Current cancer drug targets最新文献

{"title":"Enhanced Efficacy of Radiation Therapy against Glioblastoma by Attenuated Salmonella Carrying Co-Expression Plasmids with siRNA-PD-L1 and Endostatin.","authors":"Yinghua Ji, Jiaming Guo, Hanyu Jiang, Weiwei Ren, Jiaxin Geng, Mengyu Lei, Jiahang Li, Peiyuan Dang, Yu Wang, Xin Chen, Tiesuo Zhao, Chengbiao Lu, Huijie Jia, Jin Yang","doi":"10.2174/0115680096344636250101074632","DOIUrl":"https://doi.org/10.2174/0115680096344636250101074632","url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma (GBM), a common type of brain tumor, is currently treatable through radiation therapy. However, there is room for improvement in the effec-tiveness of treatment. Radiation can lead to an increase in the expression of PD-L1 and VEGF, which might reduce the responsiveness of the tumor to the therapy. This situation underlines the necessity for innovative treatment strategies.</p><p><strong>Objectives: </strong>In this study, we investigated the potential of attenuated Salmonella carrying the co-expressing plasmid siPD-L1-Endo to effectively inhibit PD-L1 and VEGF expres-sion, thereby enhancing the anti-tumor effects of radiation therapy in GBM-bearing mice.</p><p><strong>Methods: </strong>The regulatory mechanisms responsible for the treatment effect were detected by Flow cytometry, Immunohistochemistry, TUNEL, Immunofluorescence, H&E staining, and Western blot assays.</p><p><strong>Results: </strong>Upon administration of attenuated Salmonella carrying siRNA-PD-L1 and co-expressing endostatin plasmids, the results exhibited significant suppression of tumor growth and tumor cell proliferation, as well as a concurrent decrease in PD-L1 and VEGF expression in tumor tissues. Moreover, the treatment led to reduced expression levels of tumor-related proteins p-Stat3, MMP2, Cyclin D1, and PCNA, an increase in the expres-sion of the apoptosis-related protein cleaved-caspase3, facilitated infiltration of CD4+ and CD8+ T cells within tumor tissues, and an elevation of the ratios of CD4+, CD8+ T cells, and NK cells in the spleen of tumor-bearing mice.</p><p><strong>Conclusion: </strong>These findings highlight the ability of attenuated Salmonella carrying siR-NA-PD-L1 and co-expressing endostatin plasmids to effectively modulate PD-L1 and VEGF expression, thus strengthening the anti-tumor immune response in GBM-bearing mice subjected to radiation therapy. This combination therapy approach holds promise as a potential avenue for improving the efficacy of radiation therapy in the treatment of glio-blastoma.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390349","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}

{"title":"Influence of DNA Copy Number Aberrations in ABC Transporter Family Genes on the Survival of Patients with Primary Operatable Non-Small Cell Lung Cancer.","authors":"Matvey Mikhailovich Tsyganov, Marina Konstantinovna Ibragimova, Evgeny Olegovich Rodionov, Anastavia Alekseevna Frolova, Irina Aleksandrovna Tsydenova, Elizaveta Andreevna Lutzkaya, Sergey Viktorovich Miller","doi":"10.2174/0115680096336801241005173638","DOIUrl":"https://doi.org/10.2174/0115680096336801241005173638","url":null,"abstract":"<p><strong>Purpose: </strong>Previous research has shown, that ABC transporters gene expression level can predict the efficacy of therapy. However, other mechanisms of gene activity are rarely considered, especially in non-small cell lung cancer (NSCLC). Thus, the purpose of the work was to assess chromosomal aberrations of all 49 ABC transporters genes and the expression levels of some ABC genes, as well as their correlation with survival.</p><p><strong>Materials and methods: </strong>The surgical material of 104 patients with NSCLC was used in this study. Treatment included surgery and 3 courses of adjuvant chemotherapy with \"platinum doublets\". DNA and RNA were isolated from the samples, followed by microarray analysis to assess the expression and chromosomal aberrations (deletions and amplifications) of ABC genes.</p><p><strong>Results: </strong>Metastatic-free survival (MFS) was higher with ABCC1, ABCC2, and ABCG1 hypoexpression at a statistically significant level (p=0.01). The presence of deletion in ABCB1 correlates with 100% MFS (p=0.001). The survival rates with ABCG1 amplification are not higher than 45% (p<0.0001). ABCA11 deletion is associated with a low MFS rate (38%) versus 91% with normal copy number (p=0.006). ABCB9 analysis showed opposite results, with survival rates of 55% and 91% in the presence of amplification and normal copy number, respectively (p=0.006). ABCC subfamily genes showed a similar result in the presence of amplification, where ABCC3 and ABCC10 account for 64% and 60% survival, respectively (p=0.005, p=0.01).</p><p><strong>Conclusion: </strong>Thus, not only expression but also chromosomal aberrations were found to be associated with patient survival. These findings could be a potential marker of metastatic-free survival.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122350","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}

{"title":"A Novel Platinum-Resistance-related Gene Signature in Ovarian Cancer: Identification and Patient-derived Organoids Verification.","authors":"Jie Lin, Xintong Cai, Linying Liu, Anyang Li, Huaqing Huang, Yixin Fu, Zhisen Dai, Yang Sun","doi":"10.2174/0115680096326784241009113454","DOIUrl":"https://doi.org/10.2174/0115680096326784241009113454","url":null,"abstract":"<p><strong>Background: </strong>Platinum-based chemotherapy resistance is one of the main contributors to the mortality of Ovarian Cancer (OC). It is believed that sensitive biomarkers for identifying the population that is platinum-resistant are urgently needed. This study aims to develop a platinum-resistance gene-based signature to predict OC patients' responses to platinum drugs as well as survival outcomes.</p><p><strong>Methods: </strong>A platinum-resistance-related gene model was built by bioinformatics analysis. Then, its predictive power was internally validated. Continually, a nomogram was constructed to confirm the model's predictive ability. Afterward, GSEA was used to explore our model's potential functions. The ESTIMATE, CIBERSORT, TIMER, and ssGSEA were applied to estimate immune conditions. Then, somatic mutation and drug sensitivity were also analyzed. Finally, to gain insights into the roles of targeted genes in drug sensitivity, patient-derived tumor organoids (PDOs) validation was performed.</p><p><strong>Results: </strong>Nine platinum-resistance-related genes, including SLC22A2, TAP1, PC, MCM3, GTF2H2, FXYD5, SUPT6H, IGKC, and MATN2, were anchored to build the predictive model, which was well internally validated. Subsequently, GSEA unveiled that our model genes enriched in the Hedgehog signaling pathway. The predictive signature was associated with immune checkpoint inhibitors such as PD-1, PD-L1, and CTLA4, guiding immunotherapy applications for OC patients. Drugs such as dasatinib, midostaurin, metformin, MK-2206, and mitomycin C might also benefit OC patients with different risk scores. PDOs showed patients with high-risk scores were more resistant to cisplatin than patients with low-risk scores.</p><p><strong>Conclusion: </strong>The platinum-resistance-related gene signature (SLC22A2, TAP1, PC, MCM3, GTF2H2, FXYD5, SUPT6H, IGKC, and MATN2) is valuable for prognosis prediction and guidance of treatment choices for OC patients.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122348","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}

{"title":"GCN2 in Cancer: Molecular Mechanisms to Therapeutic Potential.","authors":"Hayley Prescott, Makhdoom Sarwar, Martin Dickens, Evelyn Sattlegger","doi":"10.2174/0115680096325045241120113825","DOIUrl":"10.2174/0115680096325045241120113825","url":null,"abstract":"<p><p>Virtually every mammalian cell contains the cytoplasmic protein kinase General Control Non-depressible 2 (GCN2), which allows cells to cope with stresses such as nutrient shortage. While GCN2 is not essential for normal cells, in many can-cers GCN2 assumes a pivotal role, becoming indispensable for cell growth and sur-vival. This has spurred significant interest in GCN2 as a promising target for anti-cancer therapies. In this review, we give an overview of the known links between GCN2 and cancer.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390283","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}

{"title":"Recent Advancements in Drug Targeting for Ferroptosis as an Antitumor Therapy: Development of Novel therapeutics.","authors":"Reena Rawat Negi, Sanju Singh, Neeta Gupta, Manish Upadhyay, Shilpi Shrivastava, Bhawana Jain","doi":"10.2174/0115680096337123241217070834","DOIUrl":"https://doi.org/10.2174/0115680096337123241217070834","url":null,"abstract":"<p><strong>Objectives: </strong>The primary objective of this review is to provide updated mechanisms that regulate ferroptosis sensitivity in cancer cells and recent advancements in drug targeting for ferroptosis as an antitumor therapy.</p><p><strong>Methods: </strong>To achieve these objectives, a comprehensive literature review was conducted, analyzing recent studies on ferroptosis, including its cellular, molecular, and gene-level characteristics. The review involved an evaluation of advancements in ferroptosis drug research across various medical domains, with particular attention to novel therapeutic approaches in nano-medicine, TCM, and Western medicine. The review also included an assessment of how ferroptosis influences cancer treatment, including its role in tumor drug resistance and immuno-therapy, and provided a detailed analysis of pharmacological activators of ferroptosis.</p><p><strong>Results: </strong>The review highlights several key findings, like primary mechanisms that regulate cancer cell sensitivity to ferroptosis, and provides an overview of the latest advancements in ferroptosis drug research. The review reveals that ferroptosis has both beneficial and detrimental effects on human cancer, reflecting its complex role in cancer progression and treatment. The review also emphasizes the dual nature of ferroptosis, noting its potential as both a tumor suppressor and an oncogenic factor. Additionally, it provides a comprehensive examination of various pharmacological agents that activate ferroptosis and their potential therapeutic applications.</p><p><strong>Conclusion: </strong>In conclusion, ferroptosis represents a promising target for cancer therapy, given its distinctive characteristics and significant role in tumor biology. The review underscores the need for further research to clarify the complex roles of ferroptosis in carcinogenesis and to optimize the development of novel therapeutics targeting this form of cell death. It also highlights current challenges and opportunities in the field, including the potential for overcoming cancer metastasis through ferroptosis modulation and the need for continued exploration of pharmacological activators to advance therapeutic strategies.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063889","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}

{"title":"Precision Medicine in Colorectal Cancer: Targeted Therapies and Biomarker Insights.","authors":"Shriyansh Srivastava, Amit Anand, Anil Goud Kandhula, Pooja Jaiswal, Sachin Kumar, Monica Gulati, Monika Sachdeva, Tapan Behl","doi":"10.2174/0115680096338273241224061021","DOIUrl":"https://doi.org/10.2174/0115680096338273241224061021","url":null,"abstract":"<p><p>The current review delves into the transformative role of precision medicine in addressing Colorectal Cancer [CRC], a pressing global health challenge. It examines closely signalling pathways, genetic and epigenetic modifications, and microsatellite in-stability. The primary focus is on elucidating biomarkers revolutionizing CRC diagnosis and treatment. Genetic biomarkers encompass non-coding RNA, epigenetic markers, TP53 mutations, and KRAS, NRAS, and BRAF gene alterations. Targeted therapies, including anti-EGFR, anti-VEGF, immune checkpoint inhibitors, and HER2-targeted treatments, are explored along with their mechanisms and clinical applications. Additionally, we highlight the importance of utilizing personalized treatment strategies by employing molecular pro-filing and genetic testing. These approaches facilitate the identification of appropriate pa-tients for targeted therapies. Clinical trials supporting these treatments are presented, em-phasizing response rates and survival outcomes. Detailed exploration of resistance mecha-nisms to targeted therapies and strategies to overcome resistance is also provided, paving the way for more effective regimens. Directions for future research in precision medicine, such as biomarkers, combinations, and liquid biopsy in the oncology field, are described. However, the precise application of precision medicine in CRC comes with questions such as costs, considerations of ethical factors, and the need to sensitize patients. Nonetheless, based on a meticulous analysis of several aspects, precision medicine finds itself equipped with the ability to enhance the patients' prognosis ,thereby, lessening the global oncologic burden of CRC and provide important information to the clinician-scientist and policy-maker that might benefit from the ongoing development of precision medicine.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058196","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}

{"title":"CDK8 as a therapeutic target for overall survival prediction in cervical squamous cell carcinoma (CESC).","authors":"Feiting Xie, Qiugang Zhu, Shizhou Yang, Xiaofen Jin, Danqi Ruan, Lingfang Wang, Yang Li, Fang Ren, Xiaojing Chen","doi":"10.2174/0115680096332050241022102545","DOIUrl":"https://doi.org/10.2174/0115680096332050241022102545","url":null,"abstract":"<p><p>Cyclin-dependent kinase 8 (CDK8) is a paracrine transcriptional regulator involved in regulating cellular stress response, growth, and neurological functions, in conjunction with mediator complex subunits 12 (MED12), MED13, and cyclin C.Cyclin-dependent kinase 8 (CDK8) is a paracrine transcriptional regulator involved in regulating cellular stress response, growth and neurological functions，in conjunction with mediator complex subunit 12 (MED12), MED13 and cyclin C. Studying the relationship between CDK8 and cervical squamous cell carcinoma (CESC) has significant clinical implications in diagnosis, treatment, and prognosis. We analyzed the relationship between CDK8 and poor prognosis of CESC. The results indicated that CDK8 was overexpressed in CESC, and the survival rate of patients in the CDK8 hypermethylation group was higher than that in the CDK8 hypomethylation group. In addition, CDK8 was associated with immune cell infiltration in tumor tissues. Overall, these findings provide more evidences for the relationship between CDK8 and patient's overall survival, which could provide insights into clinical diagnosis and prognosis prediction for CESC.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045708","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}

{"title":"Preventive and Therapeutic effects of Metformin in Cancer: A Meta-Analysis of RCT and Cohort Studies.","authors":"Mikiyas Amare Getu, Xianbin Zhang, Jia Wang, Kunpeng Xu, Ying Ying, Li Ma, Peng Gong","doi":"10.2174/0115680096345507241030224210","DOIUrl":"https://doi.org/10.2174/0115680096345507241030224210","url":null,"abstract":"<p><strong>Background: </strong>There is discrepancy of results among various individual and me-ta-analytical studies about the effect of metformin on cancer risk and patients' survival. Therefore, we have conducted a comprehensive, updated meta-analysis to evaluate the preventive and therapeutic effects of metformin for cancer patients, as well as the inci-dence of adverse reactions, among metformin users.</p><p><strong>Methods: </strong>A total of 18 studies (10 cohort studies and 8 randomized controlled trials) in-volving 1,300,820 participants from Europe, North America, and Asia were included in this meta-analysis.</p><p><strong>Results: </strong>No significant association was found between metformin use and overall survival (Hazard ratio = 1.02; 95% CI, 0.80 - 1.30) and progressive-free survival (Hazard ratio = 1.00; 95% CI, 0.76 - 1.31). In addition, the summary risk estimates for adverse reactions of metformin were not statistically significant between intervention and control groups (Risk Ratio = 1.11; 95% CI, 0.94 - 1.31). However, metformin use was associated with a reduction in cancer risk (Hazard ratio = 0.90, 95% CI, 0.86 - 0.94).</p><p><strong>Conclusion: </strong>Metformin does not significantly prolong the overall survival and progressive-free survival of cancer patients, but it may effectively reduce the risk of cancer occurrence.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022491","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}

{"title":"Macranthoside B Suppresses the Growth of Adenocarcinoma of Esophagogastric Junction by Regulating Iron Homeostasis and Ferroptosis through NRF2 Inhibition.","authors":"Lingling Wang, Guangzhao Pan, Sichao Tian, Che Zhang, Fangfang Tao, Jiang-Jiang Qin","doi":"10.2174/0115680096370291250109103853","DOIUrl":"https://doi.org/10.2174/0115680096370291250109103853","url":null,"abstract":"<p><strong>Background: </strong>Macranthoside B (MB) is a saponin compound extracted from hon-eysuckle that has been reported to exhibit significant medicinal values, particularly anti-tumor activities. This study aimed to evaluate the anticancer efficacy of MB in treating adenocarci-noma of the esophagogastric junction (AEG) and elucidate its underlying mechanisms.</p><p><strong>Methods: </strong>Three AEG cell lines and normal gastric epithelial cells were used to assess the an-ticancer activity of MB in vitro. A series of experiments, including RNA sequencing (RNA-seq) analysis, transmission electron microscopy (TEM), immunofluorescence, and western blot assay, were conducted to validate the molecular mechanisms by which MB may mediate these physiological changes. Finally, we used shRNA assays to silence the key gene driving these changes and examined the expression of molecules involved in the affected pathways.</p><p><strong>Results: </strong>MB exhibited significant anti-AEG cell activity with IC50 values ranging from 9.5 to 12.7 μM. RNA-seq results indicated that MB treatment in AEG cells significantly altered mRNA levels of autophagy- and ferroptosis-related genes. Further experiments revealed that MB treatment led to the up-regulation of lipid reactive oxygen species (Lip-ROS), oxidative stress-related pathway genes, and LC3B-labeled autophagic vesicles in AEG cells. Moreover, MB mediated NCOA4-dependent ferritinophagy, disrupting iron homeostasis and causing subsequent ferroptosis. We further confirmed that the intrinsic connection between autophagy and ferroptosis was due to the inhibition of NRF2 by MB. The inhibition of NRF2 by MB triggered transcriptional repression of its downstream effector molecules HERC2 and VAMP8, thus stabilizing NCOA4.</p><p><strong>Conclusion: </strong>This study demonstrated MB to inhibit AEG cell growth by regulating iron ho-meostasis and inducing ferroptosis through the inhibition of NRF2, providing a basis for the development of novel drugs for AEG treatment.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022527","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}

{"title":"Targeting Glutamine Metabolic Reprogramming in Pancreatic Cancer: Current Insights and Future Directions.","authors":"Yanhui Ma, Mingling Wang, Kexing Zhang, Fangbing Ren, Yuqun Wang, Wenqiang Zhang, Chengxia Kan, Fang Han, Hongxi Sun, Xiaodong Sun","doi":"10.2174/0115680096357993241206072609","DOIUrl":"https://doi.org/10.2174/0115680096357993241206072609","url":null,"abstract":"<p><p>Pancreatic Cancer (PC) is a devastating malignancy with a poor prognosis and in-creasing morbidity. Current treatment strategies have limited efficacy in improving patient survival. Metabolic reprogramming is a hallmark of cancer and plays a key role in the pro-gression and maintenance of PC. PC cells exhibit a unique glutamine metabolism that is dis-tinct from other cancer types. The non-classical pathway of glutamine metabolic reprogram-ming plays a \"permissive role\" in the survival and proliferation of PC cells, mainly by affect-ing the redox homeostasis of the cells. In this review, we compare and contrast the canonical and non-canonical glutamine metabolic pathways and highlight recent advances in targeting non-canonical glutamine metabolism for therapeutic intervention. This may provide novel in-sights and opportunities for exploiting glutamine metabolic reprogramming in PC treatment.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022499","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}