Recent patents on anti-cancer drug discovery最新文献

{"title":"Targeting Phosphatase and Tensin Homolog Deleted on Chromosome 10q23.3 (PTEN) as a Potential Theragnostic Biomarker in Tumors.","authors":"Ying Liu, Tian Li, Lifen Zhang, Shuhua He, Jialiang Hui","doi":"10.2174/0115748928370540250508101925","DOIUrl":"10.2174/0115748928370540250508101925","url":null,"abstract":"<p><strong>Background: </strong>Immunotherapy and targeted therapy have been shown to be notably effective in tumor treatment; however, the mechanism of PTEN function in tumorigenesis, development, and immune response of tumors remains unclear.</p><p><strong>Methods: </strong>We show that PTEN expression varies significantly in many types of tumors and affects the prognosis of patients with cancer using pan-cancer analysis. Patents were reviewed using the World Intellectual Property Organisation database. We analyzed data from GTEx, CCLE, and TCGA to study the correlation between PTEN expression and prognosis, investigated the correlation between PTEN expression and tumor-infiltrating immune cells using TIMER, analyzed the mutation pattern of PTEN and its correlation with neoantigen expression, TMB, MSI, MMRs, and DNA methyltransferases in tumors, and conducted an enrichment analysis of PTEN in tumors using GSEA.</p><p><strong>Results and discussion: </strong>PTEN expression is related to the levels of infiltrating immune cells, such as B cells, CD4+ T cells, CD8+ T cells, neutrophils, macrophages, and dendritic cells. PTEN expression is closely related to neoantigen expression, tumor mutational burden, microsatellite instability, and mismatch repair. The results of a functional enrichment analysis of PTEN showed that PTEN has the potential as a biomarker for precision immunotherapy of tumors.</p><p><strong>Conclusion: </strong>This study suggests that PTEN may be involved in the recruitment and regulation of immune-infiltrating cells, tumor development, metastasis, prognosis, tumor immune escape, and immunotherapy, indicating its importance in tumor diagnosis and treatment.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"323-337"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113159","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":"ZNF146-Mediated HMGB1-NF-κB Signaling Activation as a Therapeutic Target and Prognostic Biomarker in Osteosarcoma.","authors":"Rui Yang, Hu Feng, Sheng Li, Shenglin Xu, Qianxi Wang, Hao Wang, Longze Xiao, Yong Hu","doi":"10.2174/0115748928387577251118114459","DOIUrl":"https://doi.org/10.2174/0115748928387577251118114459","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to investigate the role of ZNF146 in osteosarcoma progression and its potential as a therapeutic target and prognostic biomarker, focusing on its interaction with the HMGB1-NF-κB signaling pathway.</p><p><strong>Methods: </strong>ZNF146 expression was analyzed in osteosarcoma tissues versus normal tissues using RNA-seq data from the TARGET database and validated in a cohort of 36 patients via RTqPCR, Western blot, and IHC. Functional assays (Transwell, wound healing, colony formation, CCK-8) and molecular analyses (dual-luciferase reporter, ChIP, Western blot) were conducted in MG63 and U2OS cells with ZNF146 modulation. An MG63 xenograft mouse model was used for in vivo validation.</p><p><strong>Results: </strong>ZNF146 was significantly upregulated in osteosarcoma tissues, correlating with poor patient prognosis (p =0.0307). Functionally, ZNF146 overexpression promoted cell proliferation, migration, and invasion, while its knockdown suppressed these effects. Mechanistically, ZNF146 directly binds to the HMGB1 promoter, thereby enhancing HMGB1 expression and activating the NF-κB pathway, which leads to increased cyclin D1 and MMP9 levels. In vivo, ZNF146 knockdown resulted in reduced tumor growth and Ki-67/PCNA expression.</p><p><strong>Discussion: </strong>These findings establish ZNF146 as a key oncogenic driver in osteosarcoma via HMGB1-NF-κB signaling. The results align with studies implicating ZNF proteins in tumor progression but highlight a novel mechanism. Limitations include unexplored effects on the tumor microenvironment and the need for validation in larger clinical cohorts.</p><p><strong>Conclusion: </strong>ZNF146 promotes osteosarcoma progression through HMGB1-mediated NF-κB activation, suggesting its potential as both a prognostic biomarker and a therapeutic target. Inhibition of ZNF146 or HMGB1 may offer novel strategies for osteosarcoma treatment.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145879691","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":"Tracing the Technological Trajectory of CAR-T Cell Therapy in Cancer Treatment through Patent Analysis.","authors":"Yilan Guan, Yunting Liu, Yuxuan Sun, Baijun Liu, Hongmei Yuan","doi":"10.2174/0115748928406285251014064259","DOIUrl":"https://doi.org/10.2174/0115748928406285251014064259","url":null,"abstract":"<p><strong>Introduction: </strong>CAR-T technology represents a state-of-the-art approach in cancer treatment. This study constructs a multi-dimensional framework for analyzing the technological trajectory to comprehensively clarify the evolution trend of CAR-T technology in cancer treatment.</p><p><strong>Methods: </strong>Based on relevant patent data, three methodologies were applied: MPA (to identify dominant technological pathways), Word2Vec (to convert textual content into semantic vectors), and PCA-Kmeans (for dimensionality reduction and clustering). These methods facilitated the construction of one comprehensive technological trajectory and three supplementary trajectories.</p><p><strong>Results: </strong>The comprehensive technological trajectory exhibits a linear evolutionary trend. In its early stages, the focus was primarily on optimizing the CAR signal transduction domain. Recently, patent technologies have predominantly focused on T-cell modification and expansion, as well as the identification of multiple target antigens. Future research is expected to emphasize the co-expression of antigen targets with immune checkpoint inhibitors. Additionally, the supplementary technology trajectories suggest that refining the CAR-T regulatory mechanism, coexpressing GPX4 to enhance cellular anti-apoptotic capabilities, and expanding investigations into NKG2D targets may represent critical strategies for addressing the high costs and limited long-term persistence associated with CAR-T technology.</p><p><strong>Discussion: </strong>Systematic guidance is provided for formulating CAR-T technology patent strategies, and limitations in the current multi-dimensional analysis framework-such as data sources, indication analysis, and modeling methods-are highlighted, necessitating further optimization through integration with clinical data and advanced algorithms.</p><p><strong>Conclusion: </strong>A systematic technical synthesis is provided for both academic investigations and enterprise R&D, revealing the intrinsic patterns and potential advancements in the technological evolution of the field.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145433655","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":"CAD is Associated with Cancer Prognosis and Promotes Enzalutamide Resistance in Prostate Cancer.","authors":"Bing-Xue Ma, Yi-You Mao, Ze-Fan Zhang, Xian-Zi Zeng, Xiao Xie, Hua Zhao, Qin Li, Ying-Hao Wen, Mao-Ping Cai, Tao Xie, Yu-Zhong Yu, Shan-Chao Zhao, Yang-Zi Ren","doi":"10.2174/0115748928412596251011092220","DOIUrl":"https://doi.org/10.2174/0115748928412596251011092220","url":null,"abstract":"<p><strong>Introduction: </strong>Preliminary investigations into the feasibility of Carbamoyl-phosphate synthetase 2, Aspartate transcarbamoylase, and Dihydroorotase (CAD)-targeted therapies have been conducted in a limited range of cancer types in pre-clinical studies. A comprehensive exploration of the diagnostic and prognostic capabilities of CAD, along with an understanding of its underlying biological mechanisms, is needed.</p><p><strong>Methods: </strong>A range of bioinformatics tools was employed to produce an extensive pan-cancer analysis of CAD expression. Experimental validation of the role of CAD in enzalutamide resistance in prostate cells was conducted. The molecular classification and drug patents of CAD were reviewed using the Worldwide Espacenet ®.</p><p><strong>Results: </strong>Our study revealed that CAD was upregulated in tumor tissues in most cancer types. The expression of CAD was significantly different in clinical stages, pathological grades, and clinical prognosis. The highest frequency of CAD mutation was shown, but CAD mutations did not affect the clinical outcome of cancer patients. Comprehensive data across different cancer types illustrate the relationship between the expression of CAD and tumor mutation burden (TMB), microsatellite instability (MSI), and homologous recombination deficiency (HRD). Immune infiltration algorithms showed a positive link between CAD level and the prevalence of tumor-associated fibroblasts, MDSC, mast cells, and CD4+T cells. CAD level was positively linked to the immune checkpoint, suggesting a potential synergistic effect between CAD and immunotherapy. The GSEA analysis revealed that CAD expression is significantly associated with angiogenesis and epithelial-mesenchymal transition (EMT) pathways. Finally, we demonstrated that knockdown of CAD inhibits the growth of prostate cancer (PCa) cells and resistance to enzalutamide.</p><p><strong>Conclusion: </strong>This study revealed the diagnostic and prognostic potential of CAD. Notably, CAD exhibits essential functions in PCa cell proliferation and enzalutamide resistance.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145433671","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":"Aucubin Inhibits Liver Cancer via HMGB1-mediated Inactivation of the PI3K/AKT/mTOR Signaling Pathway.","authors":"Weinan Li, Xuan Ma, Yong Mei, Cijun Peng, Zanjie Feng","doi":"10.2174/0115748928420661250922102242","DOIUrl":"https://doi.org/10.2174/0115748928420661250922102242","url":null,"abstract":"<p><strong>Introduction: </strong>Liver cancer remains one of the most aggressive and lethal malignancies worldwide，and current therapeutic efforts show limited survival benefits. Based on our previous findings that aucubin attenuates liver ischemia-reperfusion injury by inhibiting the HMGB1/TLR-4/NF-κB signaling pathway, this study aimed to elucidate the biological functions and molecular mechanisms of aucubin in liver cancer.</p><p><strong>Methods: </strong>In this study, the role of aucubin in liver cancer was examined using liver cancer cell models and tumor-bearing mouse models. We evaluated whether the anti-tumor effect of aucubin is dependent on HMGB1 and its key signaling pathways. Intellectual property implications related to this small molecule are also explored.</p><p><strong>Results: </strong>Results revealed that aucubin effectively reduced the Epithelial-Mesenchymal Transition (EMT) behavior of liver cancer in nude mice and inhibited the migration and invasion ability of liver cancer cells. The effect of aucubin on migration and proliferation was reversed by HMGB1 overexpression in HepG2 and HCCLM3 cells. Aucubin inhibited the levels of HMGB1, RAGE, p-PI3K, p-AKT, and p-mTOR proteins in mouse tumor tissues and this change was reversed by HMGB1 overexpression.</p><p><strong>Discussion: </strong>We identified that aucubin exerts anti-liver cancer effects. By investigating the regulatory effects of HMGB1 overexpression and AKT agonist SC79 intervention on the HMGB1/ RAGE axis and PI3K/AKT/mTOR pathway, our findings confirmed the core role of the HMGB1/RAGE axis in aucubin's anti-tumor activity, as well as aucubin's regulation of liver cancer cell proliferation, migration, and invasion via the PI3K/AKT/mTOR pathway-ultimately mediating its anti-tumor effects.</p><p><strong>Conclusion: </strong>This study indicated that aucubin inhibits the proliferation, invasion, and metastasis of liver cancer by upregulating the HMGB1/RAGE axis and targeting the PI3K/AKT/mTOR signaling pathway. The results of this study highlighted the potential of aucubin as a therapeutic agent for suppressing liver cancer.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145294927","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":"Mendelian Randomization Combined with Experimental Validation Identifies Prognostic Genes LMNB1 and PLXNB2 in the Immune Response in Multiple Myeloma.","authors":"Xiaofen Zhang, Qiuhong Kong, Jianhao Zhao, Ruifang Qiao, Fei Niu, Haipeng Jia, Yanchao Duan","doi":"10.2174/0115748928367765250925145654","DOIUrl":"https://doi.org/10.2174/0115748928367765250925145654","url":null,"abstract":"<p><strong>Introduction: </strong>Immune regulatory genes, such as PLXNB2, play critical roles in the tumor microenvironment, yet their specific functions in Multiple Myeloma [MM] remain largely unclear.</p><p><strong>Methods: </strong>Transcriptomic and clinical data for MM were retrieved from the Gene Expression Omnibus (GEO) database and analyzed alongside immune regulation-related genes identified from previous Mendelian randomization analysis. Correlations between these genes and immune functions, clinical risk scores, and survival prognosis were evaluated. Virtual drug sensitivity screening was performed for MM immune-related prognostic risk genes. In vitro experiments, including cell cloning, Transwell assays, scratch tests, and ELISA, were conducted to validate findings.</p><p><strong>Results: </strong>PLXNB2 expression was positively correlated with improved MM prognosis, whereas LMNB1 expression showed a negative correlation. MM cell lines exhibited reduced PLXNB2 and increased LMNB1 expression. Overexpression of PLXNB2 and knockdown of LMNB1 significantly inhibited MM cell proliferation, invasion, and migration. Furthermore, these manipulations decreased PD1 and CTLA-4 expression, enhancing the cytotoxic activity of immune cells against MM cells.</p><p><strong>Discussion: </strong>Our findings highlight the potential immune regulatory functions of PLXNB2 and LMNB1 in MM progression. The interplay between these genes may influence immune evasion and tumor aggressiveness, providing insights into potential therapeutic targets.</p><p><strong>Conclusion: </strong>Reduced PLXNB2 expression may drive LMNB1 upregulation, suppress immune cell responses, and promote MM progression. These genes represent promising biomarkers and therapeutic targets for improving MM treatment strategies.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145294955","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":"Diosgenin-loaded Silver Nanoparticles: Dual Protective Role and Enhanced Radiosensitivity against ENU-induced Leukemia and γ-irradiation-induced Liver Toxicity.","authors":"Amira Atef Mahmoud, Mohammed A Hussein, Ahmed M Hamdy, Ahmed A Emara, Ebtsam A Abdel-Wahab","doi":"10.2174/0115748928394316250831082610","DOIUrl":"https://doi.org/10.2174/0115748928394316250831082610","url":null,"abstract":"<p><strong>Introduction: </strong>Leukemia and radiation-induced liver toxicity are significant health challenges requiring effective therapeutic strategies. This study aimed to evaluate the therapeutic efficacy and radiosensitizing effects of Diosgenin-loaded silver nanoparticles (Dio-AgNPs) in ENU-induced leukemic mice, with a focus on their dual role in mitigating leukemia progression and γ-irradiation-induced hepatotoxicity.</p><p><strong>Methods: </strong>Dio-AgNPs were synthesized and characterized using TEM, UV-Vis spectroscopy, FT-IR spectroscopy, and encapsulation efficiency analysis. Leukemic mice were treated with Dio-AgNPs (90 mg/kg b.w.) and γ-irradiation (2 Gy). Biological assays assessed hematological parameters, liver function, oxidative stress biomarkers, and gene expression (Nrf2, ABCC1, NQO1). Molecular docking analyzed diosgenin's binding affinities to target proteins. Histological evaluation of liver tissues and in silico ADMET profiling were also performed.</p><p><strong>Results: </strong>Dio-AgNPs exhibited a mean diameter of 51.60 ± 1.54 nm, zeta potential of -19.5 ± 0.2 mV, and high encapsulation efficiency (84.98 ± 0.45%). Treatment significantly improved blood parameters (e.g., 39.4% increase in Hb, 41.5% reduction in WBCs), reduced liver enzymes (40.4% decrease in AST), and lowered oxidative stress (50.1% reduction in MDA). Synergy with γ-irradiation enhanced radiosensitivity (IC50: 24.55 μg/mL vs. 58.35 μg/mL alone). Molecular docking revealed strong binding to Nrf2 (-9.04 kcal/mol), ABCC1 (-10.05 kcal/mol), and NQO1 (-10.71 kcal/mol). Histology confirmed hepatoprotection, with minimal degeneration in combination-treated groups.</p><p><strong>Discussion: </strong>Dio-AgNPs demonstrated multifaceted benefits, including anti-leukemic, antioxidant, and anti-inflammatory effects, amplified by γ-irradiation. The activation of the Nrf2 pathway and modulation of detoxification genes (ABCC1, NQO1) underpinned their therapeutic mechanism. Limitations include a single timepoint analysis and the need for human-relevant validation.</p><p><strong>Conclusion: </strong>Dio-AgNPs are a promising dual-function therapy for leukemia and radiationinduced liver damage, combining targeted cytotoxicity with organ protection. Future research should optimize dosing and explore clinical translation.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145016995","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":"Advances in Artemisinin-based Therapies: Innovations in Synthesis, Drug Delivery, and Expanding Therapeutic Applications.","authors":"Akshay Thakur, Gaurav Thakur, Vir Vikram Sharma, Kuldeep Singh, Jeetendra Kumar Gupta, Divya Jain, Mukesh Chandra Sharma","doi":"10.2174/0115748928394599250827093709","DOIUrl":"https://doi.org/10.2174/0115748928394599250827093709","url":null,"abstract":"<p><p>Artemisinin, a natural compound derived from Artemisia annua, has significantly impacted the treatment of malaria and has shown promise in various other therapeutic applications. This review explores the molecular structure of artemisinin and its derivatives, as well as advancements in synthetic and semi-synthetic production methods, and their broader therapeutic effects beyond malaria, including potential uses in cancer, neurological disorders, and viral infections. It also discusses contemporary drug delivery innovations, such as nanoparticles and liposomal systems, which aim to enhance the bioavailability and targeted action of artemisinin, while addressing issues of drug resistance, particularly in parasitic diseases like malaria. The future of artemisinin research is expected to focus on the development of novel derivatives and innovative formulations that leverage nanomedicine, with significant implications for global health and improved therapeutic efficacy.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145016935","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":"Targeted Therapy with Dalpiciclib in a Pediatric Patient with Anaplastic Ependymoma: A Case Study and Literature Review.","authors":"Yiming Qi, Yang Li, Jia Yang, Huaguo Wu, Long Lai, Rongjie Tao, Hui Zhang","doi":"10.2174/0115748928392108250728050114","DOIUrl":"https://doi.org/10.2174/0115748928392108250728050114","url":null,"abstract":"<p><strong>Introduction: </strong>Ependymoma is the third most common brain tumor in children, with a high recurrence rate and poor prognosis. The traditional treatment of ependymoma is surgery and radiation therapy. However, the effectiveness of conventional chemotherapy has been modest. Recent breakthroughs in molecular biology and genetics have opened doors to more targeted and effective therapeutic approaches. Complex mutations, such as CDK4 amplification in anaplastic ependymoma, are infrequently documented, warranting further investigation.</p><p><strong>Case presentations: </strong>This case study presents a twelve-year-old girl with a WHO Grade III anaplastic ependymoma. She underwent two surgical procedures, followed by radiotherapy and chemotherapy. Despite this comprehensive treatment, she experienced a relapse after one year. Genetic testing identified CDK4 amplification in the tumor tissue. Subsequently, based on the genetic finding, she was treated with a CDK4/6 inhibitor, Dalpiciclib, in combination with bevacizumab. So far, she has survived for over 48 months following her surgery and continues to be monitored, underscoring the remarkable efficacy of the treatment.</p><p><strong>Conclusions: </strong>This report represents the first use of the CDK4/6 inhibitor Dalpiciclib for the treatment of anaplastic ependymoma. The treatment was guided by insights from next-generation sequencing (NGS) analysis and has shown promising results in terms of patient survival.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144839548","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":"Exploring the Molecular Mechanisms and Biological Effects of CELF2 in the Development of Gastric Cancer.","authors":"Weijian Li, Shengyong Zhai, Xuejian Wang, Xiaoke Wang, Shanyu Li, Guiyu Zhang, Minghui Duan, Xindi Huang, Wenyan Jiang, Shenshuo Gao, Chunyan Fang, Jianjun Qu","doi":"10.2174/0115748928387819250728053528","DOIUrl":"https://doi.org/10.2174/0115748928387819250728053528","url":null,"abstract":"<p><strong>Introduction: </strong>The CUGBP ELAV-like family member 2 (CELF2) gene is irregularly expressed in various types of cancer. However, the role of CELF2 in stomach adenocarcinoma (STAD) remains unclear. This study aims to elucidate its potential role in modulating tumor behavior in STAD, as well as its correlation with tumor-infiltrating immune cells.</p><p><strong>Methods: </strong>Bioinformatics analysis methods were employed to investigate the CELF2 expression levels of CELF2 in STAD and its correlation with clinicopathological factors. CELF2 expression was quantified in STAD cells using qRT-PCR and Western blot. Immunohistochemistry confirmed CELF2 expression in STAD versus adjacent normal tissues. The effects of CELF2 expression on cell proliferation were evaluated using CCK-8 and colony formation assays, and migration and invasion assays evaluate cellular motility and invasiveness. Differential expression and protein-protein interaction (PPI) network analysis were conducted to predict the downstream targets of CELF2.</p><p><strong>Results: </strong>Our findings revealed that CELF2 expression was significantly reduced in STAD tissues and was correlated with patient survival outcomes. Moreover, CELF2 overexpression demonstrated a notable inhibitory effect on cell proliferation, migration, and invasion in STAD cells. Importantly, CELF2 appeared to exert its effects through the regulation of the downstream target gene adiponectin (ADIPOQ). The knockdown of ADIPOQ effectively negated the inhibitory effects of CELF2 on cell proliferation and migration.</p><p><strong>Discussion: </strong>This study underscores CELF2 as a tumor suppressor in STAD, whose downregulation promotes progression and correlates with poor prognosis. The CELF2/ADIPOQ axis represents a new regulatory pathway with therapeutic implications. The lack of deeper mechanistic insights into how CELF2 regulates ADIPOQ also warrants further investigation.</p><p><strong>Conclusion: </strong>CELF2 acts as a tumor suppressor in STAD by inhibiting proliferation, migration, and invasion, partly through regulating ADIPOQ and influencing the immune microenvironment. It represents a promising prognostic biomarker and new therapeutic target, with the CELF2/ADIPOQ axis offering a specific pathway for future drug development.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144839546","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}