Recent patents on anti-cancer drug discovery最新文献

{"title":"Synergistic Antitumor Activity of DA-10 and Niraparib by Overcoming Platinum Resistance in Ovarian Cancer.","authors":"Ruyuan Yu, Yingru Xu, Miaoling Tang, Shengyuan Zhang, ZunFu Ke","doi":"10.2174/0115748928425406260217074420","DOIUrl":"https://doi.org/10.2174/0115748928425406260217074420","url":null,"abstract":"<p><strong>Introduction: </strong>While PARP inhibitors have shown effectiveness in treating platinumsensitive ovarian cancer, their therapeutic efficacy is notably reduced in cases of platinumresistant disease. This limitation highlights the urgent need for developing combination strategies that can enhance the response to PARP inhibitors in platinum-resistant ovarian cancer.</p><p><strong>Methods: </strong>This study explores the therapeutic potential and mechanisms of combining dolastatin 10 (DA-10) with niraparib in platinum-resistant models, highlighting their cytotoxic synergy and promising patent prospects. In vitro assays, including cell proliferation, colony formation, apoptosis, and DNA damage quantification, were conducted using cisplatin-resistant A2780 and SKOV3 cell lines. The in vivo efficacy and synergy were evaluated in xenograft tumor models. Mechanistic studies focused on DNA damage accumulation, PARP activity, and microtubule stability.</p><p><strong>Results: </strong>The co-treatment of DA-10 with niraparib significantly inhibited cell proliferation and colony formation, while substantially increasing DNA damage levels and apoptosis in platinumresistant A2780 and SKOV3 cell lines. The synergistic inhibition of tumor growth was further validated in vivo through xenograft models. Mechanistically, the combination treatment synergistically suppressed PARP activity and destabilized microtubules.</p><p><strong>Discussion: </strong>These findings suggest that concurrent disruption of DNA repair and microtubule stability contributes to the observed synergy and may help overcome mechanisms underlying platinum resistance. Further studies in broader preclinical models will be needed to refine the mechanistic basis and assess translational potential.</p><p><strong>Conclusion: </strong>The synergistic interaction between DA-10 and niraparib demonstrates significant potential to overcome platinum resistance in ovarian cancer. This novel combinatorial strategy represents a patentable therapeutic approach for platinum-resistant ovarian cancer, offering insights for future translational clinical trials assessing the efficacy of DA-10 in combination with niraparib.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancements in Sotorasib: A Comprehensive Review of its Efficacy in Non-small Lung Cancer Treatment.","authors":"Archana Tupe, Sachin Bhosale, Nirmala Shinde","doi":"10.2174/0115748928388137251204140520","DOIUrl":"https://doi.org/10.2174/0115748928388137251204140520","url":null,"abstract":"<p><p>Sotorasib (SR), a first-in-class KRAS G12C inhibitor developed by Amgen, represents a major advancement in the treatment of non-small cell lung cancer (NSCLC) with KRAS G12C mutations. This comprehensive review covers the drug's development, mechanism of action, pharmacokinetics, synthesis, and analytical methods. KRAS mutations, particularly KRAS G12C, are associated with poor prognosis in NSCLC, with approximately 13% of cases harboring this mutation. SR targets the KRAS G12C mutation by covalently binding to the cysteine residue in the KRAS protein, inhibiting its signalling pathways and promoting tumour cell death. Approved by the FDA in 2021, SR has demonstrated promising efficacy, including significant objective response rates and progression-free survival benefits in pretreated patients with NSCLC. The development of resistance mechanisms, such as secondary mutations and alternative signalling pathways, remains a challenge, underscoring the need for ongoing research into combination therapies and further trials. This review also highlights the drug's synthetic processes, structural features, and global patent coverage. SR approval marks a significant milestone in KRAS-targeted therapies, offering new hope for patients with difficult-to-treat lung cancer.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147597199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MYH9 Promotes the Proliferation and Progression of Squamous Cervical Cancer Cells.","authors":"Juanjuan Yi, Caiqiu Xu, Zhifeng Huo, Huixia Zhou, Zhaoyang Zeng, Longyang Liu","doi":"10.2174/0115748928385414251121233928","DOIUrl":"https://doi.org/10.2174/0115748928385414251121233928","url":null,"abstract":"<p><strong>Introduction: </strong>Cervical cancer (CC) is the third most commonly occurring cancer and the fourth most common cause of cancer-related death in women. Squamous cell carcinoma (SCC) comprises ~70% of CC cases; however, its detailed molecular mechanisms are still unclear.</p><p><strong>Methods: </strong>24 pairs of SCC and para-tumor tissues were detected with RT-qPCR, respectively. MTT and EdU assays were performed to demonstrate the role of MYH9 in SCC cell proliferation. Transwell and Boyden were performed to demonstrate the role of MYH9 in SCC cell progression. A Western blot was performed to demonstrate the mechanism of MYH9 in SCC.</p><p><strong>Results: </strong>The results showed that mRNA and protein levels of MYH9 were higher in SCC samples than in para-tumor samples, and MYH9 knockdown suppressed the proliferation of SCC cells, and suppressed the migration and invasion of the Siha cell line, but not the C-33A cell line. Mechanistic assays showed that knockdown of MYH9 inhibited the epithelial-mesenchymal transition (EMT) and downstream cell-cycle factors, including c-Jun and cyclin-D1.</p><p><strong>Discussion: </strong>MYH9 expression was upregulated in samples with SCC. Furthermore, the in vitro assays demonstrated that MYH9 had roles in promoting the proliferation of the SCC Siha and C- 33A cell lines and inducing the migration and invasion of Siha cells via regulating EMT signals and downstream cell-cycle factors.</p><p><strong>Conclusion: </strong>MYH9 acts as an oncogenic gene in SCC, which promotes the carcinogenesis and progression of SCC cells via EMT signaling, and it may serve as a valuable patent for targeted treatment biomarker of SCC.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147617251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lactylation Plays a Novel Role in the Tumor Microenvironment and its Prognostic Implications for Breast Cancer.","authors":"LiLi Gao, Hongfei Yao, Qing Li","doi":"10.2174/0115748928413005251129104036","DOIUrl":"https://doi.org/10.2174/0115748928413005251129104036","url":null,"abstract":"<p><strong>Introduction: </strong>This study aims to develop a predictive signature based on lactylation to complement existing staging systems and improve prognostic accuracy in clinical settings.</p><p><strong>Methods: </strong>A database of lactylation-associated genes was obtained from The Cancer Genome Atlas (TCGA). Cox and LASSO regression analyses were used to identify a risk signature. Differential expression and enrichment analyses were performed to explore functional differences between these groups, and the influence of lactylation-associated genes on the tumor immune microenvironment and chemotherapy sensitivity was evaluated. After screening for lactylationassociated genes highly expressed and prognostically relevant in BC, in vitro assays were conducted to examine the role of these genes in tumor proliferation and metastasis.</p><p><strong>Results: </strong>We identified six lactylation-associated genes, including SH3GL1, XRCC4, PCMT1, DECR1, ALDH1A1, and RPL14. XRCC4 was highly expressed and identified as a significant factor affecting patients' overall survival in BC. Patients in the high-risk groups exhibited poorer prognoses compared to those in the low-risk groups. Tumor mutation burden, chemotherapeutic sensitivity, and immune infiltration differed significantly between the two groups.</p><p><strong>Discussion: </strong>Our results propose XRCC4 as a potential therapeutic target in BC. Although the current evidence is constrained, we are actively expanding the sample size and will develop dedicated validation cohorts to corroborate the lactylation-related findings.</p><p><strong>Conclusion: </strong>Our findings highlight the potential of lactylation-associated genes, particularly XRCC4, in BC progression and clinical treatment strategies. The development of an XRCC4 inhibitor may be eligible for patent protection and could potentially serve as a novel therapeutic option for BC.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone Deacetylases as Epigenetic Regulators of EMT in Hypoxia-driven Tumor Metastasis: Mechanistic Insights and Therapeutic Implications.","authors":"Yin Bao, Jun Zhu, Hong Zhu, Jun Gao","doi":"10.2174/0115748928416410251128094143","DOIUrl":"https://doi.org/10.2174/0115748928416410251128094143","url":null,"abstract":"<p><strong>Introduction: </strong>The hypoxic microenvironment is a hallmark of solid tumors, driving metastasis through Hypoxia-Inducible Factor-1α (HIF-1α)-mediated Epithelial-Mesenchymal Transition (EMT). Histone deacetylases (HDACs) critically enhance HIF-1α signaling by deacetylation, making them a potential therapeutic target for metastasis inhibition.</p><p><strong>Methods: </strong>We conducted a systematic review of literature from PubMed, Web of Science, and Embase databases; patent data from WIPO PATENTSCOPE, USPTO, and CNIPA (January 2015 to July 2024); and clinical trial data from ClinicalTrials.gov and the Synapse database. Search terms included MeSH keywords: \"Histone Deacetylase Inhibitors,\" \"hypoxia,\" \"Epithelial- Mesenchymal Transition,\" and \"Neoplasm Metastasis.\"</p><p><strong>Results: </strong>Recent patents demonstrate improved HDAC inhibitor delivery systems and isoformselective compounds, particularly targeting HDAC1/3/6. Clinical data show that HDAC inhibitors reverse EMT markers, such as E-cadherin, in solid tumors, though efficacy varies by cancer type. Mechanistically, HDAC4/6 stabilize HIF-1α through direct deacetylation and Hsp90-P300 regulation, driving hypoxia-induced EMT across multiple cancers. Combination therapies with immunotherapy show promising synergistic effects.</p><p><strong>Discussion: </strong>HDACs regulate hypoxia-induced EMT through HIF-1α stabilization, with isoform- selective inhibitors showing improved tumor specificity. While effective at reversing EMT markers, responses vary by cancer type, necessitating biomarker-guided approaches. Combination therapies show promise but require monitoring for potential risks of EMT induction.</p><p><strong>Conclusion: </strong>HDAC inhibition represents a viable strategy against hypoxia-driven metastasis. Future work should optimize selective inhibitors, develop predictive biomarkers, and explore natural compound derivatives to enhance efficacy and reduce toxicity.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent Advances in Proton Therapy for the Treatment of Skull Base Chordoma.","authors":"Wanghan Li, Yiyuan Zhang, Xiaowen Wang, Man Hu","doi":"10.2174/0115748928402324251201133127","DOIUrl":"https://doi.org/10.2174/0115748928402324251201133127","url":null,"abstract":"<p><p>Skull base chordoma is a rare, slow-growing primary tumor. Due to its proximity to the brainstem, blood vessels, and nerves, complete surgical resection is challenging. Therefore, postoperative radiotherapy is required to achieve full disease eradication. Compared to photon therapy, proton therapy offers physical dosimetric advantages, ensuring an adequate target dose while minimizing damage to surrounding tissues. Long-term follow-up has confirmed that proton therapy provides survival benefits and enhanced safety in treating skull base chordoma. Consequently, it is considered the standard radiotherapy approach for this condition. However, due to the low incidence of skull base chordoma and the high cost of proton therapy, only a limited number of prospective studies have evaluated its use in this disorder. To date, there is no consensus on proton therapy dosage, fractionation, or target delineation. In this review, we assess the latest advancements and challenges associated with proton therapy for chordomas located at the skull base, aiming to provide a comprehensive understanding of radiotherapy strategies for this disease.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mir-338-3p Increases the Sensitivity to Oxaliplatin via Reversing Epithelialmesenchymal Transition in Hepatocellular Carcinoma Cells.","authors":"Chuan Huang, Zhenguang Huang, Jun Luo, Meiyi Wu, Kaining Cai, Ruiqiang Zhao, Yan Wen","doi":"10.2174/0115748928408751251113182005","DOIUrl":"https://doi.org/10.2174/0115748928408751251113182005","url":null,"abstract":"<p><strong>Objective: </strong>Oxaliplatin (OXA) is commonly used in combination therapy for patients with advanced hepatocellular carcinoma. While the emergence of acquired resistance dramatically reduces its efficacy. It was previously found that the sensitivity of drug-resistant hepatocellular carcinoma cells to OXA could be enhanced by a synthesized ethyl derivative (patented) of epigallocatechin-3-gallate, and also initially found that the reversal mechanism might be related to the miR-338-3p/HIF-1α/ TWIST pathway. In this study, the function of the miR-338- 3p/HIF-1α / TWIST pathway was investigated in OXA-resistant hepatocellular carcinoma cells, particularly its involvement in reversing chemoresistance mediated by EMT.</p><p><strong>Methods: </strong>The cell viability, migration, invasion, and epithelial-mesenchymal transition markers of SMMC-7721 and SMMC-7721/OXA cells were measured using the MTT assay, wound healing assay, transwell assay, western blot, and qRT-PCR. The effects of miR-338-3p overexpression were evaluated by transfecting cells with miR-338-3p mimic or negative control mimic.</p><p><strong>Results and discussion: </strong>The SMMC-7721/OXA cells exhibited an epithelial-mesenchymal transition phenotype, characterized by increased migration and invasion, reduced E-cadherin, and elevated vimentin expression. The miR-338-3p expression was dramatically downregulated in SMMC-7721/OXA cells. Overexpression of miR-338-3p enhanced OXA sensitivity, with the IC50 value of OXA decreasing from 51.23 μM to 19.26 μM, reversed the epithelialmesenchymal transition phenotype, and reduced the expression of hypoxia-inducible factor-1α and twist family bHLH transcription factor 1, key regulators of epithelial-mesenchymal transition. The results indicated that the miR-338-3p regulates epithelial-mesenchymal transition and chemoresistance in OXA-resistant hepatocellular carcinoma cells by targeting hypoxiainducible factor-1α and subsequently down-regulating twist family bHLH transcription factor 1.</p><p><strong>Conclusion: </strong>This study implies that the resistance of SMMC-7721/OXA cells to OXA is likely related to the acquisition of the EMT phenotype. The up-regulating miR-338-3p could be a new treatment method for over-coming OXA resistance in hepatocellular carcinoma.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146032225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell and Bulk RNA-Seq Analyses Reveal TOMM7-mediated Multi-cell Death Mechanisms Driving Muscle-invasive Bladder Cancer Progression.","authors":"Jinge Zhang, Li Zheng, Zhe Yu, Yuwen Chen, Feifan Jiang, Zicai Zhang, Tanghua Li, Hongfan Zhao, Yaxian Li, Fei Li","doi":"10.2174/0115748928396718251104075645","DOIUrl":"https://doi.org/10.2174/0115748928396718251104075645","url":null,"abstract":"<p><strong>Introduction: </strong>Muscle-invasive bladder cancer (MIBC) is characterized by high malignancy and poor prognosis. Advances in single-cell RNA sequencing (scRNA-seq) have provided new insights into the molecular heterogeneity and progression of MIBC.</p><p><strong>Methods: </strong>A single-cell atlas of bladder cancer (BCa) was constructed, and MIBC-related epithelial subclusters (Epi_MIBC) were identified. Key transcription factors and dysregulated cell death pathways were characterized. A prognostic model based on MIBC-related cell death genes (MIBC.CDGs) was developed using machine learning algorithms and validated across multiple cohorts. The functional role and druggability of TOMM7, a core gene, were evaluated through in vitro experiments and molecular docking analysis.</p><p><strong>Results: </strong>The MIBC-related cell death score (MIBC.CDS) was shown to effectively stratify patient prognosis and predict immunotherapy response. Multiple cell death pathways were found to be activated in MIBC. Knockdown of TOMM7 suppressed proliferation, invasion, and migration in T24 cells, while modulating apoptosis, autophagy, mitophagy, cuproptosis, and ferroptosis. Molecular docking analysis identified sorafenib as a potential TOMM7-targeted therapeutic agent.</p><p><strong>Discussion: </strong>The findings highlighted the critical role of cell death dysregulation in MIBC progression and underscored TOMM7 as a novel oncogenic regulator. The integration of multiomics data and machine learning enhanced our understanding of tumor biology and provided a foundation for developing personalized treatment strategies.</p><p><strong>Conclusion: </strong>TOMM7 was found to drive MIBC progression by regulating multiple cell death pathways. The MIBC.CDS may serve as a promising tool for prognostic evaluation and therapeutic stratification. Sorafenib was identified as a potential candidate for TOMM7-targeted therapy in MIBC.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145992258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preface.","authors":"Bohan Zhang, Zhe-Sheng Jason Chen","doi":"10.2174/0115748928455099251102183758","DOIUrl":"10.2174/0115748928455099251102183758","url":null,"abstract":"","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"i"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145508684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"L-Selenomethylselenocysteine Exerts Inhibitory Effects on the Progression of Esophageal Cancer by Targeting the PI3K/AKT Signaling Pathway.","authors":"Keyi Ji, Suhui Wu, Jiayao Yuan, Yu Wang, Genlin Li, Linlin Wang, Shuncai Wang, Longjie Wang, Hanbing Li, Chengbao Wang","doi":"10.2174/0115748928355152250527060605","DOIUrl":"10.2174/0115748928355152250527060605","url":null,"abstract":"<p><strong>Background: </strong>Esophageal cancer is a common malignant tumor, making the search for effective treatments a critical research focus. L-methylselenocysteine (L-SeMC) has been reported to exert anticancer effects in various cancers; however, its role and underlying mechanisms in esophageal cancer remain unclear. This study aimed to investigate the anticancer effects of L-SeMC on esophageal cancer both <i>in vitro</i> and <i>in vivo</i>, and to explore its potential mechanisms of action.</p><p><strong>Methods: </strong>For cellular studies, flow cytometry, colony formation assay, MTT assay, wound healing assay, and ROS measurement were employed. Western blotting was used to assess the expression levels of apoptotic proteins. A subcutaneous tumor xenograft model was established. The analysis included the evaluation of proteins related to the PI3K/AKT signaling pathway, TUNEL, and Ki-67 staining, as well as HE staining.</p><p><strong>Results: </strong>L-SeMC caused cell death and, in a concentration-dependent manner, reduced the migration, invasion, and proliferation of esophageal cancer cells. Western blot analysis showed that L-SeMC was associated with a decrease in the anti-apoptotic protein Bcl-2 and an increase in the pro-apoptotic protein Bax. It also triggered the mitochondrial apoptosis pathway, promoting the activation of caspase-3 and subsequent cancer cell death induced by L-SeMC. In a dosedependent manner, L-SeMC decreased the phosphorylation of phosphatidylinositol 3-kinase (PI3K) downstream effector molecules. This suggests that L-SeMC inhibits the PI3K/AKT signaling pathway in esophageal cancer cells, contributing to its anticancer effects.</p><p><strong>Discussion: </strong>Our results suggest that L-Selenomethylselenocysteine acts as a potential therapeutic pathway in esophageal cancer through the PI3K/AKT signaling pathway. Although the current evidence is limited, we are actively increasing the sample size to conduct further verification.</p><p><strong>Conclusion: </strong>L-SeMC has a strong anticancer effect on human esophageal cancer cells and promotes apoptosis by inhibiting the PI3K/AKT signaling pathway, suggesting that L-SeMC may represent a novel strategy for the treatment of esophageal cancer.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"161-172"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144334710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}