Ganoderma lucidum has anti-tumor effects, but its mechanism of action against lung cancer is not clear. This study aims to use molecular docking and network pharmacology to investigate how G. lucidum inhibits tumor growth in lung cancer and how this relationship relates to the degree of immune cell infiltration. By utilizing the TCMSP database, the therapeutic targets and active ingredients of G. lucidum were discovered. Based on the targets found in subsequent rounds of screening, a protein interaction (PPI) network was constructed. Additionally, enrichment analysis was conducted using GO and the KEGG. The molecular docking was conducted with the help of AutoDock Tools and PyMOL. Finally, we investigated the relationships between immune cells and the commonalities between lung cancer and. The primary targets of G. lucidum’s anti-lung cancer activities, according to network pharmacology studies, are ADRB2, OPRM1, SLC6A4, and JUN. The primary components of the lung cancer fighter Ergosterol are ganoderal B, ganolucidic acid E, and beta-sitosterol. The molecular docking analysis revealed that beta-sitosterol had the highest degree of stability in its docking interaction with JUN. The immune infiltration analysis indicated a potential correlation between the biomarkers associated with G. lucidum treatment for lung cancer and the immune infiltrating cells. G. lucidum combats lung cancer by targeting multiple components and signaling pathways, facilitating cancer cell apoptosis and interacting with immune responses. This elucidates potential avenues for future research into G. lucidum’s mechanisms in lung cancer therapy.
灵芝具有抗肿瘤作用，但其对肺癌的作用机制尚不清楚。本研究旨在利用分子对接和网络药理学研究灵芝如何抑制肺癌肿瘤的生长，以及这种关系与免疫细胞浸润程度的关系。 通过利用 TCMSP 数据库，发现了鹿角胶的治疗靶点和活性成分。根据随后几轮筛选中发现的靶点，构建了蛋白质相互作用（PPI）网络。此外，还利用 GO 和 KEGG 进行了富集分析。在 AutoDock Tools 和 PyMOL 的帮助下进行了分子对接。最后，我们研究了免疫细胞与肺癌之间的关系以及肺癌与免疫细胞之间的共性。 根据网络药理学研究，绿藻抗肺癌活性的主要靶点是ADRB2、OPRM1、SLC6A4和JUN。肺癌斗士麦角甾醇的主要成分是甘露醇 B、甘露酸 E 和 beta-谷甾醇。分子对接分析表明，β-谷甾醇与 JUN 的对接作用稳定性最高。免疫浸润分析表明，绿藻治疗肺癌的相关生物标志物与免疫浸润细胞之间存在潜在的相关性。 绿藻通过靶向多种成分和信号通路、促进癌细胞凋亡以及与免疫反应相互作用来抗击肺癌。这为今后研究绿巨人治疗肺癌的机制提供了潜在的途径。
{"title":"Exploring the anti-lung cancer mechanism of Ganoderma lucidum and its relationship with the level of immune cell infiltration based on network pharmacology and molecular docking","authors":"Yuanyuan Luo, Xuehua Luo, Zhijian Xue, Miao Wu, Qiufang Chen, Ling Jin","doi":"10.1515/oncologie-2024-0194","DOIUrl":"https://doi.org/10.1515/oncologie-2024-0194","url":null,"abstract":"\u0000 \u0000 \u0000 \u0000 Ganoderma lucidum has anti-tumor effects, but its mechanism of action against lung cancer is not clear. This study aims to use molecular docking and network pharmacology to investigate how G. lucidum inhibits tumor growth in lung cancer and how this relationship relates to the degree of immune cell infiltration.\u0000 \u0000 \u0000 \u0000 By utilizing the TCMSP database, the therapeutic targets and active ingredients of G. lucidum were discovered. Based on the targets found in subsequent rounds of screening, a protein interaction (PPI) network was constructed. Additionally, enrichment analysis was conducted using GO and the KEGG. The molecular docking was conducted with the help of AutoDock Tools and PyMOL. Finally, we investigated the relationships between immune cells and the commonalities between lung cancer and.\u0000 \u0000 \u0000 \u0000 The primary targets of G. lucidum’s anti-lung cancer activities, according to network pharmacology studies, are ADRB2, OPRM1, SLC6A4, and JUN. The primary components of the lung cancer fighter Ergosterol are ganoderal B, ganolucidic acid E, and beta-sitosterol. The molecular docking analysis revealed that beta-sitosterol had the highest degree of stability in its docking interaction with JUN. The immune infiltration analysis indicated a potential correlation between the biomarkers associated with G. lucidum treatment for lung cancer and the immune infiltrating cells.\u0000 \u0000 \u0000 \u0000 \u0000 G. lucidum combats lung cancer by targeting multiple components and signaling pathways, facilitating cancer cell apoptosis and interacting with immune responses. This elucidates potential avenues for future research into G. lucidum’s mechanisms in lung cancer therapy.\u0000","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141919511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ganoderma lucidum has anti-tumor effects, but its mechanism of action against lung cancer is not clear. This study aims to use molecular docking and network pharmacology to investigate how G. lucidum inhibits tumor growth in lung cancer and how this relationship relates to the degree of immune cell infiltration. By utilizing the TCMSP database, the therapeutic targets and active ingredients of G. lucidum were discovered. Based on the targets found in subsequent rounds of screening, a protein interaction (PPI) network was constructed. Additionally, enrichment analysis was conducted using GO and the KEGG. The molecular docking was conducted with the help of AutoDock Tools and PyMOL. Finally, we investigated the relationships between immune cells and the commonalities between lung cancer and. The primary targets of G. lucidum’s anti-lung cancer activities, according to network pharmacology studies, are ADRB2, OPRM1, SLC6A4, and JUN. The primary components of the lung cancer fighter Ergosterol are ganoderal B, ganolucidic acid E, and beta-sitosterol. The molecular docking analysis revealed that beta-sitosterol had the highest degree of stability in its docking interaction with JUN. The immune infiltration analysis indicated a potential correlation between the biomarkers associated with G. lucidum treatment for lung cancer and the immune infiltrating cells. G. lucidum combats lung cancer by targeting multiple components and signaling pathways, facilitating cancer cell apoptosis and interacting with immune responses. This elucidates potential avenues for future research into G. lucidum’s mechanisms in lung cancer therapy.
灵芝具有抗肿瘤作用，但其对肺癌的作用机制尚不清楚。本研究旨在利用分子对接和网络药理学研究灵芝如何抑制肺癌肿瘤的生长，以及这种关系与免疫细胞浸润程度的关系。 通过利用 TCMSP 数据库，发现了鹿角胶的治疗靶点和活性成分。根据随后几轮筛选中发现的靶点，构建了蛋白质相互作用（PPI）网络。此外，还利用 GO 和 KEGG 进行了富集分析。在 AutoDock Tools 和 PyMOL 的帮助下进行了分子对接。最后，我们研究了免疫细胞与肺癌之间的关系以及肺癌与免疫细胞之间的共性。 根据网络药理学研究，绿藻抗肺癌活性的主要靶点是ADRB2、OPRM1、SLC6A4和JUN。肺癌斗士麦角甾醇的主要成分是甘露醇 B、甘露酸 E 和 beta-谷甾醇。分子对接分析表明，β-谷甾醇与 JUN 的对接作用稳定性最高。免疫浸润分析表明，绿藻治疗肺癌的相关生物标志物与免疫浸润细胞之间存在潜在的相关性。 绿藻通过靶向多种成分和信号通路、促进癌细胞凋亡以及与免疫反应相互作用来抗击肺癌。这为今后研究绿巨人治疗肺癌的机制提供了潜在的途径。
{"title":"Exploring the anti-lung cancer mechanism of Ganoderma lucidum and its relationship with the level of immune cell infiltration based on network pharmacology and molecular docking","authors":"Yuanyuan Luo, Xuehua Luo, Zhijian Xue, Miao Wu, Qiufang Chen, Ling Jin","doi":"10.1515/oncologie-2024-0194","DOIUrl":"https://doi.org/10.1515/oncologie-2024-0194","url":null,"abstract":"\u0000 \u0000 \u0000 \u0000 Ganoderma lucidum has anti-tumor effects, but its mechanism of action against lung cancer is not clear. This study aims to use molecular docking and network pharmacology to investigate how G. lucidum inhibits tumor growth in lung cancer and how this relationship relates to the degree of immune cell infiltration.\u0000 \u0000 \u0000 \u0000 By utilizing the TCMSP database, the therapeutic targets and active ingredients of G. lucidum were discovered. Based on the targets found in subsequent rounds of screening, a protein interaction (PPI) network was constructed. Additionally, enrichment analysis was conducted using GO and the KEGG. The molecular docking was conducted with the help of AutoDock Tools and PyMOL. Finally, we investigated the relationships between immune cells and the commonalities between lung cancer and.\u0000 \u0000 \u0000 \u0000 The primary targets of G. lucidum’s anti-lung cancer activities, according to network pharmacology studies, are ADRB2, OPRM1, SLC6A4, and JUN. The primary components of the lung cancer fighter Ergosterol are ganoderal B, ganolucidic acid E, and beta-sitosterol. The molecular docking analysis revealed that beta-sitosterol had the highest degree of stability in its docking interaction with JUN. The immune infiltration analysis indicated a potential correlation between the biomarkers associated with G. lucidum treatment for lung cancer and the immune infiltrating cells.\u0000 \u0000 \u0000 \u0000 \u0000 G. lucidum combats lung cancer by targeting multiple components and signaling pathways, facilitating cancer cell apoptosis and interacting with immune responses. This elucidates potential avenues for future research into G. lucidum’s mechanisms in lung cancer therapy.\u0000","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141918967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-09DOI: 10.1515/oncologie-2024-0132
Wenyang Lei, Wenting Yu, Yu Zhong, Ti Li, Hongjun Xiao, S. Zong
Cancer is a major cause of death worldwide and a serious threat to human health. Cisplatin, a widely used first-line chemotherapeutic agent for various solid tumors, is renowned for its efficacy but is limited by significant cytotoxicity. Cisplatin triggers pyroptosis in tumor cells by activating Gasdermin proteins, thereby enhancing its anticancer efficacy. However, this same mechanism can induce pyroptosis in normal cells, causing inflammation and toxicity in healthy tissues, such as nephrotoxicity and ototoxicity. The objective of this review is to identify the major molecular targets for optimizing the cisplatin treatment window by summarizing recent advances in the pyroptosis caused by cisplatin in different cancer types and normal tissues. Among them, gasdermin D and gasdermin E are the main molecular targets involved in cisplatin-induced pyroptosis, and GSDMB also has similar effects. Future research directions include exploring targeted drug delivery systems and target regulating GSDMs (gasdermin protein family) to selectively modulate pyroptosis, thereby maximizing cisplatin’s anticancer effects while minimizing its side effects. Therefore, this review provides a comprehensive overview of cisplatin-induced pyroptosis, offering new insights into therapeutic strategies in cancer treatment.
{"title":"Cisplatin-induced pyroptosis: a double-edged sword in cancer treatment","authors":"Wenyang Lei, Wenting Yu, Yu Zhong, Ti Li, Hongjun Xiao, S. Zong","doi":"10.1515/oncologie-2024-0132","DOIUrl":"https://doi.org/10.1515/oncologie-2024-0132","url":null,"abstract":"\u0000 Cancer is a major cause of death worldwide and a serious threat to human health. Cisplatin, a widely used first-line chemotherapeutic agent for various solid tumors, is renowned for its efficacy but is limited by significant cytotoxicity. Cisplatin triggers pyroptosis in tumor cells by activating Gasdermin proteins, thereby enhancing its anticancer efficacy. However, this same mechanism can induce pyroptosis in normal cells, causing inflammation and toxicity in healthy tissues, such as nephrotoxicity and ototoxicity. The objective of this review is to identify the major molecular targets for optimizing the cisplatin treatment window by summarizing recent advances in the pyroptosis caused by cisplatin in different cancer types and normal tissues. Among them, gasdermin D and gasdermin E are the main molecular targets involved in cisplatin-induced pyroptosis, and GSDMB also has similar effects. Future research directions include exploring targeted drug delivery systems and target regulating GSDMs (gasdermin protein family) to selectively modulate pyroptosis, thereby maximizing cisplatin’s anticancer effects while minimizing its side effects. Therefore, this review provides a comprehensive overview of cisplatin-induced pyroptosis, offering new insights into therapeutic strategies in cancer treatment.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141924328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-09DOI: 10.1515/oncologie-2024-0177
Alessandro Cioce, Renato Franco
Colorectal cancer (CRC) remains a prevalent malignancy worldwide, with a significant burden on public health despite advancements in screening and treatment modalities. While the majority of CRC cases are histologically classified as adenocarcinomas not otherwise specified (NOS), there exists a subset characterized by clear cell features or enteroblastic differentiation, which pose diagnostic and therapeutic challenges. This commentary explores the clinical and pathological aspects of these rare colorectal neoplasms, highlighting their distinct characteristics and aggressive behavior. Despite their rarity, clear cell adenocarcinomas or those with enteroblastic differentiation represent a notable proportion of CRC cases and are associated with adverse prognostic implications, including higher TNM stage and poorer survival outcomes. We advocate for a clearer recognition and classification of these entities within the framework of colorectal carcinoma, analogous to existing categorizations in other gastrointestinal malignancies, to facilitate optimal management strategies and further elucidate their underlying biology.
{"title":"Unveiling the unexplored: shedding light on a novel aspect of colorectal carcinoma","authors":"Alessandro Cioce, Renato Franco","doi":"10.1515/oncologie-2024-0177","DOIUrl":"https://doi.org/10.1515/oncologie-2024-0177","url":null,"abstract":"\u0000 Colorectal cancer (CRC) remains a prevalent malignancy worldwide, with a significant burden on public health despite advancements in screening and treatment modalities. While the majority of CRC cases are histologically classified as adenocarcinomas not otherwise specified (NOS), there exists a subset characterized by clear cell features or enteroblastic differentiation, which pose diagnostic and therapeutic challenges. This commentary explores the clinical and pathological aspects of these rare colorectal neoplasms, highlighting their distinct characteristics and aggressive behavior. Despite their rarity, clear cell adenocarcinomas or those with enteroblastic differentiation represent a notable proportion of CRC cases and are associated with adverse prognostic implications, including higher TNM stage and poorer survival outcomes. We advocate for a clearer recognition and classification of these entities within the framework of colorectal carcinoma, analogous to existing categorizations in other gastrointestinal malignancies, to facilitate optimal management strategies and further elucidate their underlying biology.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141923488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-24DOI: 10.1515/oncologie-2024-0246
Valentina Zagardo, Francesco Cuccia, Antonio Piras, Silvana Parisi, M. Sciacca, G. Ferrantelli, Fiorenza Latteri, G. Ferini
Renal cell carcinoma (RCC) often presents with tumor thrombus (TT) in the inferior vena cava (IVC), posing significant therapeutic challenges, particularly in cases of metastatic or inoperable disease. While surgical excision remains the standard treatment approach, recent advancements in radiotherapy techniques may offer alternative strategies. We present the clinical picture of a 74-year-old male with metastatic RCC, who presented with recurrent IVC-TT, detected by surveillance computed tomography imaging, and complained of mild lower leg edema. This was successfully managed with stereotactic body radiotherapy (SBRT), resulting in a slow but continuous shrinkage of the IVC-TT with almost complete regression of most lung, liver, and lymph node metastases, obtaining a full resolution of the mild bilateral leg edema. The case described here highlights the possibility of using radiotherapy as a safe and tolerable treatment for inoperable or metastatic patients with IVC-TT. Additionally, we conducted a literature review looking for evidence of the effectiveness of radiotherapy in RCC patients with IVC-TT across different treatment settings. This case-based review ultimately aims to shed light on the emerging evidence supporting the usefulness of radiotherapy in such complex clinical challenges, hopefully paving the way for well-organized trials.
{"title":"Radiotherapy directed to inferior vena cava tumor thrombus among patients with renal cell carcinoma: an illustrative case and review of the literature","authors":"Valentina Zagardo, Francesco Cuccia, Antonio Piras, Silvana Parisi, M. Sciacca, G. Ferrantelli, Fiorenza Latteri, G. Ferini","doi":"10.1515/oncologie-2024-0246","DOIUrl":"https://doi.org/10.1515/oncologie-2024-0246","url":null,"abstract":"\u0000 Renal cell carcinoma (RCC) often presents with tumor thrombus (TT) in the inferior vena cava (IVC), posing significant therapeutic challenges, particularly in cases of metastatic or inoperable disease. While surgical excision remains the standard treatment approach, recent advancements in radiotherapy techniques may offer alternative strategies. We present the clinical picture of a 74-year-old male with metastatic RCC, who presented with recurrent IVC-TT, detected by surveillance computed tomography imaging, and complained of mild lower leg edema. This was successfully managed with stereotactic body radiotherapy (SBRT), resulting in a slow but continuous shrinkage of the IVC-TT with almost complete regression of most lung, liver, and lymph node metastases, obtaining a full resolution of the mild bilateral leg edema. The case described here highlights the possibility of using radiotherapy as a safe and tolerable treatment for inoperable or metastatic patients with IVC-TT. Additionally, we conducted a literature review looking for evidence of the effectiveness of radiotherapy in RCC patients with IVC-TT across different treatment settings. This case-based review ultimately aims to shed light on the emerging evidence supporting the usefulness of radiotherapy in such complex clinical challenges, hopefully paving the way for well-organized trials.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141808508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-16DOI: 10.1515/oncologie-2024-0166
Xiaoxiong Wu, Zhendong Zhang, Xiaoping Wang
MiRNA (MicroRNA) can target and regulate mRNA, thereby influencing the biological processes of tumors. The extract of Tibetan medicine Rhodiola demonstrates anti-tumor effects by targeting and regulating cancer-related signaling molecules and pathways. This review aims to pave the way for integrating salidroside into clinical practice, fully leverage its multi-effective and multi-targeted biological effects, and innovate approaches to tumor prevention and management, thus enhancing cancer prognosis. We initially delve into the occurrence and mechanism of action of miRNA, as well as the anti-tumor mechanism of the miRNA-mRNA signaling axis. Additionally, it was described that salidroside can hinder cancer cell proliferation by inducing autophagy and apoptosis, inhibiting cell metastasis and invasion, and modulating the tumor microenvironment and cell cycle. Moreover, examples from lung cancer, gastric cancer, and nasopharyngeal carcinoma confirm that salidroside regulates the onset and progression of tumors through the miRNA-mRNA signaling axis. This groundbreaking discovery carries significant implications for cancer diagnosis and treatment, offering a novel pathway for therapeutic intervention.
{"title":"Research progress on anti-cancer mechanism of salidroside regulating miRNA-mRNA signaling axis","authors":"Xiaoxiong Wu, Zhendong Zhang, Xiaoping Wang","doi":"10.1515/oncologie-2024-0166","DOIUrl":"https://doi.org/10.1515/oncologie-2024-0166","url":null,"abstract":"\u0000 MiRNA (MicroRNA) can target and regulate mRNA, thereby influencing the biological processes of tumors. The extract of Tibetan medicine Rhodiola demonstrates anti-tumor effects by targeting and regulating cancer-related signaling molecules and pathways. This review aims to pave the way for integrating salidroside into clinical practice, fully leverage its multi-effective and multi-targeted biological effects, and innovate approaches to tumor prevention and management, thus enhancing cancer prognosis. We initially delve into the occurrence and mechanism of action of miRNA, as well as the anti-tumor mechanism of the miRNA-mRNA signaling axis. Additionally, it was described that salidroside can hinder cancer cell proliferation by inducing autophagy and apoptosis, inhibiting cell metastasis and invasion, and modulating the tumor microenvironment and cell cycle. Moreover, examples from lung cancer, gastric cancer, and nasopharyngeal carcinoma confirm that salidroside regulates the onset and progression of tumors through the miRNA-mRNA signaling axis. This groundbreaking discovery carries significant implications for cancer diagnosis and treatment, offering a novel pathway for therapeutic intervention.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141643854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study aimed to investigate the efficacy of boanmycin, a clinical drug used for head and neck cancers, in the treatment of acute myeloid leukemia (AML), particularly in venetoclax-resistant AML cells. The cell viability assay was conducted to measure the inhibitory effects of boanmycin on the AML cell lines and patient primary cells using the CCK8 reagent. The colony formation assay was performed to evaluate the colony formation ability of HL60 and venetoclax-resistant HL60 (HL60-res) cells with or without boanmycin treatment. Flow cytometry was performed to detect cell apoptosis level, and Western blot was used to assess changes in apoptosis-related proteins. Our findings reveal that boanmycin significantly inhibits AML cell proliferation and colony formation, and induces apoptosis. Importantly, boanmycin exhibits substantial inhibitory effects on venetoclax-resistant cells, and suppresses the proliferation of peripheral blood mononuclear cells (PBMCs) or bone marrow mononuclear cells (BMMCs) derived from newly diagnosed and relapsed AML patients. Boanmycin may overcome venetoclax resistance and offer therapeutic benefits for patients with venetoclax-resistant AML.
{"title":"Boanmycin induces apoptosis and overcomes venetoclax resistance in acute myeloid leukemia","authors":"Jin-Xing Wang, Peng-Wei Zhang, Luo-Wei Yuan, Jian Jiang, Xiao-Hui Cheng, Ju-Heng Li, Mei-Qin Tang, Jiao-Yang Fan, Wei Zhu, Yong Lei, Faqing Tian","doi":"10.1515/oncologie-2024-0140","DOIUrl":"https://doi.org/10.1515/oncologie-2024-0140","url":null,"abstract":"\u0000 \u0000 \u0000 This study aimed to investigate the efficacy of boanmycin, a clinical drug used for head and neck cancers, in the treatment of acute myeloid leukemia (AML), particularly in venetoclax-resistant AML cells.\u0000 \u0000 \u0000 \u0000 The cell viability assay was conducted to measure the inhibitory effects of boanmycin on the AML cell lines and patient primary cells using the CCK8 reagent. The colony formation assay was performed to evaluate the colony formation ability of HL60 and venetoclax-resistant HL60 (HL60-res) cells with or without boanmycin treatment. Flow cytometry was performed to detect cell apoptosis level, and Western blot was used to assess changes in apoptosis-related proteins.\u0000 \u0000 \u0000 \u0000 Our findings reveal that boanmycin significantly inhibits AML cell proliferation and colony formation, and induces apoptosis. Importantly, boanmycin exhibits substantial inhibitory effects on venetoclax-resistant cells, and suppresses the proliferation of peripheral blood mononuclear cells (PBMCs) or bone marrow mononuclear cells (BMMCs) derived from newly diagnosed and relapsed AML patients.\u0000 \u0000 \u0000 \u0000 Boanmycin may overcome venetoclax resistance and offer therapeutic benefits for patients with venetoclax-resistant AML.\u0000","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141641950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-16DOI: 10.1515/oncologie-2024-0147
Lu Qi, Zhongwen Li
Iron metabolism plays a crucial role in various physiological processes, and its dysregulation has been implicated in many cancers. Epidemiological studies have confirmed a significant correlation between iron overload and an increased risk of oesophageal cancer. The purpose of this review is to investigate the relationship between iron metabolism imbalance and oesophageal cancer and to explore the potential application of iron metabolism regulatory mechanisms in the treatment of oesophageal cancer. This paper details the physiological mechanisms that regulate cellular iron homeostasis, including absorption, storage, utilization, and excretion and focuses on changes in iron homeostasis in oesophageal cancer cells. In addition, the paper discusses the multifaceted roles of iron in tumourigenesis, progression and metastasis, as well as the impact of iron metabolism in the tumour microenvironment. Finally, this paper discusses the potential impact of ferroptosis on cancer cell survival, highlights the importance of iron metabolism in oesophageal cancer, and provides new ideas for the prevention, diagnosis and treatment of oesophageal cancer. Future research should further elucidate the specific role of iron metabolism in esophageal cancer pathogenesis and explore new therapeutic approaches using these mechanisms for more effective treatment strategies.
{"title":"Exploring the interplay between iron metabolism imbalance and esophageal cancer","authors":"Lu Qi, Zhongwen Li","doi":"10.1515/oncologie-2024-0147","DOIUrl":"https://doi.org/10.1515/oncologie-2024-0147","url":null,"abstract":"\u0000 Iron metabolism plays a crucial role in various physiological processes, and its dysregulation has been implicated in many cancers. Epidemiological studies have confirmed a significant correlation between iron overload and an increased risk of oesophageal cancer. The purpose of this review is to investigate the relationship between iron metabolism imbalance and oesophageal cancer and to explore the potential application of iron metabolism regulatory mechanisms in the treatment of oesophageal cancer. This paper details the physiological mechanisms that regulate cellular iron homeostasis, including absorption, storage, utilization, and excretion and focuses on changes in iron homeostasis in oesophageal cancer cells. In addition, the paper discusses the multifaceted roles of iron in tumourigenesis, progression and metastasis, as well as the impact of iron metabolism in the tumour microenvironment. Finally, this paper discusses the potential impact of ferroptosis on cancer cell survival, highlights the importance of iron metabolism in oesophageal cancer, and provides new ideas for the prevention, diagnosis and treatment of oesophageal cancer. Future research should further elucidate the specific role of iron metabolism in esophageal cancer pathogenesis and explore new therapeutic approaches using these mechanisms for more effective treatment strategies.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141643244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-15DOI: 10.1515/oncologie-2024-0157
A. Phull, Sadia Qamar Arain, Abdul Majid, Humaira Fatima, Madiha Ahmed, Song-Ja Kim
Cancer is a serious public health issue and cases are rising at a high rate around the world. Altered production of reactive oxygen species (ROS) causes oxidative stress (OS) which plays a vital role in cancer development by disrupting signaling pathways and genomic integrity in the cellular microenvironment. In this study, we reviewed the regulation of noncoding RNAs, histone modifications, and DNA methylation which OS is involved in. These mechanisms promote cancer growth, metastasis, and resistance to chemotherapeutic agents. There is significant potential to improve patient outcomes through the development of customized medications and interventions that precisely address the role of OS in the onset and progression of cancer. Redox-modulating drugs, antioxidant-based therapies, and measures to restore regular cellular activity and OS-modulated signaling pathways are some examples of these strategies. One other hypothesis rationalizes the cancer-suppressing effect of OS, which acts as a two-edged condition that warns against the use of antioxidants for cancer treatment and management. The present study was executed to review the impact of OS on epigenetic machinery, the evolution of metastatic cancer, and how OS mediates cellular signaling. Along with, insights into the potential of targeting OS-mediated mechanisms for cancer therapy.
癌症是一个严重的公共卫生问题，全世界的癌症病例都在高速上升。活性氧（ROS）产生的变化会导致氧化应激（OS），而氧化应激会破坏细胞微环境中的信号通路和基因组完整性，从而在癌症发展过程中扮演重要角色。在本研究中，我们回顾了 OS 所涉及的非编码 RNA、组蛋白修饰和 DNA 甲基化的调控。这些机制促进了癌症的生长、转移和对化疗药物的耐药性。通过开发定制药物和干预措施，精确解决操作系统在癌症发生和发展中的作用，在改善患者预后方面大有可为。氧化还原调节药物、抗氧化疗法以及恢复正常细胞活动和OS调节信号通路的措施就是这些策略的一些例子。还有一种假说认为操作系统具有抑制癌症的作用，它是一把双刃剑，警告人们不要使用抗氧化剂来治疗和控制癌症。本研究旨在回顾 OS 对表观遗传机制的影响、转移性癌症的演变以及 OS 如何介导细胞信号传导。此外，本研究还深入探讨了针对操作系统介导的癌症治疗机制的潜力。
{"title":"Oxidative stress-mediated epigenetic remodeling, metastatic progression and cell signaling in cancer","authors":"A. Phull, Sadia Qamar Arain, Abdul Majid, Humaira Fatima, Madiha Ahmed, Song-Ja Kim","doi":"10.1515/oncologie-2024-0157","DOIUrl":"https://doi.org/10.1515/oncologie-2024-0157","url":null,"abstract":"\u0000 Cancer is a serious public health issue and cases are rising at a high rate around the world. Altered production of reactive oxygen species (ROS) causes oxidative stress (OS) which plays a vital role in cancer development by disrupting signaling pathways and genomic integrity in the cellular microenvironment. In this study, we reviewed the regulation of noncoding RNAs, histone modifications, and DNA methylation which OS is involved in. These mechanisms promote cancer growth, metastasis, and resistance to chemotherapeutic agents. There is significant potential to improve patient outcomes through the development of customized medications and interventions that precisely address the role of OS in the onset and progression of cancer. Redox-modulating drugs, antioxidant-based therapies, and measures to restore regular cellular activity and OS-modulated signaling pathways are some examples of these strategies. One other hypothesis rationalizes the cancer-suppressing effect of OS, which acts as a two-edged condition that warns against the use of antioxidants for cancer treatment and management. The present study was executed to review the impact of OS on epigenetic machinery, the evolution of metastatic cancer, and how OS mediates cellular signaling. Along with, insights into the potential of targeting OS-mediated mechanisms for cancer therapy.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141649073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-18DOI: 10.1515/oncologie-2024-0106
Huimei Zou, Peilei Chen, Zhongkui Li, Tingliang Yan, Daolin Cui, Lei Gong, Jie Fang, Yu Ren, Min Chen, Jie Yu, Jun Yu, Juan Luo, Fan Zhang
Abstract Objectives Despite the involvement of the G protein beta-1 (GNB1) protein in various cancer types, its relationship to breast tumours is presently uncertain. This research focused on the expression of GNB1 in breast cancer and its possible biological ramifications in an effort to explain this confusion. Methods The expression levels of GNB1 in adjacent normal tissues and breast cancer were compared. We next constructed GNB1-overexpressed or -knockdown MDA-MB-231 cell lines in order to clarify GNB1’s function in breast cancer. We used colony-formation assays, CCK-8 assays, xenograft models, and transwell migration/invasion assays to evaluate the effect of GNB1 on tumorigenicity, migration, and invasion. Moreover, we used western blot analysis to investigate the significance of FAK/mTOR signalling in GNB1-regulated tumour stimulatory effects in breast cancer. Finally, we investigated the upstream regulatory signaling of GNB1 using luciferase reporter and functional repair assays. Results When comparing human breast cancer specimens to specimens of normal tissue, we discovered that GNB1 was noticeably overexpressed. This phenotype was also found to be substantially associated with unfavourable clinical outcomes. Functional research findings indicate that elevated expression of GNB1 stimulated the proliferation and metastasis of breast cancer cells. Additionally, we discovered that GNB1 activated the FAK/mTOR signalling cascade by directly inducing the phosphorylation of the FAK protein through specific contacts. According to the results of the RNA pull-down assays and dual-luciferase reporter, we concluded that circRNA-0133711 functions as a competitive endogenous RNA (ceRNA) that sequesters miR-145-5p and thereby relieves its repressive effect on GNB1 expression. Conclusions Collectively, our research findings elucidate the hitherto unexplored important role of the circRNA-0133711/miR-145-5p/GNB1 axis in the formation of breast cancer, and provide a new biomarker for clinical diagnosis and treatment of breast cancer.
{"title":"Identification of GNB1 as a downstream effector of the circRNA-0133711/miR-145-5p axis involved in breast cancer proliferation and metastasis","authors":"Huimei Zou, Peilei Chen, Zhongkui Li, Tingliang Yan, Daolin Cui, Lei Gong, Jie Fang, Yu Ren, Min Chen, Jie Yu, Jun Yu, Juan Luo, Fan Zhang","doi":"10.1515/oncologie-2024-0106","DOIUrl":"https://doi.org/10.1515/oncologie-2024-0106","url":null,"abstract":"Abstract Objectives Despite the involvement of the G protein beta-1 (GNB1) protein in various cancer types, its relationship to breast tumours is presently uncertain. This research focused on the expression of GNB1 in breast cancer and its possible biological ramifications in an effort to explain this confusion. Methods The expression levels of GNB1 in adjacent normal tissues and breast cancer were compared. We next constructed GNB1-overexpressed or -knockdown MDA-MB-231 cell lines in order to clarify GNB1’s function in breast cancer. We used colony-formation assays, CCK-8 assays, xenograft models, and transwell migration/invasion assays to evaluate the effect of GNB1 on tumorigenicity, migration, and invasion. Moreover, we used western blot analysis to investigate the significance of FAK/mTOR signalling in GNB1-regulated tumour stimulatory effects in breast cancer. Finally, we investigated the upstream regulatory signaling of GNB1 using luciferase reporter and functional repair assays. Results When comparing human breast cancer specimens to specimens of normal tissue, we discovered that GNB1 was noticeably overexpressed. This phenotype was also found to be substantially associated with unfavourable clinical outcomes. Functional research findings indicate that elevated expression of GNB1 stimulated the proliferation and metastasis of breast cancer cells. Additionally, we discovered that GNB1 activated the FAK/mTOR signalling cascade by directly inducing the phosphorylation of the FAK protein through specific contacts. According to the results of the RNA pull-down assays and dual-luciferase reporter, we concluded that circRNA-0133711 functions as a competitive endogenous RNA (ceRNA) that sequesters miR-145-5p and thereby relieves its repressive effect on GNB1 expression. Conclusions Collectively, our research findings elucidate the hitherto unexplored important role of the circRNA-0133711/miR-145-5p/GNB1 axis in the formation of breast cancer, and provide a new biomarker for clinical diagnosis and treatment of breast cancer.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":0.9,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141335006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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