Current cancer drug targets最新文献

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Magnesium as a Co-Factor: A Vital Cation with Pro- and Anti-Tumor Effects. 作为辅助因子的镁:具有促进和抗肿瘤作用的重要阳离子
IF 2.3 4区 医学
Current cancer drug targets Pub Date : 2024-09-12 DOI: 10.2174/0115680096346615240907210849
Muthu Krishnan Dhivya Dharshini, Dhamodharan Prabhu, Subash C B Gopinath
{"title":"Magnesium as a Co-Factor: A Vital Cation with Pro- and Anti-Tumor Effects.","authors":"Muthu Krishnan Dhivya Dharshini, Dhamodharan Prabhu, Subash C B Gopinath","doi":"10.2174/0115680096346615240907210849","DOIUrl":"https://doi.org/10.2174/0115680096346615240907210849","url":null,"abstract":"","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281669","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}
引用次数: 0
Progressive Dynamics of Cancer Stem Cells in Oral Squamous Cell Carcinoma. 口腔鳞状细胞癌中癌症干细胞的进展动态
IF 2.3 4区 医学
Current cancer drug targets Pub Date : 2024-09-12 DOI: 10.2174/0115680096340994240906111400
Gopalakrishnan Shankari, Rajmichael Raji, Dhamodharan Prabhu, Jeyaraman Jeyakanthan, Subash C B Gopinath
{"title":"Progressive Dynamics of Cancer Stem Cells in Oral Squamous Cell Carcinoma.","authors":"Gopalakrishnan Shankari, Rajmichael Raji, Dhamodharan Prabhu, Jeyaraman Jeyakanthan, Subash C B Gopinath","doi":"10.2174/0115680096340994240906111400","DOIUrl":"https://doi.org/10.2174/0115680096340994240906111400","url":null,"abstract":"","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281670","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}
引用次数: 0
SELENBP1 Inhibits the Warburg Effect and Tumor Growth by Reducing the HIF1α Expression in Colorectal Cancer. SELENBP1 通过降低结直肠癌中 HIF1α 的表达抑制沃伯格效应和肿瘤生长
IF 2.3 4区 医学
Current cancer drug targets Pub Date : 2024-09-12 DOI: 10.2174/0115680096320837240806172245
Tao Song, Xiaotian Zhang, Jun Ren, Zhiqing Hu, Xin Wang, Gengming Niu
{"title":"SELENBP1 Inhibits the Warburg Effect and Tumor Growth by Reducing the HIF1α Expression in Colorectal Cancer.","authors":"Tao Song, Xiaotian Zhang, Jun Ren, Zhiqing Hu, Xin Wang, Gengming Niu","doi":"10.2174/0115680096320837240806172245","DOIUrl":"https://doi.org/10.2174/0115680096320837240806172245","url":null,"abstract":"<p><strong>Introduction: </strong>Colorectal cancer (CRC) is experiencing a significant increase in both incidence and mortality rates globally. The expression of Selenium-binding protein 1 (SELENBP1) has been reported to be notably downregulated in various malignancies, yet its biological functions and cellular mechanisms in CRC remain incompletely understood.</p><p><strong>Method: </strong>In our investigation, we observed the downregulation of SELENBP1 in CRC tissues through quantitative real-time PCR and western blotting and identified a positive correlation between higher SELENBP1 expression and improved survival prognosis using Kaplan-Meier survival analysis. Through loss-of-function and gain-of-function studies, we demonstrated the tumor-suppressive roles of SELENBP1 in CRC, supported by results from both in vitro and in vivo experiments. Furthermore, we uncovered the pivotal functions of SELENBP1 in suppressing aerobic glycolysis in CRC cells by regulating glucose uptake, lactate generation, and extracellular acidification rate.</p><p><strong>Result: </strong>At a mechanistic level, we found that SELENBP1 inhibits the expression of the key glycolytic modulator hypoxia-inducible factor 1 subunit alpha (HIF1α), and the inhibition of glycolysis by SELENBP1 can be reversed by ectopic expression of HIF1α. Therefore, our study highlights the potential of SELENBP1 as a promising target for CRC therapy, given its significant impact on tumor suppression and reprogrammed glucose metabolism.</p><p><strong>Conclusion: </strong>These findings contribute to a deeper understanding of the molecular mechanisms underlying CRC progression and may pave the way for the development of targeted therapies for this challenging disease.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281671","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}
引用次数: 0
Antibody-drug conjugates (ADCs): a novel therapy for triple-negative breast cancer (TNBC). 抗体药物共轭物 (ADC):治疗三阴性乳腺癌 (TNBC) 的新型疗法。
IF 2.3 4区 医学
Current cancer drug targets Pub Date : 2024-09-07 DOI: 10.2174/0115680096343056240828190900
Gaurav Gupta, Md Sadique Hussain, Kumud Pant, Haider Ali, Riya Thapa, Asif Ahmad Bhatt
{"title":"Antibody-drug conjugates (ADCs): a novel therapy for triple-negative breast cancer (TNBC).","authors":"Gaurav Gupta, Md Sadique Hussain, Kumud Pant, Haider Ali, Riya Thapa, Asif Ahmad Bhatt","doi":"10.2174/0115680096343056240828190900","DOIUrl":"https://doi.org/10.2174/0115680096343056240828190900","url":null,"abstract":"<p><p>NA.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153279","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}
引用次数: 0
Quantum Dots Functionalized Polymeric Nanoparticles as Cancer Theranostics: An Advanced Nanomedicine Strategy. 量子点功能化聚合物纳米粒子作为癌症治疗药物:一种先进的纳米医学策略
IF 2.3 4区 医学
Current cancer drug targets Pub Date : 2024-09-04 DOI: 10.2174/0115680096299455240621070820
Honey Panchal, Drishti Panjwani, Shruti Patel, Priyanka Ahlawat, L D Patel, Abhay Dharamsi, Asha Patel
{"title":"Quantum Dots Functionalized Polymeric Nanoparticles as Cancer Theranostics: An Advanced Nanomedicine Strategy.","authors":"Honey Panchal, Drishti Panjwani, Shruti Patel, Priyanka Ahlawat, L D Patel, Abhay Dharamsi, Asha Patel","doi":"10.2174/0115680096299455240621070820","DOIUrl":"https://doi.org/10.2174/0115680096299455240621070820","url":null,"abstract":"<p><strong>Background: </strong>Cancer is a life-threatening disease prevalent worldwide, but its proper treatment has not yet been developed. Conventional therapies, like chemotherapy, sur-gery, and radiation, have shown relapse and drug resistance. Nanomedicine comprising cancer theranostics based on imaging probes functionalized with polymeric nanoconjugates is acquir-ing importance due to its targeting capability, biodegradability, biocompatibility, capacity for drug loading, and long blood circulation time. The application of synthetic polymers contain-ing anti-cancer agents and functionalizing their surface amenities with diagnostic probes offer a nano-combinatorial model in cancer theranostics.</p><p><strong>Objective: </strong>This study aimed to highlight the recent advancements in quantum dots-functionalized nanoconjugates and substantial progress in advanced polymeric nanomaterials in cancer theragnostics.</p><p><strong>Methods: </strong>This review details the synthetic methods for fabricating Quantum Dots (QDs) and QDs-functionalized polymeric nanoparticles, such as the hydrothermal method, solvothermal technique, atomic layer desorption, electrochemical method, microwave, and ultrasonic method.</p><p><strong>Results: </strong>Conjugating nanoparticles with photo-emitting quantum dots has shown efficacy for real-time monitoring and treating multi-drug-resistant cancer.</p><p><strong>Conclusion: </strong>Quantum dots are used in phototherapy, bioimaging, and medication delivery for cancer therapy. Real-time monitoring of therapy is possible and multiple models of hybridized quantum dots may be created to treat cancer. This review has discovered that numerous at-tempts have been made to conjugate carbon and graphene-based quantum dots with various biomolecules.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142132078","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}
引用次数: 0
CNDP1 Suppresses the Malignant Behavior of Hepatoma Cell via Restricting PI3K-AKT-mTOR Activation. CNDP1 通过限制 PI3K-AKT-mTOR 激活抑制肝癌细胞的恶性行为
IF 2.3 4区 医学
Current cancer drug targets Pub Date : 2024-09-03 DOI: 10.2174/0115680096332450240827070033
Youwen Du, Linxin Pan, Wenchen Zhang, Shuangbiao Wei, Xu Fan, Na Zhang, Pengjun Wei, Xiaoqian Chen, Zhi Qiao, Li Xie
{"title":"CNDP1 Suppresses the Malignant Behavior of Hepatoma Cell via Restricting PI3K-AKT-mTOR Activation.","authors":"Youwen Du, Linxin Pan, Wenchen Zhang, Shuangbiao Wei, Xu Fan, Na Zhang, Pengjun Wei, Xiaoqian Chen, Zhi Qiao, Li Xie","doi":"10.2174/0115680096332450240827070033","DOIUrl":"https://doi.org/10.2174/0115680096332450240827070033","url":null,"abstract":"<p><strong>Introduction: </strong>Hepatocellular carcinoma (HCC) is a global health problem with increasing morbidity and mortality, and exploring the diagnosis and treatment of HCC at the gene level has been a research hotspot in recent years.</p><p><strong>Methods: </strong>In this paper, a series of differentially expressed genes were found from the biochip related to HCC by bioinformatic analysis, then CNDP1 was finally selected for in-depth study according to the function and research progress of each gene. As the rate-limiting enzyme of carnosine hydrolysis, CNDP1 participates in the progress of many diseases, but its function has not been revealed in HCC. In the follow-up study, the low expression of CNDP1 in liver cancer tissues and cells was verified, then the pcDNA3.1-CNDP1 was used to improve the expression level of CNDP1 in HCC cell lines. Furthermore, this paper found that CNDP1 overexpression could significantly suppress cell prolifer-ation, migration, and invasion of HCC cell lines.</p><p><strong>Results: </strong>Mechanismly, the GeneMANIA database predicted that CNDP1 could interact with various proteins that regulate the PI3K-AKT-mTOR signaling pathway, which is overactivated in HCC. And this study showed that CNDP1 overexpression could effectively inhibit the activation of PI3K-AKT-mTOR signaling pathways, more significantly, inhibition of PI3K-AKT-mTOR signaling pathway could disrupt the anti-cancer effect of CNDP1 on HCC.</p><p><strong>Conclusion: </strong>In conclusion, we confirmed that CNDP1 was lowly expressed in HCC tissues and cells, and had potential anti-cancer activity. This discovery will lay a cytological foundation for expanding the biological function of CNDP1 and the diagnosis and treatment of HCC in the future.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142124997","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}
引用次数: 0
Regulation and Crosstalk of Cells and Factors in the Pancreatic Cancer Microenvironment. 胰腺癌微环境中细胞和因子的调节与相互影响
IF 2.3 4区 医学
Current cancer drug targets Pub Date : 2024-09-02 DOI: 10.2174/0115680096317840240723071018
Jia Xu, Songmei Lou, Hui Huang, Jian Xu, Feng Luo
{"title":"Regulation and Crosstalk of Cells and Factors in the Pancreatic Cancer Microenvironment.","authors":"Jia Xu, Songmei Lou, Hui Huang, Jian Xu, Feng Luo","doi":"10.2174/0115680096317840240723071018","DOIUrl":"https://doi.org/10.2174/0115680096317840240723071018","url":null,"abstract":"<p><p>Pancreatic cancer is a highly malignant form of cancer that distinguishes itself from other gastrointestinal tumors through significant fibrosis and unique perineural invasion. These characteristics underscore the complexity of neural regulation within the pancreatic cancer Tumor Microenvironment (TME). This review aimed to explore the regulatory mechanisms and crosstalk among stromal cells and their factors within the pancreatic cancer microenvironment. We begin by reviewing the major components of the pancreatic cancer microenvironment, analyzing interactions among crucial cell types, such as Cancer-associated Fibroblasts (CAFs) and immune cells, and revealing the dynamic changes between tumor cells and surrounding nerves, immune, and stromal cells. We discuss the role of neural factors, including the Nerve Growth Factor (NGF) and Brain-derived Neurotrophic Factor (BDNF), in the progression of pancreatic cancer and the mechanisms by which the sympathetic and parasympathetic nervous systems regulate tumor cell growth, migration, and invasion. Interactions among stromal cells, cytokines, and neural factors in the pancreatic cancer microenvironment promote fibrosis and perineural invasion. A deeper understanding of the regulation and crosstalk among components in the pancreatic cancer microenvironment offers new perspectives for inhibiting fibrosis and perineural invasion in pancreatic cancer.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119195","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}
引用次数: 0
Neomorphic IDH Heterodimer Mutants: An Underestimated Point in Cancer Pathogenesis. 新形的 IDH 杂二聚体突变体:癌症发病机制中被低估的一点
IF 2.3 4区 医学
Current cancer drug targets Pub Date : 2024-08-28 DOI: 10.2174/0115680096317314240723054739
Olga V Dorovatovskaia, Mikhail Yu Oliferenko, Anatoly A Sorokin, Daniil I Sobolev, Galina S Stupnikova, Danil S Sobakin, Eugene N Nikolaev, Igor A Popov, Stanislav I Pekov
{"title":"Neomorphic IDH Heterodimer Mutants: An Underestimated Point in Cancer Pathogenesis.","authors":"Olga V Dorovatovskaia, Mikhail Yu Oliferenko, Anatoly A Sorokin, Daniil I Sobolev, Galina S Stupnikova, Danil S Sobakin, Eugene N Nikolaev, Igor A Popov, Stanislav I Pekov","doi":"10.2174/0115680096317314240723054739","DOIUrl":"https://doi.org/10.2174/0115680096317314240723054739","url":null,"abstract":"<p><p>Mutations in an essential metabolic enzyme, isocitrate dehydrogenase (IDH), were found in many cancers. The impact of IDH1 and IDH2 proteoforms mutations can vary and de-pend on the cancer type and other genetic alterations. The wild-type IDH1/2 consists of two identical subunits, but the mutant enzyme is a heterodimer of mutant and wild-type subunits, while the mutant homodimer loses its catalytic activity. Thus, the balance of expression of wild-type and mutant proteoforms directly affects enzyme neomorphic activity, cell metabolic por-trait, and, therefore, cell survival and proliferation rates. Here, we generalize the influence of the presence of IDH mutations and the expression of mutant and wild-type proteoforms for various nosologies to demonstrate the deficiency in knowledge about the mutual distribution of the pro-teoforms in cancer cells. The review is supplemented with a brief description of IDH mutations' role in cell metabolic reprogramming and a summary of methods for IDH mutation detection. Eventually, we highlight the necessity of assessing the expression of wild-type and mutated IDH quantitatively, which can help create and deliver personalized approaches for tumor therapy.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142105192","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}
引用次数: 0
Targeting the Tumor Epigenetic Regulator SETDB1 for Tumor Therapy 靶向肿瘤表观遗传调节剂 SETDB1 治疗肿瘤
IF 3 4区 医学
Current cancer drug targets Pub Date : 2024-08-28 DOI: 10.2174/0115680096311909240721160523
Cheng Peng, Nini Zhou, Tengjiang Chen, Jie Lei, Changwen Chen, Shunqin Zhu
{"title":"Targeting the Tumor Epigenetic Regulator SETDB1 for Tumor Therapy","authors":"Cheng Peng, Nini Zhou, Tengjiang Chen, Jie Lei, Changwen Chen, Shunqin Zhu","doi":"10.2174/0115680096311909240721160523","DOIUrl":"https://doi.org/10.2174/0115680096311909240721160523","url":null,"abstract":": Epigenetic alterations are implicated in the early stages of tumorigenesis and are widely recognized as a ubiquitous phenomenon in cancer development. Aberrant epigenetic modifications can alter the expression of target genes, induce heterochromatin formation, and gradually drive normal cells towards immortalized tumor cells with significant consequences. SETDB1 (SET domain bifurcated histone lysine methyltransferase 1), a typical histone me-thyltransferase, promotes the formation of heterochromatin and inhibits the transcription of genes by modifying the methylation of lysine 9 of histone 3. SETDB1 is usually highly ex-pressed in tumors with high copy numbers, accompanied by poor prognosis and low patient survival rates, which is a typical case of abnormal epigenetic modification. We discuss the mechanism of SETDB1 in a variety of cancers and review the epigenetic inhibitors that have been reported in recent years, along with their anti-tumor effects. In addition, we summarize the role of SETDB1 in a variety of diseases and cell functions.","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142200231","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}
引用次数: 0
GPX4 Inhibition Enhances the Antitumor Effect of PARP Inhibitor on Homologous Recombination Proficient Ovarian Cancer Cells. 抑制 GPX4 可增强 PARP 抑制剂对具有同源重组能力的卵巢癌细胞的抗肿瘤作用
IF 2.3 4区 医学
Current cancer drug targets Pub Date : 2024-08-26 DOI: 10.2174/0115680096334278240821100404
Jiaxin Gu, Senmi Qian, Fangfang Qian, Xiaodong Wu, Lifeng Chen, Xiaojing Chen, Zhuoye Chen, Feifei Song, Mengxia Zheng, Lingfang Wang, Xiaodong Cheng
{"title":"GPX4 Inhibition Enhances the Antitumor Effect of PARP Inhibitor on Homologous Recombination Proficient Ovarian Cancer Cells.","authors":"Jiaxin Gu, Senmi Qian, Fangfang Qian, Xiaodong Wu, Lifeng Chen, Xiaojing Chen, Zhuoye Chen, Feifei Song, Mengxia Zheng, Lingfang Wang, Xiaodong Cheng","doi":"10.2174/0115680096334278240821100404","DOIUrl":"https://doi.org/10.2174/0115680096334278240821100404","url":null,"abstract":"<p><strong>Background: </strong>Poly (ADP-ribose) polymerase inhibitors (PARPi) are now widely used in BRCA1/2 mutation or homologous recombination (HR) deficiency ovarian cancer but have limited efficacy in HR-proficient patients. GPX4 is a key regulator of ferroptosis and has been proven to be associated with multiple drug sensitivities. As a molecule that regulates the sensitivity of multiple drugs, the relationship between GPX4 and the efficacy of PARPi in HR-proficient ovarian cancer has not been elucidated.</p><p><strong>Methods: </strong>In this study, siRNA transfection was used to regulate the expression of GPX4. The effect of GPX4 inhibition on HR-proficient ovarian cancer was determined by CCK-8 assay and flow cytometry. Immunofluorescence and comet assays were used to reflect DNA dam-age. ROS production was measured using DCFH-DA and flow cytometry. The combination index of PARP inhibitors and RSL3 was calculated using CompuSyn software based on Chou-Talalay methodology.</p><p><strong>Results: </strong>GPX4 inhibition confers HR-proficient ovarian cancer cells sensitive to PARPi due to ROS generation and oxidative stress caused by DNA double-strand breakage. The combina-tion of olaparib and niraparib with GPX4 inhibitor RSL3 also showed a synergistic effect.</p><p><strong>Conclusion: </strong>Combining GPX4 inhibition with PARP inhibitors resulted in a notable increase in DNA damage, ultimately causing the death of cancer cells with proficient HR pathways. Our findings may provide new therapeutic options for HR-proficient patients to benefit from PARP inhibitors and improve outcomes.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142079473","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}
引用次数: 0
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