Medical Oncology最新文献

{"title":"Botanical sources, biopharmaceutical profile, anticancer effects with mechanistic insight, toxicological and clinical evidence of prunetin: a literature review.","authors":"Sumaya Akter Bithi, Md Sakib Al Hasan, Md Shimul Bhuia, Emon Mia, Noshin Tasnim Yana, Ali Mohamod Wasaf Hasan, Mohammed Burhan Uddin, Md Abu Sayeed, Yasin Emon, Rubel Hasan, Raihan Chowdhury, Muhammad Torequl Islam","doi":"10.1007/s12032-025-02646-z","DOIUrl":"10.1007/s12032-025-02646-z","url":null,"abstract":"<p><p>Prunetin (PRU), a naturally occurring flavonoid, has gained recognition for its wide-ranging therapeutic benefits, though its anticancer properties have yet to be extensively reviewed. This study explores the potential of PRU in targeting critical molecular pathways involved in tumor progression, including oxidative stress, apoptosis, cell cycle regulation, and metastasis. Data were compiled from reputable sources, including PubMed, Springer Link, Scopus, Wiley Online, Web of Science, ScienceDirect, and Google Scholar. The findings emphasize PRU's ability to mitigate oxidative stress, promote apoptosis, and regulate the cell cycle in cancer cells. Its anti-inflammatory and anti-angiogenic properties further enhance its effectiveness against cancer. Mechanistic studies reveal that PRU suppresses oncogenic pathways such as PI3K/Akt/mTOR (Phosphoinositide 3-kinase/Protein kinase B/Mammalian target of rapamycin) while activating tumor-suppressor mechanisms. Experimental models show that PRU effectively inhibits cancer cell proliferation and metastasis. Additionally, PRU exhibits favorable pharmacokinetics, demonstrating high intestinal absorption (95.5%), good Caco-2 permeability, and metabolism via CYP1A2, CYP2C19, CYP2C9, and CYP3A4, though it has poor blood-brain barrier (BBB) permeability and limited aqueous solubility, posing challenges for systemic bioavailability. Beyond its anticancer properties, PRU displays broad pharmacological relevance, including anti-inflammatory, cardioprotective, neuroprotective, anti-obesity, and osteoprotective effects, mediated through pathways, such as NF-κB, MAPK, and AMPK. Toxicological studies indicate a favorable safety profile, with low cytotoxicity in normal cells and no significant toxicity at high doses in preclinical models. While clinical evidence on PRU remains limited, studies on structurally related isoflavones suggest promising therapeutic potential, necessitating further clinical trials to establish its efficacy and safety in humans.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"87"},"PeriodicalIF":2.8,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542589","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":"Deciphering FOXM1 regulation: implications for stemness and metabolic adaptations in glioblastoma.","authors":"Kumari Swati, Saniya Arfin, Kirti Agrawal, Saurabh Kumar Jha, Ramya Lakshmi Rajendran, Anand Prakash, Dhruv Kumar, Prakash Gangadaran, Byeong-Cheol Ahn","doi":"10.1007/s12032-025-02639-y","DOIUrl":"10.1007/s12032-025-02639-y","url":null,"abstract":"<p><p>The Forkhead box M1 (FOXM1) gene-mediated Wnt signaling pathway plays a significant role in the development and growth of glioblastoma multiforme (GBM), an exceptionally aggressive form of brain cancer. Our research explores the crucial involvement of the FOXM1 gene, a key transcription factor within the Wnt signaling pathway using bioinformatics techniques in both GBM and glioma stem cells (GSCs). Elevated FOXM1 gene expression is strongly associated with poor patient survival in GBM. Furthermore, FOXM1 gene expression is correlated with stemness-related factors, such as SOX2 and SOX9, which act as key drivers in the progression of cancer stem cells. Moreover, we specifically look into the direct associations of the FOXM1 gene with angiogenetic-related factors, metabolic genes, metastatic genes, pluripotency-related factors, immune cell infiltration, transcriptional networks, and functional category enrichment analysis, shedding light on the intricate molecular mechanisms involved in GBM initiation and progression. Additionally, our research identifies FOXM1-targeting miRNAs, revealing their potential as therapeutic candidates with implications for patient survival rates and DNA methylation patterns of the FOXM1 gene, uncovering insights into its epigenetic regulation. This knowledge contributes to a comprehensive understanding of the molecular landscape and potential avenues for developing more effective therapeutic approaches against GBM and GSCs.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"88"},"PeriodicalIF":2.8,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542593","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 reciprocal effects of autophagy and the Warburg effect in pancreatic ductal adenocarcinoma: an in vitro study.","authors":"Bita Azizzadeh, Maryam Majidinia, Ali Gheysarzadeh","doi":"10.1007/s12032-025-02631-6","DOIUrl":"10.1007/s12032-025-02631-6","url":null,"abstract":"<p><p>Autophagy and the Warburg effect are two common pathways in pancreatic ductal adenocarcinoma (PDAC). To date, the reciprocal effects of these pathways have not yet been elucidated. Therefore, this study was designed to investigate the relationship between these factors in vitro and may provide therapeutic targets in the future. The Mia-Paca-2 and AsPc-1 cell lines were cultured under normal conditions. To achieve autophagy, starvation was induced by Hank's balanced salt solution (HBSS), whereas autophagy was inhibited by 3-methyladenine (3-MA). The Warburg effect is mimicked by lactic acid, and the Warburg effect is inhibited by oxamate, the main inhibitor of lactate dehydrogenase. Cell viability was checked through the MTT assay method. Autophagy was checked via evaluation of Beclin-1 via western blotting. The amount of lactic acid was also measured with a lactate dehydrogenase (LDH) assay kit. The cells were incubated with different concentrations of 3-MA, lactic acid and oxamate. The viability of AsPc-1 cells decreased, and the IC₅₀ values were 1195 µM, 23.06 mM and 8.617 mM for 3-MA, lactic acid and oxamate, respectively. Similarly, the IC₅₀ values of Mia-Paca-2 were 873.9 µM, 35.9 mM and 26.74 mM for 3-MA, lactic acid and oxamate, respectively. Our data revealed that starvation increased the expression of the autophagy-related protein Beclin-1 (P value < 0.05); however, 3-MA significantly reduced its expression (P value < 0.05). In addition, lactic acid alone did not affect the expression level of Beclin-1 (P value > 0.05), but oxamate treatment increased its expression (P value < 0.05). We also showed that starvation reduced lactic acid levels, but an autophagy inhibitor, 3MA, significantly increased lactic acid production (P value < 0.05). Our findings showed that lactic acid alone has no significant effect on autophagy and that oxamate induces autophagy, possibly because of caloric restriction. On the other hand, autophagy inhibits lactic acid production, whereas the inhibition of autophagy leads to increased lactic acid production.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"86"},"PeriodicalIF":2.8,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531242","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 the TGF-β-p21 axis: a critical regulator of bleomycin-induced cell cycle arrest and apoptosis in vitro-implication for progressive cervical cancer therapy.","authors":"Somi Shrivastava, Chandrahas Koumar Ratnacaram","doi":"10.1007/s12032-025-02624-5","DOIUrl":"10.1007/s12032-025-02624-5","url":null,"abstract":"<p><p>Cervical cancer signifies a global health concern and is a major cause of cancer mortality in women worldwide. Dysregulation of apoptotic pathway and cell cycle play a role in cancer development. Aberrant signalling pathways leads to complex mechanisms leading to the severity. Bleomycin is an anti-tumor glycopeptide molecule which exhibits impressive cytotoxicity in cancer cells. However, its modulating significance on TGF-β induced cell cycle arrest and apoptosis in cervical cancer remains elusive. We confirmed the cytotoxicity, anti proliferative effect of bleomycin in HeLa cells. Meanwhile, bleomycin also led to the suppression of cell migration, invasion. Relative gene expression quantification for cell cycle regulatory, apoptotic, and TGF-β member's genes was done by qRT-PCR. Bleomycin markedly downregulated the expression of cyclin A2, cyclin B1 and cell cycle arrest at G₂/M phase in vitro. Dual AO/EB and Propidium iodide staining was done to evaluate early and late apoptosis in cervical cancer cells. Bleomycin prompts early and late apoptosis in cervical cancer cells by chromatin condensation and blebbing. Mechanistically, bleomycin activates TGF-β induced p21 cascade by upregulation of GADD45A and GDF11, stabilizing p53, to induce cell cycle arrest and apoptosis. Bleomycin induces DNA damage triggering TGF-β pathway. This study can broaden our understanding of the signalling mechanisms that could develop effective strategies for cancer therapy. Elucidation of these pathways in cervical cancer may ultimately lead to novel and more effective treatments. Here, we highlight apoptosis-inducing drug as a therapeutic strategy to regulate the process of carcinogenesis, and regulating apoptosis could benefit cancer treatment and prevention.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"85"},"PeriodicalIF":2.8,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143523767","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":"Characterization of lncRNAs contributing to drug resistance in epithelial ovarian cancer.","authors":"Ehteram Khademi Siahestalkhi, Aydin Demiray, Arzu Yaren, Atike Gökçen Demiray, Seçil Tan, Hakan Akça","doi":"10.1007/s12032-025-02628-1","DOIUrl":"10.1007/s12032-025-02628-1","url":null,"abstract":"<p><p>Epithelial ovarian cancer (EOC) is the second leading cause of death among women with gynecological cancers, particularly in high-income countries. Despite significant advancements in molecular oncology and an initially positive response to primary chemotherapy, the development of drug resistance remains a major challenge in the effective management of EOC. Consequently, there is an urgent need for innovative biological markers that can enable early diagnosis and provide more accurate predictions of recurrence risk in ovarian cancer patients. This study investigated the expression profiles of seven specific long noncoding RNAs (lncRNAs)-SNHG7, TUG1, XIST1, PRLB, TLR8-AS1, ZFAS1, and PVT1-associated with epithelial ovarian cancer and their relationship with drug resistance. To achieve this, drug-resistant subtypes of aggressive EOC cell lines, including carboplatin/paclitaxel-resistant OVCAR3 and SKOV3 lines, were developed. The expression profiles of the selected lncRNAs were quantitatively analyzed using RT-qPCR across various ovarian cancer cell lines and in serum samples from 25 patients before chemotherapy, six months after treatment, and 23 healthy controls. The findings revealed that the target lncRNAs were significantly upregulated under drug-resistant conditions and in post-chemotherapy serum samples, suggesting their involvement in a complex regulatory network. These results highlight the critical roles of lncRNAs in the progression and treatment response of EOC, positioning them as potential therapeutic targets and biomarkers for early diagnosis and treatment stratification. Identifying reliable lncRNA biomarkers could enable the early detection of patients at risk for developing drug resistance, thereby facilitating personalized treatment strategies to improve patient outcomes and survival rates.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"84"},"PeriodicalIF":2.8,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11850566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metal nanoparticles as a promising therapeutic approach for prostate cancer diagnosis and therapy: a comprehensive review.","authors":"Mohamed J Saadh, Wajida Ataallah Khidr, Karar H Alfarttoosi, Ashok Kumar Bishoyi, Subbulakshmi Ganesan, Aman Shankhyan, S Gayathri, Jasur Rizaev, Waam Mohammed Taher, Mariem Alwan, Mahmood Jasem Jawad, Ali M Ali Al-Nuaimi","doi":"10.1007/s12032-025-02633-4","DOIUrl":"10.1007/s12032-025-02633-4","url":null,"abstract":"<p><p>Prostate cancer is a leading cause of mortality among men worldwide, particularly in the USA and European nations, with an estimated 1.9 million new cases and over 580,000 deaths annually, according to recent global statistics. The treatment of prostate tumors presents significant clinical challenges, due to the disease's high metastatic potential, specifically to vital organs, such as the liver, lungs, bones, and brain. The intrinsic heterogeneity of prostate cancer cells, characterized by diverse genetic, molecular, and phenotypic profiles, complicates conventional therapeutic strategies, highlighting the need for advanced diagnostic and treatment modalities. Nanoparticles play a critical role in oncology field due to their unique physicochemical properties, including high surface area-to-volume ratio and the ability to be functionalized with targeting ligands. Metallic-based nanoparticles exhibits significant potential for applications in field of nanomedicine, drug delivery systems, gene silencing methods, radiotherapy enhancement, cancer diagnostics, and targeted therapeutic interventions. Metal nanoparticles have substantially improved the sensitivity and specificity of major imaging modalities and have demonstrated remarkable efficacy as biosensors for the detection of prostate cancer-specific biomarkers. This review article provides an in-depth analysis of the utilization of metal nanomaterials in prostate cancer, focusing on their roles in enhancing therapeutic efficacy, advancing diagnostic precision, and supporting the development of novel treatment strategies.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"83"},"PeriodicalIF":2.8,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483681","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":"STM2457 impairs the proliferation of esophageal squamous cell carcinoma by activating DNA damage response through ATM-Chk2 axis.","authors":"Chuanli Gao, Hui Yang, Jiao Cheng, Shuang He, Yong Yang, Lei Xu, Qiang Ma, Xiaolan Guo, Xiaowu Zhong","doi":"10.1007/s12032-025-02634-3","DOIUrl":"10.1007/s12032-025-02634-3","url":null,"abstract":"<p><p>METTL3 has been proven to play an important role in the proliferation of Esophageal squamous cell carcinoma (ESCC). In this study, we focused on investigating the therapeutic role and molecular mechanism of STM2457 in ESCC, which is a novel small-molecule inhibitor of METTL3. The effect of STM2457 on ESCC was evaluated using ESCC cell lines by the cell viability measurement, cloning formation assay, scratching assay, transwell assay, and flow cytometry techniques. Furthermore, the molecular mechanism study was employed to evaluate by RT-qPCR, Western blotting, proteomics analysis, comet assay, etc. Additionally, the anticancer effect of STM2457 was carried out by nude mice tumor xenograft in vivo. This study showed STM2457 could significantly inhibit the proliferation and migration of Eca109 and KYSE150 cells, which promoted G0/G1 phase arrest and apoptosis in a dose-dependent manners in vitro. Moreover, proteomics analysis suggested the important role of ATM in action mechanism of STM2457. Further studies showed that STM2457 may activate DNA damage response and the expression of ATM, p-ATM, p-Chk2, and γ-H2AX protein in ATM-Chk2 pathway. Intriguingly, ATM inhibitor CGK-733 and knocking down ATM significantly reduced the expression of ATM in Eca109 and KYSE150 cells treated with STM2457. Importantly, STM2457 significantly upregulated the expression of ATM and γ-H2AX protein and inhibited the growth of ESCC in vivo. Finally, STM2457 combined with PTX could also significantly inhibit the proliferation and migration ability of Eca109 and KYSE150 cells by targeting the ATM-mediated DDR pathway. In tumor-bearing nude mice model, STM2457 combined with Paclitaxel can inhibit the growth of ESCC and increased the expression of ATM and γ-H2AX protein. These findings revealed ATM-Chk2 pathway is a promising therapeutic target for STM2457 to effectively inhibit the proliferation of ESCC.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"82"},"PeriodicalIF":2.8,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476088","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":"From conventional to cutting edge: an exploration of osteosarcoma treatments.","authors":"Garen S Sellers, McKade A Poirier, Trenton G Mayberry, Braydon C Cowan, Mark R Wakefield, Yujiang Fang","doi":"10.1007/s12032-025-02629-0","DOIUrl":"10.1007/s12032-025-02629-0","url":null,"abstract":"<p><p>Osteosarcoma is a highly aggressive cancer in children and young adults that has a remarkably high mortality rate upon metastasis. Current standard treatments have remained largely unchanged for nearly five decades, focusing on a combination of chemotherapy with high-dose methotrexate, doxorubicin, and cisplatin, complemented by aggressive surgical resections. Despite this lack of change, recent advancements in medical research have spurred hope for more effective and less invasive approaches to managing osteosarcoma. In this review, we provide an overview of existing therapeutic modalities, including chemotherapy regimens tailored to tumor stage and patient response, radiation therapies aimed at local tumor control, and advanced surgical techniques such as limb-sparing procedures. Additionally, we explore two promising future treatments that are currently under investigation for osteosarcoma cases: targeted therapies utilizing nanomaterials like graphene oxide and innovative oncolytic viruses. This review highlights potential breakthroughs in treatment options while identifying areas that warrant further investigation in the management of osteosarcoma. Considering the limited advancements in treatment over the past decades, identifying and highlighting novel and effective therapies is vital for improving patient outcomes and survival rates.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"81"},"PeriodicalIF":2.8,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468502","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":"PHLPP1 depletion promotes tumorigenesis and stemness in triple-negative breast cancer cells through AKT signaling.","authors":"Md Anwarul Haque, Thanasis Poullikkas, F M Al-Amin Kaisar, Shariful Haque, Mst Hajera Khatun, Al Mamun, Alam Khan","doi":"10.1007/s12032-025-02630-7","DOIUrl":"10.1007/s12032-025-02630-7","url":null,"abstract":"<p><p>Breast cancer, particularly triple-negative breast cancer (TNBC), is a major cause of women's mortality, and effective treatment options are still lacking due to the absence of known mechanisms and biomarkers. Therefore, unveiling novel molecular mechanisms to identify potential biomarkers is urgently needed to ensure an effective TNBC treatment. In this study, we investigated the role of PHLPP1, a tumor suppressor gene, in the tumorigenesis and induction of cancer stem cells in TNBC using publicly available data and experimental protocols. Our study found that lower levels of PHLPP1 contributed negatively to patient overall survival. In addition, loss of PHLPP1 increased breast cancer cell proliferation, long-term colony regrowth ability, and the number of migrated and invaded cells. Consequently, we designed a stable PHLPP1 knockdown (KD) cell line to understand its impact through its stemness potential. As expected, PHLPP1 KD dramatically upregulated breast cancer stemness markers (NANOG, OCT4, and SOX2) expression and significantly increased cancer stem cell frequencies in TNBC cells. Mechanistically, PHLPP1 loss enhanced AKT phosphorylation at Ser473, thus activating AKT signaling, leading to larger tumor formation in vivo and elevated stemness expression. This study concludes that PHLPP1 has the capability to reduce the expression of cancer stemness genes by negatively regulating the AKT signaling pathway. Therefore, these findings may pave the way for discoveries in the context of cancer stemness and future strategies for developing effective treatment options for TNBC patients.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"80"},"PeriodicalIF":2.8,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468519","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":"In vitro cytotoxic and apoptotic effects of boric acid on endometrial adenocarcinoma cell lines (HEC-1B and Ischikawa).","authors":"Nazlı Çil, Elif Önder, Ayşe Nur Damar, Seyedmahdi Tabatabaei, Ümit Çabuş, Gülçin Abban Mete","doi":"10.1007/s12032-025-02625-4","DOIUrl":"10.1007/s12032-025-02625-4","url":null,"abstract":"<p><p>Endometrial carcinoma, the most common malignancy of the female genital tract, remains challenging to treat despite early-stage dominance. Surgical interventions and irradiation are insufficient for advanced endometrial cancer. Our aim was to investigate to explore the in vitro cytotoxicity and apoptotic effects of boric acid (BA) on endometrial adenocarcinoma cell lines (Ishikawa and HEC-1B cell lines), providing experimental evidence for the potential application of boric acid as an anticancer drug. Time- and dose-dependent cell viability was determined with the XTT cell proliferation test. Differences in mRNA levels were determined by RT-PCR using cDNAs and SYBR green assay. Colony formation and the effect of BA on wound healing were evaluated. Immunocytochemistry and TUNEL tests were performed to evaluate apoptosis. BA increased the expression of Caspase 3 and Bax in HEC-1B and Ischikawa cell lines. It was determined that BA significantly decreased the number of colonies in both cell lines (p < 0.05). In HEC-1B and Ishikawa cell lines, there was an increase in cell migration in the control group at 16 and 24 h. The apoptotic index was higher in the BA group, although it was not statistically significant. According to immunohistochemistry results, Caspase 3 and Bax expression in HEC-1B and Ishikawa cell lines were statistically increased in BA group. The expression of Bcl-2 was decreased statistically with BA treatment in both cell lines (p = 0.0001). BA treatment inhibited cell migration and colony formation, which are important for carcinogenesis, in endometrial adenocarcinoma cell lines. This inhibition was shown to occur through the apoptotic pathway.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"79"},"PeriodicalIF":2.8,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11839787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}