Current cancer drug targets最新文献

{"title":"EVI5 Drives Lung Adenocarcinoma Progression through Modulation of the ERK1/2-c-Myc Signaling Axis","authors":"Peipei Zhang, Xinyang Zhang, Tingting Cai, Yangyang Xu, Yiqing Xie, Chong Li","doi":"10.2174/0115680096384104250529115246","DOIUrl":"10.2174/0115680096384104250529115246","url":null,"abstract":"<p><strong>Introduction: </strong>Lung adenocarcinoma (LUAD) remains a lethal disease worldwide\u0000with a poor prognosis. The ecotropic viral integration site 5 (EVI5) is a crucial oncogene and\u0000mediator of cell division processes, and it extensively participates in tumorigenesis and progression. However, the role of EVI5 in LUAD progression remains elusive. This study aimed\u0000to further explore the underlying mechanisms of EVI5's involvement in LUAD development.</p><p><strong>Methods: </strong>The GEO database was employed to investigate the expression of EVI5 in LUAD and normal tissues, while the Kaplan-Meier Plotter database was utilized to assess its correlation with patient prognosis. Stable cell lines with EVI5 knockout and overexpression were constructed, and Western blotting was performed to detect EVI5 protein expression levels to validate the successful establishment of the stable cell lines. The abilities of proliferation, invasion, and migration of LUAD cells after transfection were analyzed using CCK-8, colony formation, transwell, and wound healing assays. Western blotting, immunofluorescence, and qRT-PCR were further carried out to measure the protein and mRNA expression levels associated with the ERK1/2-c-Myc signaling pathway. Finally, functional rescue experiments were performed on LUAD cells to further explore and verify the signaling pathway.</p><p><strong>Results: </strong>EVI5 was found to be highly expressed in lung adenocarcinoma tissues and correlated with poor prognosis. EVI5 overexpression promoted the malignant behavior of lung adenocarcinoma, whereas its knockout produced the opposite effect. Mechanistically, ERK1/2-cMyc, the key signaling pathway in the malignant progression of LUAD, was further validated by an ERK1/2 pathway inhibitor.</p><p><strong>Conclusion: </strong>Our study demonstrated for the first time that EVI5 promotes malignant progression through the activation of the ERK1/2-c-Myc signaling axis, providing new insights into the pathogenesis of LUAD.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316065","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":"Mechanism of Bispecific Antibodies and Clinical Research Advances in Lung Cancer.","authors":"Jie Yang, Yangyueying Liang, Meiying Zhu, Yuan Meng, Xuerui Wang, Minghui Yu, Longhui Li, Fanming Kong","doi":"10.2174/0115680096353819250127065001","DOIUrl":"https://doi.org/10.2174/0115680096353819250127065001","url":null,"abstract":"<p><p>Lung cancer is an aggressive malignancy and one of the leading causes of cancer-related mortality worldwide. Compared with traditional treatments, the development of pre-cision treatment programs, such as targeted therapy and immunotherapy, has progressively transformed non-small cell lung cancer (NSCLC) with driver mutations, becoming a clini-cally controllable chronic disease. Among the treatments for lung cancer, monospecific anti-bodies gradually show effectiveness but also expose their susceptibility to drug resistance, off-target effects, and other limitations. Therefore, bispecific antibodies have been developed, which have two different antigen-binding sites so that they can bind two distinct antigens or two distinct epitopes of the same antigen with adjustable specificity and do not easily produce drug resistance. This article reviews the design strategies and mechanism of bispecific anti-bodies, summarizes the latest progress in clinical trials involving bispecific antibodies for lung cancer, and analyzes the current challenges and future directions in this area of research.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282792","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":"Comprehensive Pan-cancer Analysis and Experimental Verification of EGLN Family: Potential Biomarkers in Cervical Cancer.","authors":"Dongli Zhang, Ruifang Fu, Guixia Sun, Junfang Yan, Xiaofeng Yang","doi":"10.2174/0115680096362252250527060004","DOIUrl":"https://doi.org/10.2174/0115680096362252250527060004","url":null,"abstract":"<p><strong>Background: </strong>Hypoxia plays a crucial role in malignant tumor formation, primarily mediated by hypoxia-inducible factors (HIFs). Despite extensive research, the complexities and prognostic implications of the EGLN gene family (EGLN1, EGLN2, EGLN3) in cancers remain unclear.</p><p><strong>Methods: </strong>Utilizing public databases (TCGA, GTEx, TARGET, GEO) and bioinformatics tools, a comprehensive analysis of EGLN genes across various cancer types was conducted. Gene ex-pression, mutation data, stemness scores, and clinical information were integrated to evaluate the mutation landscape, expression levels, and prognostic values of EGLNs. Enrichment and pathway analyses explored EGLN-associated biological processes and functional networks. ssGSEA con-structed EGLN scores for prognostic evaluation. Colocalization analysis combined eQTL and GWAS data to investigate genetic variations in cervical cancer. Immunohistochemistry validated EGLN expression in cervical cancer tissues.</p><p><strong>Results: </strong>EGLN genes showed differential expression across cancer types. EGLN1 overexpres-sion was associated with worse survival in cervical squamous cell carcinoma (CESC), pancreatic adenocarcinoma (PAAD), and neuroblastoma (NB), while EGLN3 was linked to poor survival in CESC, lung adenocarcinoma (LUAD), and kidney cancers. EGLNs also demonstrated varied roles in modulating tumor immune activity and heterogeneity.</p><p><strong>Conclusion: </strong>This study provides new insights into EGLN biology and identifies EGLN1 as a potential biomarker for cervical cancer.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215184","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":"Raddeanoside R13 Inhibits Proliferation, Invasion, and Metastasis of Gastric Cancer Cells Based on Network Pharmacology and Experimental Validation.","authors":"Tiantian Zhao, Qiong Wu, Mingxu Da, Chenglou Zhu","doi":"10.2174/0115680096379893250523102125","DOIUrl":"https://doi.org/10.2174/0115680096379893250523102125","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to explore the potential mechanisms by which Rad-deanoside R13 (R13) inhibits the proliferation, invasion, and metastasis of gastric cancer (GC) cells through network pharmacology analysis and experimental validation.</p><p><strong>Methods: </strong>First, network pharmacology was used to explore the potential mechanisms of R13 in treating gastric cancer. The effects of R13 on GC cell proliferation were assessed using CCK-8 and colony formation assays. Apoptosis was measured by flow cytometry, while the effects of R13 on invasion and metastasis were evaluated through wound healing and Transwell invasion assays. Finally, Western blotting was performed to investigate the impact of R13 on the expression of epithelial-to-mesenchymal transition (EMT) markers, PI3K/AKT signaling pathway proteins, and apoptosis-related proteins in GC cells.</p><p><strong>Results: </strong>A total of 58 potential targets of R13 in the treatment of GC were identified. R13 was found to affect the development of GC by regulating pathways, such as NFKB1, mTOR, apoptosis, and the PI3K-Akt signaling pathway. In vitro experiments confirmed that R13 inhibited the proliferation, invasion, and metastasis of GC cells while promoting apoptosis. Additionally, we found that R13 suppressed the EMT of GC cells and reduced the phos-phorylation levels of PI3K, Akt, and mTOR. When this pathway was activated, it partially reversed these effects.</p><p><strong>Conclusion: </strong>R13 inhibited the proliferation, invasion, and metastasis of GC cells while in-ducing apoptosis. Furthermore, R13 may suppress the EMT process in GC cells by inhibit-ing the PI3K/Akt/mTOR signaling pathway. These findings provide a foundation for the potential use of R13 as a therapeutic strategy for gastric cancer.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207909","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":"Extracellular Vesicles-Associated tRFs as Emerging Biomarkers in Breast Cancer.","authors":"Md Sadique Hussain, Liming Zhang, Sumel Ashique","doi":"10.2174/0115680096388071250527074008","DOIUrl":"https://doi.org/10.2174/0115680096388071250527074008","url":null,"abstract":"<p><p>Breast cancer (BC) remains a leading cause of cancer-related mortality among women worldwide, underscoring the urgent need for sensitive, non-invasive biomarkers to improve diagnosis, prognosis, and treatment monitoring. Traditional biomarkers like ER, PR, and HER2 offer limited efficacy, particularly for heterogeneous subtypes such as triple-nega-tive breast cancer (TNBC). Extracellular vesicles (EVs), including exosomes and microvesi-cles, have emerged as promising biomarker carriers due to their stability and ability to encap-sulate diverse bioactive molecules reflective of the parental cell's state. Among EV cargoes, tRNA-derived fragments (tRFs), which are small non-coding RNAs produced by precise cleavage of tRNAs, have gained increasing attention. Once considered mere degradation prod-ucts, tRFs are now recognized for their roles in gene regulation, translation control, apoptosis modulation, and immune response. Recent studies have revealed the selective enrichment of tRFs within EVs, highlighting their role in intercellular communication in breast cancer. Dif-ferential expression of EV-associated tRFs correlates with BC subtype, stage, and patient prog-nosis, highlighting their potential as minimally invasive biomarkers. Specifically, altered lev-els of certain 5'- and 3'-tRFs in patient sera and tumor tissues have been associated with poor survival, metastasis, and therapeutic resistance. Despite these promising findings, gaps remain regarding the mechanisms of tRF sorting into EVs and their functional impact on the tumor microenvironment. This review systematically examines the current understanding of EV-as-sociated tRFs in breast cancer, emphasizing their clinical relevance, detection strategies, and translational potential. By addressing existing challenges, we aim to provide insights into the utility of EV-tRFs as novel biomarkers and therapeutic targets in BC.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207908","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":"Etiology-based Molecular Characterization of Hepatocellular Carcinoma Reveals SQLE's Contribution to Immunosuppressive Microenvironment.","authors":"Kangkang Yu, Qisheng Zhong, Jubo Zhang, Chong Huang","doi":"10.2174/0115680096370558250514063841","DOIUrl":"https://doi.org/10.2174/0115680096370558250514063841","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is a kind of fatal cancer with a variety of risk factors. However, a pan-etiology molecular characterization of HCC has not been explored.</p><p><strong>Objective: </strong>The objective of this study is to explore etiology-specific features of HCC and im-prove our understanding of tumorigenesis, thereby revealing potential therapeutic targets.</p><p><strong>Methods: </strong>RNA-seq, genetic alteration, copy number alteration, and clinicopathological data of The Cancer Genome Atlas -Liver Hepatocellular Carcinoma cohort were downloaded and explored. Immune-related features and single-cell and spatial transcriptomic data were adopted and analyzed.</p><p><strong>Results: </strong>Etiology-based analyses revealed that HCC with different etiologies showed different clinical features, including gender composition, ethnic composition, clinical stage distribution, and survival. In addition, distinct genetic alterations, copy number alterations, and tumor microenvironment were observed in HCC patients with different etiologies. Significantly enhanced expression of squalene epoxidase (SQLE) was observed in viral hepatitis-related HCC and was associated with poor tumor grade and overall survival. Correlation analysis revealed a negative relationship between SQLE expression and anti-tumor immunity. Single-cell and spatial transcriptomics demonstrated that SQLE contributed to reduced T cell and NK cell infiltration while increasing macrophage and monocyte infiltration.</p><p><strong>Conclusion: </strong>The current study demonstrated that HCC has etiology-specific clinical features, genetic alteration, copy number alteration, and tumor microenvironment. Overexpression of SQLE in viral hepatitis-related HCC correlate with poor clinical outcome and may contribute to reduce T cell and NK cell infiltration while increased macrophage and monocyte infiltration, which lead to immunosuppressive microenvironment and can be an actionable target.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141657","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":"Genetic Distinctiveness in Lung Adenocarcinoma and Lung Squamous Cell Carcinoma Cancer: Identifying Key Genomic Signatures through Differentially Expressed Gene Analysis.","authors":"Patrick Shi, Wenqiang Chen","doi":"10.2174/0115680096372957250322174718","DOIUrl":"https://doi.org/10.2174/0115680096372957250322174718","url":null,"abstract":"<p><strong>Background: </strong>Lung cancer is the most commonly diagnosed cancer type and the leading cause of cancer death worldwide. Non-small cell lung cancer (NSCLC) accounts for more than 80% of all lung cancer cases and includes two main subtypes: lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Understanding the differences in genes causing the proliferation of LUAD and LUSC is key to advancing the diagnosis and targeted treatment development.</p><p><strong>Aims: </strong>The aim of this study was to identify candidate genes and potential tumorigenesis mechanisms distinguishing LUAD and LUSC.</p><p><strong>Methods: </strong>Three pooled transcriptomic datasets (GSE10245, GSE37745, and GSE43580) were analyzed from the Gene Expression Omnibus (GEO) database, with each dataset statistically tested for differentially expressed genes (DEGs). DEGs between lung LUAD and LUSC of the three datasets were analyzed with Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. A protein-protein interaction (PPI) network was constructed to screen candidate genes.</p><p><strong>Results: </strong>This study identified 138 shared DEGs among three patient-level gene expression datasets, containing 39 upregulated genes and 99 downregulated genes. The GO and KEGG enrichment analysis results showed the functions of DEGs to be mainly associated with epidermis development, cornified envelope, structural constituent of epidermis, and estrogen signaling pathway. Finally, through the PPI network, eight core genes were identified, including KRT14, KRT5, KRT6A, KRT16, SPRR1A, SPRR1B, SPRR3, and KRT6B.</p><p><strong>Conclusion: </strong>We have elucidated key genes and molecular mechanisms linked to NSCLC subtypes. These findings have the potential to facilitate improved diagnostic and therapeutic targets for LUAD and LUSC biomarkers.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141780","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":"Trimethylamine N-oxide Impairs Oocyte Maturation and Embryogenesis via NF-κB/NLRP3 Pathway Modulation.","authors":"Fengping He, Yongmei Zhang, Yanle Guo, Tizhen Yan, Jiwu Lou","doi":"10.2174/0115680096364675250419135908","DOIUrl":"https://doi.org/10.2174/0115680096364675250419135908","url":null,"abstract":"<p><strong>Background: </strong>The role of Trimethylamine N-oxide (TMAO) in oocyte maturation and embryogenesis remains unclear, particularly its impact on ovarian granulosa cells (OGCs) and its underlying mechanisms.</p><p><strong>Methods: </strong>This study examined the effects of TMAO (100-400 μmol/L) on oocyte maturation, cumulus cell expansion, mitochondrial distribution, and embryonic development in vitro and in a BALB/c mouse model. The involvement of the NF-κB/NLRP3 signaling pathway in TMAO-induced ovarian dysfunction was assessed using Western blotting and gene expression analyses. The potential therapeutic effect of miRNA-146, an NF-κB inhibitor, was also explored.</p><p><strong>Results: </strong>Western blotting confirmed that TMAO activates the NF-κB signaling pathway and induces the synthesis of caspase 3 and NLRP3 complexes. However, pretreatment with miRNA-146, an NF-κB inhibitor, significantly reduced inflammation and inflammatory gene expression during TMAO therapy. Additionally, miRNA-146 pretreatment promoted oocyte maturation by suppressing NF-κB/NLRP3 activation, OGCs apoptotic inflammatory factor expression, and the gene expression of NF-κB, caspase 3, and NLRP3.</p><p><strong>Conclusion: </strong>Findings demonstrate that TMAO disrupts oocyte development through NF- κB/NLRP3 activation, contributing to ovarian dysfunction. Notably, targeting TMAO and its downstream signaling could serve as a novel therapeutic strategy for premature ovarian insufficiency (POI).</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141784","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":"Extraordinary Benefit of Regorafenib in Metastatic Cholangiocarcinoma: A Case Report.","authors":"Ayberk Bayramgil, Tugce Kubra Gunes, Fatma Gulcicek Ayranci, Duygu Yoruk Atik, Busra Nigdelioglu, Melike Ozcelik, Ozgecan Dulgar Kaya","doi":"10.2174/0115680096378189250422100120","DOIUrl":"https://doi.org/10.2174/0115680096378189250422100120","url":null,"abstract":"<p><strong>Introduction/background: </strong>Cholangiocarcinoma (CC) is a rare, aggressive cancer of the bile ducts with limited treatment advancements over recent decades. The five-year survival rate for CC remains low, around 10%, and even lower for advanced cases.</p><p><strong>Case presentation: </strong>This case report discusses a 46-year-old woman with metastatic CC who achieved remarkable progression-free survival with regorafenib, a multikinase inhibitor typi-cally used in other cancers. After multiple lines of treatment, regorafenib was given as a 7th-line therapy. Despite initial intolerance requiring dose reduction, the patient achieved 22 months of progression-free survival (PFS) with stable disease and partial regression in some areas. Her response to regorafenib significantly exceeded typical outcomes in the literature, where PFS generally ranges from 3 to 4 months. This improvement may be attributed to an FGFR2 mutation identified via next-generation sequencing, which regorafenib may effec-tively target.</p><p><strong>Conclusion: </strong>This case suggests that patients with FGFR2 mutations might benefit from regorafenib, warranting further studies to explore this associationAs can be applied as a promising target gene to develop drug resistance and remedial efficacy.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101502","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":"Evaluation of the Antitumoral Effect of PI3K/AKT/mTOR Pathway Inhibition and Antioxidant Combination on Burkitt Lymphoma Cell Line.","authors":"Ibrahim Karaduman, Hatice Terzi, Seyma Tastemur, Mehmet Şencan","doi":"10.2174/0115680096366040250414114030","DOIUrl":"https://doi.org/10.2174/0115680096366040250414114030","url":null,"abstract":"<p><strong>Background and aim: </strong>Burkitt lymphoma is a highly aggressive type of B-cell non-Hodgkin lymphoma. While it is more commonly seen in children and adolescents, it accounts for about 1-2% of adult lymphomas. Since it has high Ki-67 ratios, both its progression rate and sensitivity to chemotherapy are high. However, treatment success decreases in chemotherapy-resistant relapsed/refractory groups. Therefore, new and less toxic therapeutic agents targeting biological pathways related to Burkitt lymphoma pathogenesis are needed. In our study, we aimed to determine the antitumoral efficacy of PI3K/AKT/mTOR pathway inhibitor ETP 45658 and antioxidant Resveratrol, which play a role in Burkitt lymphoma pathogenesis on a Burkitt lymphoma cell line.</p><p><strong>Methods: </strong>Burkitt lymphoma Raji cell line was used in our study. ETP 45658 was applied to the cell line at concentrations of 50, 25, 12.5, 1, 0.1, and 0.01 μM, both alone and in combination with 100 μM resveratrol. The cytotoxic effects of ETP 45658 and the combination treatment on Raji cells were then evaluated using an in vitro XTT cell viability test. IC50 value was calculated according to the results obtained in the XTT test. Based on the IC50 value, the apoptosis assay was studied using the flow cytometry method.</p><p><strong>Results: </strong>Our research showed that increasing doses of ETP 45658, individually and in combination, had a statistically significant cytotoxic effect on Burkitt lymphoma Raji cells. This cytotoxic effect was found to be higher in combination treatment. In apoptosis experiments with the calculated IC50 value, it induced apoptosis weakly.</p><p><strong>Conclusion: </strong>Our study showed that ETP 45668 alone and in combination with resveratrol has antitumoral activity on the Burkitt lymphoma cell line. PI3K/Akt/mTOR pathway inhibitors may be an alternative treatment option in patients with relapsed/refractory Burkitt lymphoma. However, more preclinical and clinical studies are needed.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076561","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}