increased malignancy and poorer patient outcomes. Elevated HGF levels and activation of its receptor were found to be associated with TMZ resistance in GBM cells. Lidocaine effectively suppressed the HGF/MET pathway, thereby restoring TMZ sensitivity in TMZ‑resistant cells. Furthermore, lidocaine also inhibited cell migration. Overall, these results indicated that inhibiting the HGF/MET pathway using lidocaine can enhance the sensitivity of GBM cells to TMZ and reduce cell migration, providing a potential basis for developing novel therapeutic strategies for GBM.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140564595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Retracted] Chronic oxymatrine treatment induces resistance and epithelial‑mesenchymal transition through targeting the long non‑coding RNA MALAT1 in colorectal cancer cells. [撤稿】通过靶向长非编码 RNA MALAT1,慢性氧化苦参碱治疗可诱导结直肠癌细胞的抗药性和上皮-间质转化。
IF 4.2 3区 医学 Q1 Medicine Pub Date : 2024-04-12 DOI: 10.3892/or.2024.8732
Yibai Xiong, Jun Wang, Huirong Zhu, Lingshuang Liu, Yi Jiang
Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the cell migration and invasion assay data featured in Figs. 2B, 5C, 6B and C were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been submitted elsewhere prior to the submission of this paper to Oncology Reports, or were under consideration for publication at around the same time (one of which has been retracted). In view of the fact that certain of these data had already apparently been submitted for publication prior to the submission of this article to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 39: 967‑976, 2018; DOI: 10.3892/or.2018.6204].
上述文章发表后,一位相关读者提请编辑注意,图 2B、5C、6B 和 C 中的某些细胞迁移和侵袭实验数据与不同研究机构不同作者撰写的其他文章中的数据极为相似,而这些文章要么在本文提交至《肿瘤学报告》之前已在其他地方发表,要么在同一时间正在考虑发表(其中一篇已被撤稿)。鉴于其中某些数据在本文提交给《肿瘤学报告》之前显然已经提交发表,编辑决定将本文从《肿瘤学报告》中撤回。经与作者联系,他们同意撤稿决定。对于给读者带来的不便,编辑深表歉意。[Oncology Reports 39: 967-976, 2018; DOI: 10.3892/or.2018.6204]。
{"title":"[Retracted] Chronic oxymatrine treatment induces resistance and epithelial‑mesenchymal transition through targeting the long non‑coding RNA MALAT1 in colorectal cancer cells.","authors":"Yibai Xiong, Jun Wang, Huirong Zhu, Lingshuang Liu, Yi Jiang","doi":"10.3892/or.2024.8732","DOIUrl":"https://doi.org/10.3892/or.2024.8732","url":null,"abstract":"Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the cell migration and invasion assay data featured in Figs. 2B, 5C, 6B and C were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been submitted elsewhere prior to the submission of this paper to Oncology Reports, or were under consideration for publication at around the same time (one of which has been retracted). In view of the fact that certain of these data had already apparently been submitted for publication prior to the submission of this article to <i>Oncology Reports</i>, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 39: 967‑976, 2018; DOI: 10.3892/or.2018.6204].","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140564601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Targeting BRD4: Potential therapeutic strategy for head and neck squamous cell carcinoma (Review). 靶向 BRD4:头颈部鳞状细胞癌的潜在治疗策略(综述)。
IF 4.2 3区 医学 Q1 Medicine Pub Date : 2024-04-12 DOI: 10.3892/or.2024.8733
Voraporn Yongprayoon, Napasporn Wattanakul, Winnada Khomate, Nathakrit Apithanangsiri, Tarathip Kasitipradit, Danupon Nantajit, Mahvash Tavassoli
As a member of BET (bromodomain and extra-terminal) protein family, BRD4 (bromodomain‑containing protein 4) is a chromatin‑associated protein that interacts with acetylated histones and actively recruits regulatory proteins, leading to the modulation of gene expression and chromatin remodeling. The cellular and epigenetic functions of BRD4 implicate normal development, fibrosis and inflammation. BRD4 has been suggested as a potential therapeutic target as it is often overexpressed and plays a critical role in regulating gene expression programs that drive tumor cell proliferation, survival, migration and drug resistance. To address the roles of BRD4 in cancer, several drugs that specifically target BRD4 have been developed. Inhibition of BRD4 has shown promising results in preclinical models, with several BRD4 inhibitors undergoing clinical trials for the treatment of various cancers. Head and neck squamous cell carcinoma (HNSCC), a heterogeneous group of cancers, remains a health challenge with a high incidence rate and poor prognosis. Conventional therapies for HNSCC often cause adverse effects to the patients. Targeting BRD4, therefore, represents a promising strategy to sensitize HNSCC to chemo‑ and radiotherapy allowing de‑intensification of the current therapeutic regime and subsequent reduced side effects. However, further studies are required to fully understand the underlying mechanisms of action of BRD4 in HNSCC in order to determine the optimal dosing and administration of BRD4‑targeted drugs for the treatment of patients with HNSCC.
BRD4(含溴多模域蛋白4)是BET(溴多模域和外端)蛋白家族的成员,是一种染色质相关蛋白,能与乙酰化组蛋白相互作用,并积极招募调控蛋白,从而调节基因表达和染色质重塑。BRD4 的细胞和表观遗传功能涉及正常发育、纤维化和炎症。BRD4被认为是一个潜在的治疗靶点,因为它经常被过度表达,并在调控基因表达程序中发挥着关键作用,而基因表达程序驱动着肿瘤细胞的增殖、存活、迁移和耐药性。为了研究 BRD4 在癌症中的作用,已经开发出了几种专门针对 BRD4 的药物。抑制 BRD4 在临床前模型中显示出良好的效果,目前有几种 BRD4 抑制剂正在用于治疗各种癌症的临床试验中。头颈部鳞状细胞癌(HNSCC)是一类异质性癌症,发病率高、预后差,仍然是一项健康挑战。治疗 HNSCC 的传统疗法往往会对患者造成不良影响。因此,以 BRD4 为靶点是使 HNSCC 对化疗和放疗敏感的一种有前途的策略,它能使目前的治疗方法不再强化,从而减少副作用。不过,还需要进一步研究,以充分了解 BRD4 在 HNSCC 中的基本作用机制,从而确定治疗 HNSCC 患者的 BRD4 靶向药物的最佳剂量和给药方式。
{"title":"Targeting BRD4: Potential therapeutic strategy for head and neck squamous cell carcinoma (Review).","authors":"Voraporn Yongprayoon, Napasporn Wattanakul, Winnada Khomate, Nathakrit Apithanangsiri, Tarathip Kasitipradit, Danupon Nantajit, Mahvash Tavassoli","doi":"10.3892/or.2024.8733","DOIUrl":"https://doi.org/10.3892/or.2024.8733","url":null,"abstract":"As a member of BET (bromodomain and extra-terminal) protein family, BRD4 (bromodomain‑containing protein 4) is a chromatin‑associated protein that interacts with acetylated histones and actively recruits regulatory proteins, leading to the modulation of gene expression and chromatin remodeling. The cellular and epigenetic functions of BRD4 implicate normal development, fibrosis and inflammation. BRD4 has been suggested as a potential therapeutic target as it is often overexpressed and plays a critical role in regulating gene expression programs that drive tumor cell proliferation, survival, migration and drug resistance. To address the roles of BRD4 in cancer, several drugs that specifically target BRD4 have been developed. Inhibition of BRD4 has shown promising results in preclinical models, with several BRD4 inhibitors undergoing clinical trials for the treatment of various cancers. Head and neck squamous cell carcinoma (HNSCC), a heterogeneous group of cancers, remains a health challenge with a high incidence rate and poor prognosis. Conventional therapies for HNSCC often cause adverse effects to the patients. Targeting BRD4, therefore, represents a promising strategy to sensitize HNSCC to chemo‑ and radiotherapy allowing de‑intensification of the current therapeutic regime and subsequent reduced side effects. However, further studies are required to fully understand the underlying mechanisms of action of BRD4 in HNSCC in order to determine the optimal dosing and administration of BRD4‑targeted drugs for the treatment of patients with HNSCC.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140564606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Compound 225# inhibits the proliferation of human colorectal cancer cells by promoting cell cycle arrest and apoptosis induction. 化合物 225#通过促进细胞周期停滞和诱导细胞凋亡来抑制人类结直肠癌细胞的增殖。
IF 4.2 3区 医学 Q1 Medicine Pub Date : 2024-04-05 DOI: 10.3892/or.2024.8729
Xiaoxue Zhang, Liujun He, Yong Li, Yifei Qiu, Wujing Hu, Wanying Lu, Huihui Du, Donglin Yang
Colorectal cancer (CRC) ranks as the second leading cause of cancer‑related death worldwide due to its aggressive nature. After surgical resection, >50% of patients with CRC require adjuvant therapy. As a result, eradicating cancer cells with medications is a promising method to treat patients with CRC. In the present study, a novel compound was synthesized, which was termed compound 225#. The inhibitory activity of compound 225# against CRC was determined by MTT assay, EdU fluorescence labeling and colony formation assay; the effects of compound 225# on the cell cycle progression and apoptosis of CRC cells were detected by flow cytometry and western blotting; and the changes in autophagic flux after the administration of compound 225# were detected using the double fluorescence fusion protein mCherry‑GFP‑LC3B and western blotting. The results demonstrated that compound 225# exhibited antiproliferative properties, inhibiting the proliferation and expansion of CRC cell lines in a time‑ and dose‑dependent manner. Furthermore, compound 225# triggered G2/M cell cycle arrest by influencing the expression of cell cycle regulators, such as CDK1, cyclin A1 and cyclin B1, which is also closely related to the activation of DNA damage pathways. The cleavage of PARP and increased protein expression levels of PUMA suggested that apoptosis was triggered after treatment with compound 225#. Moreover, the increase in LC3‑II expression and stimulation of autophagic flux indicated the activation of an autophagy pathway. Notably, compound 225# induced autophagy, which was associated with endoplasmic reticulum (ER) stress. In accordance with the in vitro findings, the in vivo results demonstrated that compound 225# effectively inhibited the growth of HCT116 tumors in mice without causing any changes in their body weight. Collectively, the present results demonstrated that compound 225# not only inhibited proliferation and promoted G2/M‑phase cell cycle arrest and apoptosis, but also initiated cytoprotective autophagy in CRC cells by activating ER stress pathways. Taken together, these findings provide an experimental basis for the evaluation of compound 225# as a novel potential medication for CRC treatment.
结肠直肠癌(CRC)因其侵袭性而成为全球癌症相关死亡的第二大原因。手术切除后,50% 的 CRC 患者需要进行辅助治疗。因此,用药物消灭癌细胞是治疗 CRC 患者的一种很有前景的方法。本研究合成了一种新型化合物,称为化合物 225#。化合物 225#对 CRC 的抑制活性通过 MTT 试验、EdU 荧光标记和集落形成试验进行测定;化合物 225#对 CRC 细胞周期进展和细胞凋亡的影响通过流式细胞术和 Western 印迹法进行检测;服用化合物 225#后自噬通量的变化通过双荧光融合蛋白 mCherry-GFP-LC3B 和 Western 印迹法进行检测。结果表明,化合物 225#具有抗增殖特性,能以时间和剂量依赖的方式抑制 CRC 细胞株的增殖和扩增。此外,化合物 225# 通过影响 CDK1、细胞周期蛋白 A1 和细胞周期蛋白 B1 等细胞周期调节因子的表达,引发 G2/M 细胞周期停滞,这也与 DNA 损伤通路的激活密切相关。PARP 的裂解和 PUMA 蛋白表达水平的升高表明,在使用化合物 225#处理后,细胞凋亡被触发。此外,LC3-II 表达的增加和自噬通量的刺激表明自噬途径被激活。值得注意的是,化合物 225#诱导的自噬与内质网(ER)应激有关。与体外研究结果一致,体内研究结果表明,化合物 225# 能有效抑制小鼠 HCT116 肿瘤的生长,且不会引起体重变化。综上所述,本研究结果表明,化合物 225#不仅能抑制增殖、促进 G2/M 期细胞周期停滞和细胞凋亡,还能通过激活 ER 应激途径启动 CRC 细胞的细胞保护性自噬。综上所述,这些发现为评估化合物 225#作为治疗 CRC 的新型潜在药物提供了实验依据。
{"title":"Compound 225# inhibits the proliferation of human colorectal cancer cells by promoting cell cycle arrest and apoptosis induction.","authors":"Xiaoxue Zhang, Liujun He, Yong Li, Yifei Qiu, Wujing Hu, Wanying Lu, Huihui Du, Donglin Yang","doi":"10.3892/or.2024.8729","DOIUrl":"https://doi.org/10.3892/or.2024.8729","url":null,"abstract":"Colorectal cancer (CRC) ranks as the second leading cause of cancer‑related death worldwide due to its aggressive nature. After surgical resection, &gt;50% of patients with CRC require adjuvant therapy. As a result, eradicating cancer cells with medications is a promising method to treat patients with CRC. In the present study, a novel compound was synthesized, which was termed compound 225#. The inhibitory activity of compound 225# against CRC was determined by MTT assay, EdU fluorescence labeling and colony formation assay; the effects of compound 225# on the cell cycle progression and apoptosis of CRC cells were detected by flow cytometry and western blotting; and the changes in autophagic flux after the administration of compound 225# were detected using the double fluorescence fusion protein mCherry‑GFP‑LC3B and western blotting. The results demonstrated that compound 225# exhibited antiproliferative properties, inhibiting the proliferation and expansion of CRC cell lines in a time‑ and dose‑dependent manner. Furthermore, compound 225# triggered G<sub>2</sub>/M cell cycle arrest by influencing the expression of cell cycle regulators, such as CDK1, cyclin A1 and cyclin B1, which is also closely related to the activation of DNA damage pathways. The cleavage of PARP and increased protein expression levels of PUMA suggested that apoptosis was triggered after treatment with compound 225#. Moreover, the increase in LC3‑II expression and stimulation of autophagic flux indicated the activation of an autophagy pathway. Notably, compound 225# induced autophagy, which was associated with endoplasmic reticulum (ER) stress. In accordance with the <i>in vitro</i> findings, the <i>in vivo</i> results demonstrated that compound 225# effectively inhibited the growth of HCT116 tumors in mice without causing any changes in their body weight. Collectively, the present results demonstrated that compound 225# not only inhibited proliferation and promoted G<sub>2</sub>/M‑phase cell cycle arrest and apoptosis, but also initiated cytoprotective autophagy in CRC cells by activating ER stress pathways. Taken together, these findings provide an experimental basis for the evaluation of compound 225# as a novel potential medication for CRC treatment.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140564515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Butyrate increases methylglyoxal production through regulation of the JAK2/Stat3/Nrf2/Glo1 pathway in castration‑resistant prostate cancer cells. 丁酸盐通过调节耐阉割前列腺癌细胞中的JAK2/Stat3/Nrf2/Glo1途径增加甲基乙二酸的产生。
IF 4.2 3区 医学 Q1 Medicine Pub Date : 2024-04-05 DOI: 10.3892/or.2024.8730
Yi-Jan Hsia, Zhang-Min Lin, Taolan Zhang, Tz-Chong Chou
Cancer cells are characterized by increased glycolysis, known as the Warburg effect, which leads to increased production of cytotoxic methylglyoxal (MGO) and apoptotic cell death. Cancer cells often activate the protective nuclear factor erythroid 2‑related factor2 (Nrf2)/glyoxalase1 (Glo1) system to detoxify MGO. The effects of sodium butyrate (NaB), a product of gut microbiota, on Nrf2/Glos/MGO pathway and the underlying mechanisms in prostate cancer (PCa) cells were investigated in the present study. Treatment with NaB induced the cell death and reduced the proliferation of PCa cells (DU145 and LNCap). Moreover, the protein kinase RNA-like endoplasmic reticulum kinase/Nrf2/Glo1 pathway was greatly inhibited by NaB, thereby accumulating MGO-derived adduct hydroimidazolone (MG-H1). In response to a high amount of MGO, the expression of Nrf2 and Glo1 was attenuated, coinciding with an increased cellular death. NaB also markedly inhibited the Janus kinase 2 (JAK2)/Signal transducer and activator of transcription 3 (Stat3) pathway. Conversely, co‑treatment with Colivelin, a Stat3 activator, significantly reversed the effects of NaB on Glo1 expression, MG-H1 production, and the cell migration and viability. As expected, overexpression of Stat3 or Glo1 reduced NaB‑induced cell death. The activation of calcium/calmodulin dependent protein kinase II gamma and reactive oxygen species production also contributed to the anticancer effect of NaB. The present study, for the first time, demonstrated that NaB greatly increases MGO production through suppression of the JAK2/Stat3/Nrf2/Glo1 pathway in DU145 cells, a cell line mimicking castration‑resistant PCa (CRPC), suggesting that NaB may be a potential agent for PCa therapy.
癌细胞的特点是糖酵解增加,即所谓的沃伯格效应,这会导致细胞毒性甲基乙二醛(MGO)的产生和细胞凋亡增加。癌细胞通常会激活保护性核因子红细胞2相关因子2(Nrf2)/乙二醛酶1(Glo1)系统来解毒MGO。本研究探讨了肠道微生物群产物丁酸钠(NaB)对前列腺癌(PCa)细胞中Nrf2/Glos/MGO通路的影响及其内在机制。用 NaB 处理可诱导 PCa 细胞(DU145 和 LNCap)死亡并减少其增殖。此外,NaB还极大地抑制了蛋白激酶RNA样内质网激酶/Nrf2/Glo1通路,从而积累了MGO衍生的加合物氢咪唑酮(MG-H1)。在大量 MGO 的作用下,Nrf2 和 Glo1 的表达减弱,同时细胞死亡增加。NaB 还明显抑制了 Janus 激酶 2(JAK2)/信号转导和转录激活因子 3(Stat3)通路。相反,与 Stat3 激活剂 Colivelin 联合处理可显著逆转 NaB 对 Glo1 表达、MG-H1 生成以及细胞迁移和活力的影响。正如预期的那样,Stat3 或 Glo1 的过表达可减少 NaB 诱导的细胞死亡。钙/钙调蛋白依赖性蛋白激酶Ⅱγ的活化和活性氧的产生也有助于NaB的抗癌作用。本研究首次证明,NaB 通过抑制 JAK2/Stat3/Nrf2/Glo1 通路大大增加了 DU145 细胞(一种模拟阉割耐药 PCa(CRPC)的细胞系)中 MGO 的产生,这表明 NaB 可能是一种治疗 PCa 的潜在药物。
{"title":"Butyrate increases methylglyoxal production through regulation of the JAK2/Stat3/Nrf2/Glo1 pathway in castration‑resistant prostate cancer cells.","authors":"Yi-Jan Hsia, Zhang-Min Lin, Taolan Zhang, Tz-Chong Chou","doi":"10.3892/or.2024.8730","DOIUrl":"https://doi.org/10.3892/or.2024.8730","url":null,"abstract":"Cancer cells are characterized by increased glycolysis, known as the Warburg effect, which leads to increased production of cytotoxic methylglyoxal (MGO) and apoptotic cell death. Cancer cells often activate the protective nuclear factor erythroid 2‑related factor2 (Nrf2)/glyoxalase1 (Glo1) system to detoxify MGO. The effects of sodium butyrate (NaB), a product of gut microbiota, on Nrf2/Glos/MGO pathway and the underlying mechanisms in prostate cancer (PCa) cells were investigated in the present study. Treatment with NaB induced the cell death and reduced the proliferation of PCa cells (DU145 and LNCap). Moreover, the protein kinase RNA-like endoplasmic reticulum kinase/Nrf2/Glo1 pathway was greatly inhibited by NaB, thereby accumulating MGO-derived adduct hydroimidazolone (MG-H1). In response to a high amount of MGO, the expression of Nrf2 and Glo1 was attenuated, coinciding with an increased cellular death. NaB also markedly inhibited the Janus kinase 2 (JAK2)/Signal transducer and activator of transcription 3 (Stat3) pathway. Conversely, co‑treatment with Colivelin, a Stat3 activator, significantly reversed the effects of NaB on Glo1 expression, MG-H1 production, and the cell migration and viability. As expected, overexpression of Stat3 or Glo1 reduced NaB‑induced cell death. The activation of calcium/calmodulin dependent protein kinase II gamma and reactive oxygen species production also contributed to the anticancer effect of NaB. The present study, for the first time, demonstrated that NaB greatly increases MGO production through suppression of the JAK2/Stat3/Nrf2/Glo1 pathway in DU145 cells, a cell line mimicking castration‑resistant PCa (CRPC), suggesting that NaB may be a potential agent for PCa therapy.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140564518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Retracted] Sulforaphane sensitizes human cholangiocarcinoma to cisplatin via the downregulation of anti‑apoptotic proteins. [撤稿] 透骨草素通过下调抗凋亡蛋白使人胆管癌对顺铂敏感。
IF 4.2 3区 医学 Q1 Medicine Pub Date : 2024-04-05 DOI: 10.3892/or.2024.8728
Rokas Račkauskas, Dachen Zhou, Simonas Ūselis, Kęstutis Strupas, Ingrid Herr, Peter Schemmer
Following the publication of the above article and a corrigendum that was published in October 2023 to address the issue of misplaced control β‑actin western blots comparing between Figs. 3 and 4A (doi: 10.3892/or.2023.8646), an attentive reader drew to the authors' attention that the first author had apparently made additional unreported corrections to the revised version of Fig. 4 presented in the corrigendum. Although these image discrepancies did not alter the study's primary conclusions, they were such that they did cast doubt on the data's integrity. Consequently, the authors have decided to retract the paper and the Editor of Oncology Reports has agreed to the authors' request. The authors deeply regret any confusion or inconvenience this retraction may cause, and offer their sincere apologies to the Editor of Oncology Reports and the readership. [Oncology Reports 37: 3660‑3666, 2017; DOI: 10.3892/or.2017.5622].
上述文章发表后,作者于2023年10月发表了更正,以解决图3和图4A对照β-肌动蛋白Western印迹对比错位的问题(doi: 10.3892/or.2023.8646),一位细心的读者提请作者注意,第一作者显然对更正中的图4修订版做了更多未报告的更正。尽管这些图像差异并没有改变研究的主要结论,但它们确实对数据的完整性产生了怀疑。因此,作者决定撤回论文,《肿瘤学报告》编辑也同意了作者的请求。作者对撤稿可能造成的混乱或不便深表遗憾,并向《肿瘤学报告》编辑和读者致以诚挚的歉意。[Oncology Reports 37: 3660-3666, 2017; DOI: 10.3892/or.2017.5622]。
{"title":"[Retracted] Sulforaphane sensitizes human cholangiocarcinoma to cisplatin via the downregulation of anti‑apoptotic proteins.","authors":"Rokas Račkauskas, Dachen Zhou, Simonas Ūselis, Kęstutis Strupas, Ingrid Herr, Peter Schemmer","doi":"10.3892/or.2024.8728","DOIUrl":"https://doi.org/10.3892/or.2024.8728","url":null,"abstract":"Following the publication of the above article and a corrigendum that was published in October 2023 to address the issue of misplaced control β‑actin western blots comparing between Figs. 3 and 4A (doi: 10.3892/or.2023.8646), an attentive reader drew to the authors' attention that the first author had apparently made additional unreported corrections to the revised version of Fig. 4 presented in the corrigendum. Although these image discrepancies did not alter the study's primary conclusions, they were such that they did cast doubt on the data's integrity. Consequently, the authors have decided to retract the paper and the Editor of <i>Oncology Reports</i> has agreed to the authors' request. The authors deeply regret any confusion or inconvenience this retraction may cause, and offer their sincere apologies to the Editor of <i>Oncology Reports</i> and the readership. [Oncology Reports 37: 3660‑3666, 2017; DOI: 10.3892/or.2017.5622].","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140564596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Retracted] Downregulation of microRNA-206 suppresses clear cell renal carcinoma proliferation and invasion by targeting vascular endothelial growth factor A. [撤稿】通过靶向血管内皮生长因子 A 下调 microRNA-206 可抑制透明细胞肾癌的增殖和侵袭。
IF 4.2 3区 医学 Q1 Medicine Pub Date : 2024-04-01 Epub Date: 2024-03-01 DOI: 10.3892/or.2024.8717
Yi Cai, Hanzhong Li, Yushi Zhang

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that there appeared to be several instances of overlapping data panels comparing between the Transwell invasion and migration assay images shown in Figs. 2E and 4G, such that data which were intended to show the results from differently performed experiments were apparently derived from a (much) smaller number of original sources. Given the number of cases of overlapping data panels both within and between this pair of figures in the article itself, the Editor of Oncology Reports has decided that this paper should be retracted from the Journal on the basis of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 35: 1778-1786, 2016; DOI: 10.3892/or.2015.4538].

上述论文发表后,一位相关读者提请编辑注意,在图 2E 和图 4G 所示的 Transwell 侵袭和迁移实验图像之间,似乎有多处数据板重叠的情况,这样一来,原本用于显示不同实验结果的数据显然来自(少得多的)原始来源。鉴于文章本身的这对图中和这对图之间存在大量数据面板重叠的情况,《肿瘤学报告》的编辑决定以对所提供的数据缺乏信心为由从杂志上撤回这篇论文。作者被要求解释这些问题,但编辑部没有收到回复。对于给读者带来的不便,编辑深表歉意。[肿瘤学报告 35: 1778-1786, 2016; DOI: 10.3892/or.2015.4538]。
{"title":"[Retracted] Downregulation of microRNA-206 suppresses clear cell renal carcinoma proliferation and invasion by targeting vascular endothelial growth factor A.","authors":"Yi Cai, Hanzhong Li, Yushi Zhang","doi":"10.3892/or.2024.8717","DOIUrl":"10.3892/or.2024.8717","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that there appeared to be several instances of overlapping data panels comparing between the Transwell invasion and migration assay images shown in Figs. 2E and 4G, such that data which were intended to show the results from differently performed experiments were apparently derived from a (much) smaller number of original sources. Given the number of cases of overlapping data panels both within and between this pair of figures in the article itself, the Editor of <i>Oncology Reports</i> has decided that this paper should be retracted from the Journal on the basis of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 35: 1778-1786, 2016; DOI: 10.3892/or.2015.4538].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10915703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139996933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
α‑Phellandrene enhances the apoptosis of HT‑29 cells induced by 5‑fluorouracil by modulating the mitochondria‑dependent pathway. α-黄柏烯通过调节线粒体依赖途径,增强 5-氟尿嘧啶诱导的 HT-29 细胞凋亡。
IF 4.2 3区 医学 Q1 Medicine Pub Date : 2024-04-01 Epub Date: 2024-03-08 DOI: 10.3892/or.2024.8720
Anita Caroline Susanto, Laksmi Hartajanie, Chih-Chung Wu

α‑Phellandrene (α‑PA), a natural constituent of herbs, inhibits cancer cell viability and proliferation. 5‑Fluorouracil (5‑FU) is a frequently utilized chemotherapeutic medicine for the treatment of colon cancer, which works by triggering cancer cell apoptosis. The present study examined how the combination of α‑PA and 5‑FU affects the suppression of human colon cancer cells by promoting apoptosis. The impact of this treatment on cell viability, apoptosis, and the expression levels of Bcl‑2 family members, caspase family members and mitochondria‑related molecules in HT‑29 cells was assessed by the MTT assay, immunocytochemistry, western blotting and quantitative PCR. The combination of 5‑FU and α‑PA had a synergistic inhibitory effect on cell viability, as determined by assessing the combination index value. Bax protein expression levels were higher in the 50, 100 or 250 µM α‑PA combined with 5‑FU groups compared with those in the 5‑FU alone group (P<0.05). By contrast, Bcl‑2 protein expression levels and mitochondrial membrane potential (MMP, ΔΨm) were lower in the 100 or 250 µM α‑PA combined with 5‑FU groups than those in the 5‑FU alone group (P<0.05). In addition, hexokinase‑2 (HK‑2) protein expression levels were lower in the 50, 100 or 250 µM α‑PA combined with 5‑FU groups than those in the 5‑FU alone group (P<0.05). Compared with 5‑FU alone, after HT‑29 cells were treated with 50, 100 or 250 µM α‑PA combined with 5‑FU, the mRNA expression levels of extrinsic‑induced apoptotic molecules, including caspase‑8 and Bid, were higher (P<0.05). Treatment with 50, 100 or 250 µM α‑PA combined with 5‑FU also increased the mRNA expression levels of cytochrome c, caspase‑9 and caspase‑3, regulating intrinsic apoptosis (P<0.05). These results showed that α‑PA and 5‑FU had a synergistic effect on reducing the viability of human colon cancer HT‑29 cells by inducing extrinsic and intrinsic apoptosis pathways. The mechanism by which apoptosis is induced may involve the intrinsic apoptosis pathway that activates the mitochondria‑dependent pathway, including regulating the expression levels of Bcl‑2 family members, including Bax, Bcl‑2 and Bid, regulating MMP and HK‑2 expression levels, and increasing the expression of caspase cascade molecules, including caspase‑9 and caspase‑3. In addition, it may involve the extrinsic apoptosis pathway that activates caspase‑8 and caspase‑3 leading to apoptosis.

α-黄柏烯(α-PA)是一种天然草药成分,可抑制癌细胞的活力和增殖。5-氟尿嘧啶(5-FU)是治疗结肠癌的常用化疗药物,它通过诱导癌细胞凋亡发挥作用。本研究探讨了 α-PA 和 5-FU 如何通过促进细胞凋亡来抑制人结肠癌细胞。本研究通过 MTT 检测法、免疫细胞化学法、Western 印迹法和定量 PCR 法评估了该疗法对 HT-29 细胞活力、凋亡以及 Bcl-2 家族成员、caspase 家族成员和线粒体相关分子表达水平的影响。5-FU和α-PA的组合对细胞活力有协同抑制作用,这可以通过评估组合指数值来确定。与单用 5-FU 组相比,50、100 或 250 µM α-PA 联合 5-FU 组的 Bax 蛋白表达水平更高(P<0.05)。
{"title":"α‑Phellandrene enhances the apoptosis of HT‑29 cells induced by 5‑fluorouracil by modulating the mitochondria‑dependent pathway.","authors":"Anita Caroline Susanto, Laksmi Hartajanie, Chih-Chung Wu","doi":"10.3892/or.2024.8720","DOIUrl":"10.3892/or.2024.8720","url":null,"abstract":"<p><p>α‑Phellandrene (α‑PA), a natural constituent of herbs, inhibits cancer cell viability and proliferation. 5‑Fluorouracil (5‑FU) is a frequently utilized chemotherapeutic medicine for the treatment of colon cancer, which works by triggering cancer cell apoptosis. The present study examined how the combination of α‑PA and 5‑FU affects the suppression of human colon cancer cells by promoting apoptosis. The impact of this treatment on cell viability, apoptosis, and the expression levels of Bcl‑2 family members, caspase family members and mitochondria‑related molecules in HT‑29 cells was assessed by the MTT assay, immunocytochemistry, western blotting and quantitative PCR. The combination of 5‑FU and α‑PA had a synergistic inhibitory effect on cell viability, as determined by assessing the combination index value. Bax protein expression levels were higher in the 50, 100 or 250 µM α‑PA combined with 5‑FU groups compared with those in the 5‑FU alone group (P<0.05). By contrast, Bcl‑2 protein expression levels and mitochondrial membrane potential (MMP, ΔΨm) were lower in the 100 or 250 µM α‑PA combined with 5‑FU groups than those in the 5‑FU alone group (P<0.05). In addition, hexokinase‑2 (HK‑2) protein expression levels were lower in the 50, 100 or 250 µM α‑PA combined with 5‑FU groups than those in the 5‑FU alone group (P<0.05). Compared with 5‑FU alone, after HT‑29 cells were treated with 50, 100 or 250 µM α‑PA combined with 5‑FU, the mRNA expression levels of extrinsic‑induced apoptotic molecules, including caspase‑8 and Bid, were higher (P<0.05). Treatment with 50, 100 or 250 µM α‑PA combined with 5‑FU also increased the mRNA expression levels of cytochrome c, caspase‑9 and caspase‑3, regulating intrinsic apoptosis (P<0.05). These results showed that α‑PA and 5‑FU had a synergistic effect on reducing the viability of human colon cancer HT‑29 cells by inducing extrinsic and intrinsic apoptosis pathways. The mechanism by which apoptosis is induced may involve the intrinsic apoptosis pathway that activates the mitochondria‑dependent pathway, including regulating the expression levels of Bcl‑2 family members, including Bax, Bcl‑2 and Bid, regulating MMP and HK‑2 expression levels, and increasing the expression of caspase cascade molecules, including caspase‑9 and caspase‑3. In addition, it may involve the extrinsic apoptosis pathway that activates caspase‑8 and caspase‑3 leading to apoptosis.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10940876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Oncology reports
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1