Current cancer drug targets最新文献

{"title":"Artificial Intelligence (AI) and Liquid Biopsy Transforming Early Detection of Liver Metastases in Gastrointestinal Cancers.","authors":"Thilagesh P, Anand Kumar S, Aiswarya Nair U, Rabiniraj S, Shobana P, Subramani M, Sriram K","doi":"10.2174/0115680096331238241125051307","DOIUrl":"https://doi.org/10.2174/0115680096331238241125051307","url":null,"abstract":"<p><p>Liver metastases from Gastrointestinal (GI) cancers present significant challenges in oncology, often signaling poor prognosis. Traditional detection methods like imaging and tissue biopsies have limitations in sensitivity, specificity, and tumor heterogeneity represen-tation. The advent of artificial intelligence (AI) in healthcare, driven by advancements in ma-chine learning, algorithms, and data science, offers a promising frontier for early detection and management of liver metastases. This review explores the integration of AI and liquid biopsy technologies as transformative tools in the proactive detection of liver metastases aris-ing from GI malignancies. Liquid biopsy, a non-invasive method, analyzes circulating tumor cells (CTCs), cell-free DNA (cfDNA), and circulating tumor DNA (ctDNA) in bodily fluids. It provides a compre-hensive overview of tumor heterogeneity and enables real-time monitoring of tumor evolu-tion and treatment response. Despite its advantages, liquid biopsy faces challenges such as low sensitivity for early-stage metastases, reduced detectability due to liver filtration, and technical limitations. AI enhances the potential of liquid biopsies by improving diagnostic accuracy through ad-vanced algorithms like Convolutional Neural Networks (CNNs) and Natural Language Pro-cessing (NLP). These AI models analyze complex biomedical data, offering higher sensitivity and specificity in cancer detection. The synergy between AI and liquid biopsies promises early detection, better disease monitoring, and personalized treatment strategies. This review underscores the significant advancements AI and liquid biopsy technologies bring to oncological precision medicine, particularly in improving overall survival (OS) and disease-free survival (DFS) for patients with GI cancer metastases. As we transition into the era of precision medicine, the integration of these technologies holds the potential to redefine cancer care and patient management.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022509","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":"Engineering Pancreatic Organoids.","authors":"Samaneh Mollazadeh, Abdulridha Mohammed Al-Asady, Nikoo Saeedi, Amir Avan, Majid Khazaei, Mikhail Ryzhikov, Seyed Mahdi Hasanian Mehr","doi":"10.2174/0115680096326562241112061426","DOIUrl":"https://doi.org/10.2174/0115680096326562241112061426","url":null,"abstract":"<p><p>Experimental cell culture models that mimic the intricate features of organs offer significant potential for fundamental research and clinical applications. In order to enhance the growth of organoids, various matrices have been developed to replicate the essential character-istics of the tissue microenvironment through physical, chemical, and mechanical cues. Recent advancements in biomaterial technology have further refined the cultivation of organoids. This review provides an overview of the effect of different matrices, whether natural or synthetic, on the fabrication of pancreatic and islet clusters. Through a comprehensive examination of ongoing research, this paper aims to increase an understanding of pancreatic organoid genera-tion, with implications for modeling pancreatic disorders and advancing regenerative medicine.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022513","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":"TCF19 Enhances Glioma Cell Proliferation via Modulating the Β-Catenin Signaling Pathway through Accelerating DHX32 Transcription.","authors":"Jing Tan, Haiping Lian, Qi Zheng, Tingting Yang, Tuo Wang","doi":"10.2174/0115680096360071241215171342","DOIUrl":"https://doi.org/10.2174/0115680096360071241215171342","url":null,"abstract":"<p><strong>Background: </strong>Transcription factor 19 (TCF19) is considered a crucial transcription factor and acts as an oncogene in a few cancers. Nevertheless, the effect and mechanism of TCF19 on glioma remain unknown.</p><p><strong>Objective: </strong>This research aimed to explore the function of TCF19 on glioma progression and clarify the potential mechanism.</p><p><strong>Methods: </strong>TCF19 and DHX32 expressions in glioma were determined using bioinformatics, Quantitative real-time PCR, and immunohistochemistry. MTT assay was carried out to detect the biological function of TCF19 and DHX32 in glioma cell multiplication. Cell-cycle distri-bution and apoptosis were measured by using FACS. The function of TCF19 on glioma growth was examined using tumor xenografts assay. Bioinformatics analysis, ChIP-qRT-PCR, and reporter gene assay were employed to illustrate the TCF19 target regulating DHX32 tran-scription.</p><p><strong>Results: </strong>TCF19 was observably upregulated in glioma and has important clinical significance. Overexpressing TCF19 expedited glioma cell multiplication and cell-cycle transition, mean-while preventing apoptosis. TCF19 knockdown inhibited cell proliferation, cell-cycle transi-tion, and tumour growth, simultaneously accelerating apoptosis. TCF19 expressions had a positive correlation with DHX32 expressions in glioma. It was demonstrated that TCF19 acti-vated DHX32 transcriptional activity in glioma by combining it with the promoter of DHX32. DHX32 promoted glioma cell growth and cell-cycle transition while restraining apoptosis. Overexpressing DHX32 eliminated the function of TCF19 knockdown on cell multiplication, cell-cycle transition, and apoptosis. Moreover, TCF19 activated the β-catenin pathway by en-hancing DHX32 transcriptional activity.</p><p><strong>Conclusion: </strong>TCF19 promotes glioma cell multiplication and cell-cycle transition while sup-pressing apoptosis by modulating the β-catenin signaling pathway via accelerating DHX32 transcription. These findings provide a promising therapeutic target for glioma.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001607","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":"Efficacy and Safety of PD-1/L1 Inhibitors Combined with Anlotinib versus PD-1 /L1 Inhibitors Combined with Bevacizumab in Second-Line Treatment of Advanced Non-Small Cell Lung Cancer Patients: A Comparative Cohort Study.","authors":"Xiaobing Li, De Wu, Yi Peng, Jing Tang, Yuebing Wu","doi":"10.2174/0115680096338045241117161228","DOIUrl":"https://doi.org/10.2174/0115680096338045241117161228","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to compare the efficacy and safety of PD-1/L1 inhibitors combined with anlotinib versus PD-1/L1 inhibitors combined with bevacizumab as second-line treatments for advanced NSCLC patients.</p><p><strong>Methods: </strong>A retrospective analysis was carried out on data from advanced NSCLC patients who received either PD-1/L1 inhibitors combined with anlotinib or PD-1/L1 inhibitors combined with bevacizumab as second-line therapy. Clinical outcomes, including Overall Survival (OS), Progression-Free Survival (PFS), Objective Response Rate (ORR), Disease Control Rate (DCR), and Adverse Events (AEs), were compared between the two treatment groups.</p><p><strong>Results: </strong>The results revealed that patients receiving PD-1/L1 inhibitors combined with anlo-tinib exhibited better efficacy compared to patients receiving PD-1/L1 inhibitors combined with bevacizumab (mPFS 5.0m vs. 4.0m, mOS 10.0m vs. 8.0m, ORR 31.25% vs. 17.14%, DCR 65.63% vs. 45.71%). Additionally, both treatment regimens were generally well-tolerated, with most adverse events being manageable and of mild to moderate severity. However, compared with patients receiving PD-1/L1 inhibitors combined with bevacizumab, those receiving PD-1/L1 inhibitors combined with anlotinib have higher incidence rates of certain adverse reactions (hypertension: 34.38% vs. 17.14%, proteinuria: 25% vs. 14.29%), implying that drug combinations of the same treatment modality may exhibit differences in efficacy and adverse reactions.</p><p><strong>Conclusion: </strong>In this comparative study, PD-1/L1 inhibitors combined with anlotinib demonstrated superior efficacy compared to PD-1/L1 inhibitors combined with bevacizumab as second-line therapy for advanced NSCLC patients, with a manageable safety profile. These findings provide valuable clinical evidence for guiding treatment decisions in this patient population.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001600","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":"Advances in Understanding How RhoB Regulates Akt Inhibition Efficacy in NSCLC.","authors":"Nurullah Akgun, Zekai Halici, Elif Cadirci","doi":"10.2174/0115680096355061241115113703","DOIUrl":"https://doi.org/10.2174/0115680096355061241115113703","url":null,"abstract":"<p><strong>Objectives: </strong>Increasing the effectiveness and reliability of Akt inhibition in lung cancer treatment may pave the way for a more favorable use of this method in the future. Therefore, we aimed to evaluate the possible role of RhoB in the regulation of Akt inhibition in NSCLC.</p><p><strong>Material and methods: </strong>The study was conducted using the NSCLC cell line A549. Small interfering RNA (siRNA)-mediated RhoB knockdown was performed and combined with perifosine (Akt inhibitor) treatment. Cell proliferation was detected by xCELLigence® RTCA. RhoB, pAkt, and Bcl2l11 expressions were analyzed by ELISA. Apoptosis rates were determined by flow cytometry.</p><p><strong>Results: </strong>We knocked down RhoB in A549 cells using siRNA. According to the results of the 72-hour experiment, RhoB upregulation was observed to reduce the antiproliferative ac-tivity of the Akt inhibitor. The pAkt level was significantly lower in the group where the Akt inhibitor was applied to RhoB-silenced cells via siRNA compared to other treatment groups. The percentage of apoptosis in the group where the Akt inhibitor was applied to RhoB-silenced cells was found to be significantly higher than in the RhoB-suppressed group.</p><p><strong>Conclusion: </strong>Both proliferation and apoptosis tests determined that the RhoB molecule is a negative regulator of the anti-tumor activity of Akt inhibition in non-small cell lung cancer. This study suggests that RhoB expression may play a critical role in the regulation of Akt inhibition in NSCLC, potentially opening new avenues for treatment strategies.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001597","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":"Fe3O4-viral-like Mesoporous Silica Nanoparticle(Fe3O4-vMSN)-Sustained Release of Lenvatinib for Targeted Treatment of Hepatocellular Carcinoma.","authors":"Xue Wang, Tianzhao Xu, Hui Song, Lanmei Zhou, Xinyi Li, Guangli Li, Xinghui Liu","doi":"10.2174/0115680096329105241031093859","DOIUrl":"https://doi.org/10.2174/0115680096329105241031093859","url":null,"abstract":"<p><strong>Background: </strong>Lenvatinib is an oral tyrosine kinase inhibitor that selectively inhib-its receptors involved in tumor angiogenesis and tumor growth. It is an emerging first-line treatment agent for hepatocellular carcinoma (HCC). However, there is no intravenous ad-ministration of Lenvatinib.</p><p><strong>Aims: </strong>This study aimed to construct nanocomposites that can efficiently support Lenvatinib and target liver cancer tissues and cells.</p><p><strong>Objective: </strong>In this study, ferric oxide-viral-like mesoporous silica nanoparticles-folic acid (Fe3O4-vMSN-FA) nanocomposites loaded with Lenvatinib were constructed, and their anti-hepatocellular carcinoma effects were evaluated.</p><p><strong>Methods: </strong>The hydrothermal method was used to synthesize ferric oxide (Fe3O4). Ferric ox-ide-viral-like mesoporous silica nanoparticles (Fe3O4-vMSN) were synthesized using a two-phase method. Then, Fe3O4-vMSN was modified with folic acid (Fe3O4-vMSN-FA) to better target tumor cells.</p><p><strong>Results: </strong>The experimental data showed that Fe3O4-vMSN-FA nanocomposites were suc-cessfully synthesized and could be loaded with Lenvatinib (Len@ Fe3O4-vMSN-FA). Fe3O4-vMSN-FA had good stability and biocompatibility, and it can release the loaded Len-vatinib faster in an acidic environment (pH 5.5). CCK8 assay and flow cytometry showed that HepG2 cells in the Len@ Fe3O4-vMSN group had the lowest cell viability and the high-est apoptosis rate, confirming the anticancer properties of Len@ Fe3O4-vMSN-FA in vitro. In addition, transwell experiments showed that the migration and invasion ability of HepG2 cells in the Len@ Fe3O4-vMSN-FA group were significantly inhibited. In vivo fluorescence imaging in mice confirmed the enhanced tumor-targeting ability of Fe3O4-vMSN-FA. The tumor volume of the Len@ Fe3O4-vMSN-FA group was significantly reduced, and there was no significant effect on body weight. Moreover, serum liver function index (ALT and AST) and HE staining showed that Len@ Fe3O4-vMSN-FA did not cause obvious damage to organ tissue.</p><p><strong>Conclusion: </strong>Len@ Fe3O4-vMSN-FA has a good anti-liver cancer effect. Fe3O4-vMSN-FA can be used as an alternative platform for MSCs for drug delivery, providing more options for cancer therapy.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001603","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":"Value of Label-Free Ubiquitin-Proteomic Analysis on Defining the Protective Mechanism of Valsartan against Doxorubicin-Induced Heart Failure.","authors":"Liyuan Zhang, Yujing Zhang, Di Chen, Shujuan Shao, Qin Yu","doi":"10.2174/0115680096341637241231111922","DOIUrl":"https://doi.org/10.2174/0115680096341637241231111922","url":null,"abstract":"<p><strong>Introduction: </strong>The cardiotoxicity and subsequent Heart Failure (HF) induced by Doxorubicin (DOX) limit the clinical application of DOX. Valsartan (Val) is an angiotensin II receptor blocker that could attenuate the HF induced by DOX. However, the underlying mechanism of Val in this process is not fully understood.</p><p><strong>Methods: </strong>In this study, we explored the cardio-protective mechanism of Val against DOX-induced cardiotoxicity using label-free ubiquitin-proteomic analysis.</p><p><strong>Results: </strong>Results showed that 27 lysine-ubiquitination sites in 25 proteins were differentially expressed between DOX and DOX+Val treated groups. In addition, the levels of ubiquitin modification of the myosin family and Ankrd1 were upregulated post-Val. Val also in-creased ATP production and activated the Akt/mTOR pathway by regulating the sarcoplas-mic/endoplasmic reticulum calcium ATPase (SERCA2a) and cardiomyocyte calcium hemo-stasis.</p><p><strong>Conclusion: </strong>The results highlight the value of label-free ubiquitin-proteomic analysis in de-fining the molecular mechanism of Val against HF and may be helpful in the development of new therapeutic agents for HF via targeting molecules defined in this research.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001611","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":"Molecular-targeted Therapy for Precision Medicine in Gastrointestinal Cancer: Advancement in Cancer Targeting Strategies.","authors":"Rohitas Deshmukh, Shekhar Verma, Phool Singh Yaduwanshi, Anubhav Dubey, Mamta Kumari","doi":"10.2174/0115680096333058241114064802","DOIUrl":"https://doi.org/10.2174/0115680096333058241114064802","url":null,"abstract":"<p><p>Gastrointestinal (GI) cancer represent significant health challenges, affecting the digestive system with often subtle symptoms that can delay diagnosis. GI cancers account for a higher global mortality rate than any other cancer, largely due to the limited availability of highly effective treatment options.\" Due to next-generation sequencing and new preclinical model tools, that we have learned more regarding its pathophysiology and molecular changes. Every molecular subtype has been characterised molecularly and new treatment targets have been found. Furthermore, tumour xenografts and organoids are grown from patients and are increasingly powerful resources for investigating GI patients' genetic evolution, identifying biomarkers, screening drugs, and conducting preclinical evaluations of personalised medicine approaches. Gastrointestinal (GI) cancer research is rapidly evolving, with recent advance-ments in precision medicine and immunotherapy offering new treatment options. Cutting-edge therapies, such as immune checkpoint inhibitors and targeted therapies like BRAF and HER2 inhibitors, are showing promise in treating specific types of GI cancers. These changes are making it possible for the age of precision medicine to use a mix of clinical, genome-based, and phenotype-based methods to diagnose and treat each GI patient individually. Clin-ical trials are exploring novel combinations of therapies to enhance survival rates and reduce side effects for patients with GI cancers, including colorectal, gastric, and pancreatic cancers. These developments are reshaping the future of gastrointestinal oncology. The purpose of this review is to study the current state of knowledge about predictive biomarkers, prospective novel targeted treatments, potential causes of conflicting trial outcomes, and the prospects for precision medicine in gastric cancer in the future.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142983006","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":"HDAC6: Tumor Progression and Beyond.","authors":"João Marcos Oliveira-Silva, Leilane Sales de Oliveira, João Vitor Marangoni Tagliéri, Laís Bernardo Lopes, Carlos Vinicius Expedito de Souza, Hanna Karolina de Araújo Batistão, Angel Mauricio Castro-Gamero","doi":"10.2174/0115680096332732241113053459","DOIUrl":"https://doi.org/10.2174/0115680096332732241113053459","url":null,"abstract":"<p><p>Histone Deacetylase 6 (HDAC6) is an intriguing therapeutic target in cancer re-search, distinguished as the only HDAC family member predominantly located in the cyto-plasm. HDAC6 features two catalytic domains and a unique ubiquitin-binding domain, which sets it apart from other HDACs. Beyond its role in histone deacetylation, HDAC6 targets vari-ous nonhistone substrates, such as α-tubulin, cortactin, Heat Shock Protein 90 (HSP90), and Heat Shock Factor 1 (HSF1). Its involvement spans critical aspects of tumor progression, in-cluding invasion, metastasis, angiogenesis, drug resistance, stemness, and the reduction of tu-mor cell immunogenicity. Given these functions, HDAC6 inhibitors are emerging as valuable tools in the treatment of both solid and hematological tumors. Recent advancements have seen several HDAC6 inhibitors to enter clinical trials, with promising outcomes reported. This re-view covers the structural features of HDAC6, its biological roles, and its impact on tumor development, particularly focusing on progression-related events. Additionally, a detailed dis-cussion of preclinical and clinical trials involving selective HDAC6 inhibitors is provided.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945990","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":"The COX-2 Inhibitor Celecoxib Sensitizes Nasopharyngeal Carcinoma Cells to Ferroptosis.","authors":"Dawei Li, Shuang Guo, Kunrong Wang, Zhaoqi Liu, Taixin Yu, Yingqiu Zhang","doi":"10.2174/0115680096337720241030055036","DOIUrl":"https://doi.org/10.2174/0115680096337720241030055036","url":null,"abstract":"<p><strong>Background: </strong>Nasopharyngeal cancer (NPC) is prevalent in Southeast Asia and North Africa, which is generally associated with limited treatment options and poor patient prognosis.</p><p><strong>Objective: </strong>Ferroptosis is a recently observed cell death modality and has been shown to link to the efficacy of different anti-cancer treatments, thus offering opportunities to the development of novel therapies. This study aims to investigate the potentiating effects of COX-2 inhibitors on ferroptosis in nasopharyngeal cancer.</p><p><strong>Methods: </strong>The inhibitory effects of COX-2 inhibitors celecoxib and rofecoxib on nasopharyngeal cancer cells were assessed with MTT, colony formation, sphere formation, Transwell, wound healing assays. The status of COX-2 with celecoxib and rofecoxib treatment was investigated by Western blotting and immunofluorescence experiments. Ferroptosis was induced with the GPX4 inhibitor RSL3 with or without COX-2 inhibition and was monitored by fluorescence microscopy. Transcriptomic profiling was conducted with 5-8F cells treated with DMSO as control or celecoxib, and ferroptosis-related candidates were validated by RT- PCR analysis.</p><p><strong>Results: </strong>Celecoxib and rofecoxib effectively inhibited the growth and migration of nasopharyngeal cancer cells. Both inhibitors evidently sensitized nasopharyngeal cancer cells to ferroptosis induction by RSL3, with celecoxib outperforming rofecoxib. Celecoxib treatment resulted in significantly differentially expressed genes in 5-8F cells, among which CHAC1 was validated as a ferroptosis-related target.</p><p><strong>Conclusion: </strong>The COX-2 inhibitor celecoxib effectively sensitized nasopharyngeal cancer cells to ferroptosis induction.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945995","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}