Subsequently to the publication of the above paper, the authors drew to the attention of the Editorial Office that they made a couple of errors in terms of the data assembly in Figs. 2 and 4 in their paper; specifically, the Transwell assay data shown for the 'miR-320a+/FoxM1+' panel in Fig. 5D on p. 1923 also appeared as the 'ACTN/NC' data panel in Fig. 4E on the same page (Fig. 4E contained the erroneously duplicated panel). In addition, data featured in Fig. 2D of the above paper were strikingly similar to data that appeared in Fig. 6e of the following paper, published subsequently to this article, written by different authors (although a Dr Shiyue Zhao worked in the molecular biology laboratory of Harbin Medical University from 2017 to 2018, and the research collaboration was conducted with Dr Chenlong Li's research group): Li C, Zheng H, Hou W, Bao H, Xiong J, Che W, Gu Y, Sun H and Liang P: Long non-coding RNA linc00645 promotes. TGF-β-induced epithelial-mesenchymal transition by regulating miR-205-3p-ZEB1 axis in glioma. Cell Death Dis 10: 17, 2019. Finally, after having conducted an independent investigation of the data in this paper, the Editorial Office noted that one of the Petri dish images in Fig. 2C was also strikingly similar to data that appeared in Fig. 2H of the abovementioned article in the journal Cell Death & Disease. After having considered the authors' request for corrigendum, in view of the problems that were identified with the data, the Editor of Oncology Reports has decided that, owing to a lack of confidence in the presented data, the paper should instead be retracted from the journal. After having informed the authors of this decision, they accepted the decision to retract this paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 40: 1917‑1926, 2018; DOI: 10.3892/or.2018.6597].
在上述论文发表后,作者提请编辑部注意,他们在论文图 2 和图 4 的数据组合方面犯了几个错误;具体地说,第 1923 页图 5D 中 "miR-320a+/FoxM1+"板块的 Transwell 试验数据也作为 "ACTN/NC "数据板块出现在同一页的图 4E 中(图 4E 包含错误重复的板块)。此外,上述论文图 2D 中的数据与以下论文图 6e 中的数据惊人地相似,该论文发表于本文之后,由不同作者撰写(尽管赵世跃博士于 2017 年至 2018 年在哈尔滨医科大学分子生物学实验室工作,研究合作是与李晨龙博士的研究小组进行的):Li C, Zheng H, Hou W, Bao H, Xiong J, Che W, Gu Y, Sun H and Liang P: Long non-coding RNA linc00645 promotes.TGF-β- induced epithelial-mesenchymal transition by regulating miR-205-3p-ZEB1 axis in glioma.Cell Death Dis 10: 17, 2019.最后,在对本文数据进行独立调查后,编辑部注意到图 2C 中的一个培养皿图像也与上述《细胞死亡与疾病》杂志文章图 2H 中的数据惊人相似。肿瘤学报告》编辑在考虑了作者的更正请求后,鉴于发现的数据问题,决定由于对所提交的数据缺乏信心,该论文应从该杂志上撤下。在通知作者这一决定后,他们接受了撤稿的决定。对于给读者带来的不便,编辑深表歉意。 [Oncology Reports 40: 1917-1926, 2018; DOI: 10.3892/or.2018.6597].
{"title":"[Retracted] MicroRNA‑320a suppresses tumour cell proliferation and invasion of renal cancer cells by targeting FoxM1.","authors":"Shiyue Zhao, Yangwei Wang, Yan Lou, Yonggang Wang, Jing Sun, Manyu Luo, Wen Li, Lining Miao","doi":"10.3892/or.2024.8754","DOIUrl":"10.3892/or.2024.8754","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, the authors drew to the attention of the Editorial Office that they made a couple of errors in terms of the data assembly in Figs. 2 and 4 in their paper; specifically, the Transwell assay data shown for the 'miR-320a+/FoxM1+' panel in Fig. 5D on p. 1923 also appeared as the 'ACTN/NC' data panel in Fig. 4E on the same page (Fig. 4E contained the erroneously duplicated panel). In addition, data featured in Fig. 2D of the above paper were strikingly similar to data that appeared in Fig. 6e of the following paper, published subsequently to this article, written by different authors (although a Dr Shiyue Zhao worked in the molecular biology laboratory of Harbin Medical University from 2017 to 2018, and the research collaboration was conducted with Dr Chenlong Li's research group): Li C, Zheng H, Hou W, Bao H, Xiong J, Che W, Gu Y, Sun H and Liang P: Long non-coding RNA linc00645 promotes. TGF-β-induced epithelial-mesenchymal transition by regulating miR-205-3p-ZEB1 axis in glioma. Cell Death Dis 10: 17, 2019. Finally, after having conducted an independent investigation of the data in this paper, the Editorial Office noted that one of the Petri dish images in Fig. 2C was also strikingly similar to data that appeared in Fig. 2H of the abovementioned article in the journal <i>Cell Death & Disease</i>. After having considered the authors' request for corrigendum, in view of the problems that were identified with the data, the Editor of <i>Oncology Reports</i> has decided that, owing to a lack of confidence in the presented data, the paper should instead be retracted from the journal. After having informed the authors of this decision, they accepted the decision to retract this paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 40: 1917‑1926, 2018; DOI: 10.3892/or.2018.6597].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11184357/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141317898","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}
Inotuzumab ozogamicin (IO), a novel therapeutic drug for relapsed or refractory acute lymphoblastic leukemia (RR)‑(ALL), is a humanized anti‑cluster of differentiation (CD) 22 monoclonal antibody conjugated with calicheamicin that causes DNA single‑ and double‑strand breaks. Although the efficacy of IO is significantly improved compared with that of conventional chemotherapies, the prognosis for RR‑ALL remains poor, highlighting the need for more effective treatment strategies. The present study examined the role of DNA damage repair inhibition using the poly (ADP‑ribose) polymerase (PARP) inhibitors olaparib or talazoparib on the enhancement of the antitumor effects of IO on B‑ALL cells in vitro. The Reh, Philadelphia (Ph)‑B‑ALL and the SUP‑B15 Ph+ B‑ALL cell lines were used for experiments. Both cell lines were ~90% CD22+. The half‑maximal inhibitory concentration (IC50) values of IO were 5.3 and 49.7 ng/ml for Reh and SUP‑B15 cells, respectively. The IC50 values of IO combined with minimally toxic concentrations of olaparib or talazoparib were 0.8 and 2.9 ng/ml for Reh cells, respectively, and 36.1 and 39.6 ng/ml for SUP‑B15 cells, respectively. The combination index of IO with olaparib and talazoparib were 0.19 and 0.56 for Reh cells and 0.76 and 0.89 for SUP‑B15 cells, demonstrating synergistic effects in all combinations. Moreover, the addition of minimally toxic concentrations of PARP inhibitors augmented IO‑induced apoptosis. The alkaline comet assay, which quantitates the amount of DNA strand breaks, was used to investigate the degree to which DNA damage observed 1 h after IO administration was repaired 6 h later, reflecting successful repair of DNA strand breaks. However, DNA strand breaks persisted 6 h after IO administration combined with olaparib or talazoparib, suggesting inhibition of the repair processes by PARP inhibitors. Adding olaparib or talazoparib thus synergized the antitumor effects of IO by inhibiting DNA strand break repair via the inhibition of PARP.
{"title":"Combining inotuzumab ozogamicin with PARP inhibitors olaparib and talazoparib exerts synergistic cytotoxicity in acute lymphoblastic leukemia by inhibiting DNA strand break repair.","authors":"Naoko Ida, Miyuki Okura, Saki Tanaka, Naoko Hosono, Takahiro Yamauchi","doi":"10.3892/or.2024.8749","DOIUrl":"10.3892/or.2024.8749","url":null,"abstract":"<p><p>Inotuzumab ozogamicin (IO), a novel therapeutic drug for relapsed or refractory acute lymphoblastic leukemia (RR)‑(ALL), is a humanized anti‑cluster of differentiation (CD) 22 monoclonal antibody conjugated with calicheamicin that causes DNA single‑ and double‑strand breaks. Although the efficacy of IO is significantly improved compared with that of conventional chemotherapies, the prognosis for RR‑ALL remains poor, highlighting the need for more effective treatment strategies. The present study examined the role of DNA damage repair inhibition using the poly (ADP‑ribose) polymerase (PARP) inhibitors olaparib or talazoparib on the enhancement of the antitumor effects of IO on B‑ALL cells <i>in vitro</i>. The Reh, Philadelphia (Ph)<sup>‑</sup>B‑ALL and the SUP‑B15 Ph<sup>+</sup> B‑ALL cell lines were used for experiments. Both cell lines were ~90% CD22<sup>+</sup>. The half‑maximal inhibitory concentration (IC<sub>50</sub>) values of IO were 5.3 and 49.7 ng/ml for Reh and SUP‑B15 cells, respectively. The IC<sub>50</sub> values of IO combined with minimally toxic concentrations of olaparib or talazoparib were 0.8 and 2.9 ng/ml for Reh cells, respectively, and 36.1 and 39.6 ng/ml for SUP‑B15 cells, respectively. The combination index of IO with olaparib and talazoparib were 0.19 and 0.56 for Reh cells and 0.76 and 0.89 for SUP‑B15 cells, demonstrating synergistic effects in all combinations. Moreover, the addition of minimally toxic concentrations of PARP inhibitors augmented IO‑induced apoptosis. The alkaline comet assay, which quantitates the amount of DNA strand breaks, was used to investigate the degree to which DNA damage observed 1 h after IO administration was repaired 6 h later, reflecting successful repair of DNA strand breaks. However, DNA strand breaks persisted 6 h after IO administration combined with olaparib or talazoparib, suggesting inhibition of the repair processes by PARP inhibitors. Adding olaparib or talazoparib thus synergized the antitumor effects of IO by inhibiting DNA strand break repair via the inhibition of PARP.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141086311","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}
Pub Date : 2024-07-01Epub Date: 2024-06-21DOI: 10.3892/or.2024.8757
Jing Luan, Yuxin Liu, Meng Cao, Xianing Guo, Na Guo
Cytotoxic T lymphocytes (CTLs), also known as CD8+ T cells, participate in immune function by secreting various cytokines after recognizing specific antigens and class I major histocompatibility complex molecules associated with tumor cells, and thus have a key role in antitumor immunity. However, certain CD8+ T cells show low reactivity and thus cannot effectively remove tumor cells or viral antigens. Due to this heterogeneity, effective biomarkers representing these differences in CD8+ cells are needed. The identification of suitable biomarkers will also enhance the management of cancer treatment. Recent research has improved the understanding of CD8+ T lymphocytes in the tumor microenvironment and circulatory system. Treatment efficacy is impacted directly by the pathogenic response of CTLs, and thus, the use of adjuvant therapies to address these pathological changes, e.g., stimulating the increase in the proportion of reactive T cells or suppressing the proportion of terminally exhausted T cells, would be advantageous.
细胞毒性 T 淋巴细胞(CTL)又称 CD8+ T 细胞,在识别与肿瘤细胞相关的特异性抗原和 I 类主要组织相容性复合体分子后分泌各种细胞因子,从而参与免疫功能,在抗肿瘤免疫中发挥关键作用。然而,某些 CD8+ T 细胞的反应性较低,因此不能有效清除肿瘤细胞或病毒抗原。由于这种异质性,需要有效的生物标记物来代表 CD8+ 细胞的这些差异。确定合适的生物标志物也将提高癌症治疗的管理水平。最近的研究加深了人们对肿瘤微环境和循环系统中 CD8+ T 淋巴细胞的了解。CTL 的病理反应直接影响治疗效果,因此,针对这些病理变化使用辅助疗法(如刺激反应性 T 细胞比例的增加或抑制终末衰竭 T 细胞的比例)将是有利的。
{"title":"The pathogenic response of cytotoxic T‑lymphocytes, a common therapeutic target for cancer, has a direct impact on treatment outcomes (Review).","authors":"Jing Luan, Yuxin Liu, Meng Cao, Xianing Guo, Na Guo","doi":"10.3892/or.2024.8757","DOIUrl":"10.3892/or.2024.8757","url":null,"abstract":"<p><p>Cytotoxic T lymphocytes (CTLs), also known as CD8<sup>+</sup> T cells, participate in immune function by secreting various cytokines after recognizing specific antigens and class I major histocompatibility complex molecules associated with tumor cells, and thus have a key role in antitumor immunity. However, certain CD8<sup>+</sup> T cells show low reactivity and thus cannot effectively remove tumor cells or viral antigens. Due to this heterogeneity, effective biomarkers representing these differences in CD8+ cells are needed. The identification of suitable biomarkers will also enhance the management of cancer treatment. Recent research has improved the understanding of CD8<sup>+</sup> T lymphocytes in the tumor microenvironment and circulatory system. Treatment efficacy is impacted directly by the pathogenic response of CTLs, and thus, the use of adjuvant therapies to address these pathological changes, e.g., stimulating the increase in the proportion of reactive T cells or suppressing the proportion of terminally exhausted T cells, would be advantageous.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11200153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141432429","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}
Pub Date : 2024-07-01Epub Date: 2024-06-14DOI: 10.3892/or.2024.8756
Hosouk Joung, Hyunju Liu
2',3',4'‑trihydroxyflavone (2‑D08), a SUMO E2 inhibitor, has several biological functions, including anticancer activity, but its effects on uterine leiomyosarcoma (Ut‑LMS) are unknown. The anticancer activity of 2‑D08 was explored in an in vitro model using SK‑LMS‑1 and SK‑UT‑1B cells (human Ut‑LMS cells). Treatment with 2‑D08 inhibited cell viability in a dose‑ and time‑dependent manner and significantly inhibited the colony‑forming ability of Ut‑LMS cells. In SK‑UT‑1B cells treated with 2‑D08, flow cytometric analysis revealed a slight increase in apoptotic rates, while cell cycle progression remained unaffected. Western blotting revealed elevated levels of RIP1, indicating induction of necrosis, but LC3B levels remained unchanged, suggesting no effect on autophagy. A lactate dehydrogenase (LDH) assay confirmed increased LDH release, further supporting the induction of apoptosis and necrosis by 2‑D08 in SK‑UT‑1B cells. 2‑D08‑induced production of reactive oxygen species and apoptosis progression were observed in SK‑LMS‑1 cells. Using Ki67 staining and bromodeoxyuridine assays, it was found that 2‑D08 suppressed proliferation in SK‑LMS‑1 cells, while treatment for 48 h led to cell‑cycle arrest. 2‑D08 upregulated p21 protein expression in SK‑LMS‑1 cells and promoted apoptosis through caspase‑3. Evaluation of α‑SM‑actin, calponin 1 and TAGLN expression indicated that 2‑D08 did not directly initiate smooth muscle phenotypic switching in SK‑LMS‑1 cells. Transcriptome analysis on 2‑D08‑treated SK‑LMS‑1 cells identified significant differences in gene expression and suggested that 2‑D08 modulates cell‑cycle‑ and apoptosis‑related pathways. The analysis identified several differentially expressed genes and significant enrichment for biological processes related to DNA replication and molecular functions associated with the apoptotic process. It was concluded that 2‑D08 exerts antitumor effects in Ut‑LMS cells by modulating multiple signaling pathways and that 2‑D08 may be a promising candidate for the treatment of human Ut‑LMS. The present study expanded and developed knowledge regarding Ut‑LMS management and indicated that 2‑D08 represents a notable finding in the exploration of fresh treatment options for such cancerous tumors.
{"title":"2‑D08 mediates notable anticancer effects through multiple cellular pathways in uterine leiomyosarcoma cells.","authors":"Hosouk Joung, Hyunju Liu","doi":"10.3892/or.2024.8756","DOIUrl":"10.3892/or.2024.8756","url":null,"abstract":"<p><p>2',3',4'‑trihydroxyflavone (2‑D08), a SUMO E2 inhibitor, has several biological functions, including anticancer activity, but its effects on uterine leiomyosarcoma (Ut‑LMS) are unknown. The anticancer activity of 2‑D08 was explored in an <i>in vitro</i> model using SK‑LMS‑1 and SK‑UT‑1B cells (human Ut‑LMS cells). Treatment with 2‑D08 inhibited cell viability in a dose‑ and time‑dependent manner and significantly inhibited the colony‑forming ability of Ut‑LMS cells. In SK‑UT‑1B cells treated with 2‑D08, flow cytometric analysis revealed a slight increase in apoptotic rates, while cell cycle progression remained unaffected. Western blotting revealed elevated levels of RIP1, indicating induction of necrosis, but LC3B levels remained unchanged, suggesting no effect on autophagy. A lactate dehydrogenase (LDH) assay confirmed increased LDH release, further supporting the induction of apoptosis and necrosis by 2‑D08 in SK‑UT‑1B cells. 2‑D08‑induced production of reactive oxygen species and apoptosis progression were observed in SK‑LMS‑1 cells. Using Ki67 staining and bromodeoxyuridine assays, it was found that 2‑D08 suppressed proliferation in SK‑LMS‑1 cells, while treatment for 48 h led to cell‑cycle arrest. 2‑D08 upregulated p21 protein expression in SK‑LMS‑1 cells and promoted apoptosis through caspase‑3. Evaluation of α‑SM‑actin, calponin 1 and TAGLN expression indicated that 2‑D08 did not directly initiate smooth muscle phenotypic switching in SK‑LMS‑1 cells. Transcriptome analysis on 2‑D08‑treated SK‑LMS‑1 cells identified significant differences in gene expression and suggested that 2‑D08 modulates cell‑cycle‑ and apoptosis‑related pathways. The analysis identified several differentially expressed genes and significant enrichment for biological processes related to DNA replication and molecular functions associated with the apoptotic process. It was concluded that 2‑D08 exerts antitumor effects in Ut‑LMS cells by modulating multiple signaling pathways and that 2‑D08 may be a promising candidate for the treatment of human Ut‑LMS. The present study expanded and developed knowledge regarding Ut‑LMS management and indicated that 2‑D08 represents a notable finding in the exploration of fresh treatment options for such cancerous tumors.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11200159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141317899","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}
Pub Date : 2024-07-01Epub Date: 2024-05-17DOI: 10.3892/or.2024.8748
Juntao Yao, Tao Xu, Tao Tian, Xiao Fu, Wenjuan Wang, Suoni Li, Tingting Shi, Aili Suo, Zhiping Ruan, Hui Guo, Yu Yao
Following the publication of the above paper, it was drawn to the Editors' attention by a concerned reader that the data obtained from sphere‑forming assay experiments shown in Figs. 4C‑F and 8B and C, and western blotting data in Figs. 4A and 8A, were strikingly similar to data appearing in different form in other articles by different authors from different research institutes that had already been published, one of which has been retracted. Moreover, a pair of data panels comparing between Fig. 4E and 8C were partly overlapping, such that these data appear to have been derived from the same original source. Owing to the fact that the contentious data in the above article had already been published elsewhere prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. 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: 1204‑1212, 2016; DOI: 10.3892/or.2015.4437].
上述论文发表后,一位相关读者提请编者注意,图 4C-F 和图 8B 和 C 所示的成球实验数据,以及图 4A 和图 8A 所示的 Western 印迹数据,与已发表的由不同研究机构的不同作者撰写的其他文章中以不同形式出现的数据惊人地相似,其中一篇文章已被撤回。此外,图 4E 和图 8C 之间的一对数据面板有部分重叠,因此这些数据似乎来自同一原始来源。由于上述文章中有争议的数据在提交给《肿瘤学报告》之前已经在其他地方发表,因此编辑决定从杂志上撤下这篇论文。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: 1204-1212, 2016; DOI: 10.3892/or.2015.4437]。
{"title":"[Retracted] Tripartite motif 16 suppresses breast cancer stem cell properties through regulation of Gli‑1 degradation via the ubiquitin‑proteasome pathway.","authors":"Juntao Yao, Tao Xu, Tao Tian, Xiao Fu, Wenjuan Wang, Suoni Li, Tingting Shi, Aili Suo, Zhiping Ruan, Hui Guo, Yu Yao","doi":"10.3892/or.2024.8748","DOIUrl":"10.3892/or.2024.8748","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editors' attention by a concerned reader that the data obtained from sphere‑forming assay experiments shown in Figs. 4C‑F and 8B and C, and western blotting data in Figs. 4A and 8A, were strikingly similar to data appearing in different form in other articles by different authors from different research institutes that had already been published, one of which has been retracted. Moreover, a pair of data panels comparing between Fig. 4E and 8C were partly overlapping, such that these data appear to have been derived from the same original source. Owing to the fact that the contentious data in the above article had already been published elsewhere prior to its submission to <i>Oncology Reports</i>, the Editor has decided that this paper should be retracted from the Journal. 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: 1204‑1212, 2016; DOI: 10.3892/or.2015.4437].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11130747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140958407","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}
Pub Date : 2024-07-01Epub Date: 2024-06-07DOI: 10.3892/or.2024.8753
Xinhua Yang, Beibei Liang, Lisha Zhang, Mingzhu Zhang, Ming Ma, Lijuan Qing, Hao Yang, Gang Huang, Jian Zhao
Ursolic acid (UA), a pentacyclic triterpenoid that has been found in a broad variety of fruits, spices and medicinal plants, has various biological effects such as reducing inflammation, protecting cells from damage, and preserving brain function. However, its impact on ferroptosis in cancer stem‑like cells remains unexplored. The present study investigated the effect of UA on MDA‑MB‑231 and BT‑549 cell‑derived triple‑negative breast CSCs (BCSCs) and its potential ferroptosis pathway. The effects of ferroptosis on BCSCs were demonstrated by the detection of ferroptosis‑related indexes including the intracellular level of glutathione, malondialdehyde, reactive oxygen species and iron. The effects of UA on the biological behaviors of BCSCs were analyzed by Cell Counting Kit‑8, stemness indexes detection and mammosphere formation assay. The mechanism of UA induction on BCSCs was explored by reverse transcription‑quantitative PCR and western blotting. BALB/c‑nude mice were subcutaneously injected with MDA‑MB‑231‑derived BCSCs to establish xenograft models to detect the effects of UA in vivo. The results revealed that BCSCs have abnormal iron metabolism and are less susceptible to ferroptosis. UA effectively reduces the stemness traits and proliferation of BCSCs in spheroids and mice models by promoting ferroptosis. It was observed that UA stabilizes Kelch‑like ECH‑associated protein 1 and suppresses nuclear factor erythroid‑related factor 2 (NRF2) activation. These findings suggested that the ability of UA to trigger ferroptosis through the inhibition of the NRF2 pathway could be a promising approach for treating BCSCs, potentially addressing metastasis and drug resistance in triple‑negative breast cancer (TNBC). This expands the clinical applications of UA and provides a theoretical basis for its use in TNBC treatment.
熊果酸(UA)是一种五环三萜类化合物,存在于多种水果、香料和药用植物中,具有多种生物效应,如减轻炎症、保护细胞免受损伤和保护大脑功能。然而,它对癌症干样细胞中铁细胞凋亡的影响仍有待探索。本研究探讨了 UA 对 MDA-MB-231 和 BT-549 细胞衍生的三阴性乳腺癌干细胞(BCSCs)的影响及其潜在的铁氧化途径。通过检测铁变态相关指标,包括细胞内谷胱甘肽、丙二醛、活性氧和铁的水平,证明了铁变态对乳腺癌细胞间充质干细胞的影响。细胞计数试剂盒-8、干性指数检测和乳球形成试验分析了UA对BCSCs生物学行为的影响。通过逆转录-定量 PCR 和 Western 印迹分析了 UA 诱导 BCSCs 的机制。给BALB/c-nude小鼠皮下注射MDA-MB-231来源的BCSCs,建立异种移植模型,检测UA在体内的作用。结果表明,BCSCs 的铁代谢异常,对铁变态反应的敏感性较低。UA通过促进铁突变,有效降低了球形细胞和小鼠模型中碱性细胞干性特征和增殖。研究发现,UA能稳定Kelch样ECH相关蛋白1,并抑制核因子红细胞相关因子2(NRF2)的激活。这些研究结果表明,UA通过抑制NRF2通路引发铁突变的能力可能是治疗碱性细胞癌细胞的一种有前途的方法,有可能解决三阴性乳腺癌(TNBC)的转移和耐药性问题。这拓展了UA的临床应用,并为其在TNBC治疗中的应用提供了理论基础。
{"title":"Ursolic acid inhibits the proliferation of triple‑negative breast cancer stem‑like cells through NRF2‑mediated ferroptosis.","authors":"Xinhua Yang, Beibei Liang, Lisha Zhang, Mingzhu Zhang, Ming Ma, Lijuan Qing, Hao Yang, Gang Huang, Jian Zhao","doi":"10.3892/or.2024.8753","DOIUrl":"10.3892/or.2024.8753","url":null,"abstract":"<p><p>Ursolic acid (UA), a pentacyclic triterpenoid that has been found in a broad variety of fruits, spices and medicinal plants, has various biological effects such as reducing inflammation, protecting cells from damage, and preserving brain function. However, its impact on ferroptosis in cancer stem‑like cells remains unexplored. The present study investigated the effect of UA on MDA‑MB‑231 and BT‑549 cell‑derived triple‑negative breast CSCs (BCSCs) and its potential ferroptosis pathway. The effects of ferroptosis on BCSCs were demonstrated by the detection of ferroptosis‑related indexes including the intracellular level of glutathione, malondialdehyde, reactive oxygen species and iron. The effects of UA on the biological behaviors of BCSCs were analyzed by Cell Counting Kit‑8, stemness indexes detection and mammosphere formation assay. The mechanism of UA induction on BCSCs was explored by reverse transcription‑quantitative PCR and western blotting. BALB/c‑nude mice were subcutaneously injected with MDA‑MB‑231‑derived BCSCs to establish xenograft models to detect the effects of UA <i>in vivo</i>. The results revealed that BCSCs have abnormal iron metabolism and are less susceptible to ferroptosis. UA effectively reduces the stemness traits and proliferation of BCSCs in spheroids and mice models by promoting ferroptosis. It was observed that UA stabilizes Kelch‑like ECH‑associated protein 1 and suppresses nuclear factor erythroid‑related factor 2 (NRF2) activation. These findings suggested that the ability of UA to trigger ferroptosis through the inhibition of the NRF2 pathway could be a promising approach for treating BCSCs, potentially addressing metastasis and drug resistance in triple‑negative breast cancer (TNBC). This expands the clinical applications of UA and provides a theoretical basis for its use in TNBC treatment.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11184361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141284378","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}
Pub Date : 2024-07-01Epub Date: 2024-06-14DOI: 10.3892/or.2024.8755
Sarah Hsin Cheng, Kuan-Yi Tu, Hsin-Hua Lee
Immunotherapy, particularly immune checkpoint inhibitors (ICIs), is undoubtedly one of the major breakthroughs in lung cancer research. Patient survival and prognosis have all been improved as a result, although numerous patients do not respond to immunotherapy due to various immune escape mechanisms of the tumor cells. Recent preclinical and clinical evidence has shown that stereotactic body radiotherapy (SBRT), also known as stereotactic ablative radiotherapy, has a prominent immune priming effect that could elicit antitumor immunity against specific tumor antigens and destroy distant tumor cells, thereby achieving the elusive abscopal effect, with the resulting immuno‑active tumor environment also being more conducive to ICIs. Some landmark trials have already demonstrated the survival benefit of the dynamic duo of SBRT plus immunotherapy in metastatic non‑small‑cell lung cancer, while others such as PEMBRO‑RT further suggest that the addition of SBRT to immunotherapy could expand the current indication to those who have historically responded poorly to ICIs. In the present review, the biological mechanisms that drive the synergistic effect of SBRT and immunotherapy were first briefly outlined; then, the current understanding from clinical trials was summarized and new insight into the evolving role of immunotherapy and SBRT synergy in lung cancer treatment was provided. Finally, novel avenues for discovery were highlighted. The innovation of the present review lies in the inclusion of non‑ICI immunotherapy in the discussion, which provides a more comprehensive view on the current development and future trend of SBRT + immunotherapy synergy.
{"title":"The dynamic duo: A narrative review on the synergy between stereotactic body radiotherapy and immunotherapy in lung cancer treatment (Review).","authors":"Sarah Hsin Cheng, Kuan-Yi Tu, Hsin-Hua Lee","doi":"10.3892/or.2024.8755","DOIUrl":"10.3892/or.2024.8755","url":null,"abstract":"<p><p>Immunotherapy, particularly immune checkpoint inhibitors (ICIs), is undoubtedly one of the major breakthroughs in lung cancer research. Patient survival and prognosis have all been improved as a result, although numerous patients do not respond to immunotherapy due to various immune escape mechanisms of the tumor cells. Recent preclinical and clinical evidence has shown that stereotactic body radiotherapy (SBRT), also known as stereotactic ablative radiotherapy, has a prominent immune priming effect that could elicit antitumor immunity against specific tumor antigens and destroy distant tumor cells, thereby achieving the elusive abscopal effect, with the resulting immuno‑active tumor environment also being more conducive to ICIs. Some landmark trials have already demonstrated the survival benefit of the dynamic duo of SBRT plus immunotherapy in metastatic non‑small‑cell lung cancer, while others such as PEMBRO‑RT further suggest that the addition of SBRT to immunotherapy could expand the current indication to those who have historically responded poorly to ICIs. In the present review, the biological mechanisms that drive the synergistic effect of SBRT and immunotherapy were first briefly outlined; then, the current understanding from clinical trials was summarized and new insight into the evolving role of immunotherapy and SBRT synergy in lung cancer treatment was provided. Finally, novel avenues for discovery were highlighted. The innovation of the present review lies in the inclusion of non‑ICI immunotherapy in the discussion, which provides a more comprehensive view on the current development and future trend of SBRT + immunotherapy synergy.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11188053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141317900","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}
Pub Date : 2024-07-01Epub Date: 2024-06-07DOI: 10.3892/or.2024.8751
Sadaf Anwar, Mubashir Zafar, Malik Asif Hussain, Naveed Iqbal, Abrar Ali, Sadaf, Simran Kaur, Mohammad Zeeshan Najm, Mohd Adnan Kausar
Breast cancer, a prominent cause of mortality among women, develops from abnormal growth of breast tissue, thereby rendering it one of the most commonly detected cancers in the female population. Although numerous treatment strategies are available for breast cancer, discordance in terms of effective treatment and response still exists. Recently, the potential of signaling pathways and transcription factors has gained substantial attention in the cancer community; therefore, understanding their role will assist researchers in comprehending the onset and advancement of breast cancer. Forkhead box (FOX) proteins, which are important transcription factors, are considered crucial regulators of various cellular activities, including cell division and proliferation. The present study explored several subclasses of FOX proteins and their possible role in breast carcinogenesis, followed by the interaction between microRNA (miRNA) and FOX proteins. This interaction is implicated in promoting cell infiltration into surrounding tissues, ultimately leading to metastasis. The various roles that FOX proteins play in breast cancer development, their intricate relationships with miRNA, and their involvement in therapeutic resistance highlight the complexity of breast cancer dynamics. Therefore, recognizing the progress and challenges in current treatments is crucial because, despite advancements, persistent disparities in treatment effectiveness underscore the need for ongoing research, with future studies emphasizing the necessity for targeted strategies that account for the multifaceted aspects of breast cancer.
乳腺癌是女性死亡的主要原因之一,它是由乳腺组织异常增生引起的,因此也是女性人群中最常发现的癌症之一。尽管乳腺癌的治疗策略众多,但在有效治疗和反应方面仍存在不一致。最近,信号通路和转录因子的潜力受到了癌症界的广泛关注;因此,了解它们的作用将有助于研究人员理解乳腺癌的发病和发展。叉头盒(FOX)蛋白是重要的转录因子,被认为是细胞分裂和增殖等各种细胞活动的关键调节因子。本研究探讨了 FOX 蛋白的几种亚类及其在乳腺癌发生中可能扮演的角色,随后研究了微小核糖核酸(miRNA)与 FOX 蛋白之间的相互作用。这种相互作用被认为会促进细胞向周围组织渗透,最终导致转移。FOX 蛋白在乳腺癌发展过程中扮演的各种角色、它们与 miRNA 之间错综复杂的关系以及它们在治疗耐药性中的参与,都凸显了乳腺癌动态变化的复杂性。因此,认识到当前治疗的进展和挑战至关重要,因为尽管取得了进展,但治疗效果方面持续存在的差异凸显了持续研究的必要性,未来的研究将强调考虑到乳腺癌多方面因素的靶向策略的必要性。
{"title":"Unravelling the therapeutic potential of forkhead box proteins in breast cancer: An update (Review).","authors":"Sadaf Anwar, Mubashir Zafar, Malik Asif Hussain, Naveed Iqbal, Abrar Ali, Sadaf, Simran Kaur, Mohammad Zeeshan Najm, Mohd Adnan Kausar","doi":"10.3892/or.2024.8751","DOIUrl":"10.3892/or.2024.8751","url":null,"abstract":"<p><p>Breast cancer, a prominent cause of mortality among women, develops from abnormal growth of breast tissue, thereby rendering it one of the most commonly detected cancers in the female population. Although numerous treatment strategies are available for breast cancer, discordance in terms of effective treatment and response still exists. Recently, the potential of signaling pathways and transcription factors has gained substantial attention in the cancer community; therefore, understanding their role will assist researchers in comprehending the onset and advancement of breast cancer. Forkhead box (FOX) proteins, which are important transcription factors, are considered crucial regulators of various cellular activities, including cell division and proliferation. The present study explored several subclasses of FOX proteins and their possible role in breast carcinogenesis, followed by the interaction between microRNA (miRNA) and FOX proteins. This interaction is implicated in promoting cell infiltration into surrounding tissues, ultimately leading to metastasis. The various roles that FOX proteins play in breast cancer development, their intricate relationships with miRNA, and their involvement in therapeutic resistance highlight the complexity of breast cancer dynamics. Therefore, recognizing the progress and challenges in current treatments is crucial because, despite advancements, persistent disparities in treatment effectiveness underscore the need for ongoing research, with future studies emphasizing the necessity for targeted strategies that account for the multifaceted aspects of breast cancer.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11177173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141284377","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}
Bang-Hua Zhong, Yu-Teng Ma, Jian Sun, Jing-Tong Tang, Ming Dong
{"title":"Transcription factor FOXF2 promotes the development and progression of pancreatic cancer by targeting MSI2","authors":"Bang-Hua Zhong, Yu-Teng Ma, Jian Sun, Jing-Tong Tang, Ming Dong","doi":"10.3892/or.2024.8752","DOIUrl":"https://doi.org/10.3892/or.2024.8752","url":null,"abstract":"","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141265825","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}