Recent patents on anti-cancer drug discovery最新文献

{"title":"Dosimetry Comparison of 3D Conformal Radiotherapy and Intensity-modulated Radiotherapy for the Treatment of Brain Tumors: A Meta-Analysis.","authors":"Ashima Barman, Sagor Kumar Roy, Sujan Mahamud, Nupur Karmaker, Md Nurul Islam","doi":"10.2174/0115748928307224241017110758","DOIUrl":"10.2174/0115748928307224241017110758","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to evaluate IMRT and 3D-CRT in the therapy of brain tumor (BT) in relation to dose-volume histograms (DVHs) parameters, such as Heterogeneity Index (HI), Conformity index (CI), Equivalent Uniform Dose (EUD), and mean dose (Dmean) outcomes, including the program for the tumors of the brain and estimate whether a favored procedure can be found through the features of the pretreatment.</p><p><strong>Method: </strong>A search of the PubMed, Cochrane Library, and Embase datasets from their beginnings from January 2006 to September 2022 was conducted. The authors separately selected and evaluated studies for qualifying criteria and bias risk.</p><p><strong>Result and discussion: </strong>Seven studies in total were included. Of them, a total of 387 patients were integrated for the Heterogeneity index (HI), Conformity Index (CI), Equivalent Uniform Dose (EUD), and mean dose (Dmean) comparison analysis, which showed 3D-CRT & IMRT with odd ratio (OR) =1.93; 95% confidence interval (95% CI) =1.63, 2.22; and P value=0.00. For brain tumor patients, CI was higher in IMRT than 3D-CRT with OR= 0.72; 95% CI =0.41, 1.03; p value <0.001. EUD was higher in IMRT than 3D-CRT, resulting in an increased overall survival with OR=-0.86; 95% CI =-1.30, 0.42; and p value<0.001. However, no statistically significant variance was perceived in Dmean between 3D-CRT and IMRT.</p><p><strong>Conclusion: </strong>Our records suggested that IMRT with conventional linacs results in a meaningfully lower regular percentage of brain tumor volumes compared to 3D-CRT. Finally, this meta-analysis indicated that IMRT is better than 3D-CRT and decreases the average percent irradiated amount of the brain.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"102-110"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142549882","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":"Effect of Oral Posaconazole on Venetoclax Plasma Concentration and its Efficacy in Patients with Acute Myeloid Leukemia.","authors":"Mengqi Guo, Yingzhi He, Jingwen Du, Dezhi Qiu, Yinjie Qin, Yuxian Huang","doi":"10.2174/0115748928330206241104161111","DOIUrl":"10.2174/0115748928330206241104161111","url":null,"abstract":"<p><strong>Background: </strong>BCL-2 was the first gene identified to have antiapoptotic effects, and venetoclax is an oral selective BCL-2 inhibitor, which has great potential in the treatment of patients with acute myeloid leukemia (AML) who are not candidates for intensive therapy. Notably, posaconazole, an oral antifungal drug, is also a strong factor that can affect blood venetoclax concentrations. To the best of our knowledge, the relationship between BCL-2 expression, posaconazole, and venetoclax, as well as their influence on treatment efficacy and the prognosis of patients with AML, has not been reported.</p><p><strong>Objectives: </strong>In this single-center retrospective study, the relationship between BCL-2 expression and blood venetoclax concentration was analyzed in 35 patients with AML. After that, we explored the differences in curative effect, adverse reactions, and outcomes between patients with different BCL-2 expression levels and patients with different venetoclax concentration levels, respectively.</p><p><strong>Methods: </strong>BCL-2 mRNA expression levels were examined by reverse transcription quantitative PCR. Blood venetoclax concentrations were measured using high-performance liquid chromatography- tandem mass spectrometry.</p><p><strong>Results and discussion: </strong>The results revealed that among patients with AML, those with lower primary BCL-2 expression had a higher complete remission (CR) rate (p =0.005), overall response (OR) rate (p <0.0001), and progression-free survival time (p =0.04). Posaconazole was revealed to be a strong factor that was able to increase blood venetoclax concentration (p <0.001) and CR rate in the venetoclax plus posaconazole group compared to that in the venetoclax monotherapy group (p =0.002); however, no significant difference was identified in the occurrence of adverse reactions between these groups. Among low and high-blood venetoclax concentration groups, the event-free survival of the former group was significantly higher (p =0.013).</p><p><strong>Conclusion: </strong>Higher levels of BCL-2 expression at initial diagnosis may have adverse effects on the efficacy and prognosis of patients, and higher levels of venetoclax concentration may advance the time of adverse reactions in patients, thus adversely affecting event-free survival (EFS).</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"47-61"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960581","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":"Roles of TEAD Transcription Factors and their Coactivators in the Progression and Metastasis of Cancers.","authors":"Li Xiao, Ning Zhang, Peng-Quan Li, Hai-Qing Chu, Dong Zhao, Wei Qin, Shou-Ping Gong, Hui-Ling Cao","doi":"10.2174/0115748928383622250729144741","DOIUrl":"10.2174/0115748928383622250729144741","url":null,"abstract":"<p><p>The transcriptional enhanced associate domain (TEAD) family of transcription factors and their coactivators play pivotal roles in the Hippo-YAP/TAZ pathway, a critical regulatory axis involved in oncogenesis and tumor progression. To investigate the functional interactions of TEAD transcription factors, we performed comprehensive analyses of gene regulatory networks associated with TEADs. TEADs regulate oncogenesis and tumor progression through interactions with upstream oncogenic signaling pathways and the regulation of downstream target genes. As pivotal transcription factors, TEADs critically regulate multiple oncogenic processes, including epithelial-mesenchymal transition (EMT), proliferation, apoptosis, migration, invasion, metastasis, and aerobic glycolysis in cancer cells. TEADs are regulated by numerous non-coding RNAs [ncRNAs] through the Hippo, AKT, and TGF-β signaling pathways in cancers. These insights establish a strong molecular rationale for developing TEAD-targeted therapeutic strategies in cancer treatment.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"273-289"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144839547","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":"Resibufogenin and Oxaliplatin Synergistically Inhibit Diffuse Gastric Cancer by Inactivating the FAK/AKT/GSK3β/β-Catenin Signaling Pathway.","authors":"Hui-Hui Hu, Hai-Li Shang, Yongjing Ren, Hui-Fang Lv, Shuiping Tu, Jian-Zheng Wang, Ya-Nan Gong, Zhi-Fei Li, He Zhang, Tiepeng Li, Yuhang Wang, Bei-Bei Chen, Sai-Qi Wang, Xiao-Bing Chen","doi":"10.2174/0115748928320605241112094549","DOIUrl":"10.2174/0115748928320605241112094549","url":null,"abstract":"<p><strong>Background: </strong>Diffuse Gastric Cancer (DGC) is a highly aggressive form of gastric cancer with a poor prognosis. Oxaliplatin (OX) is one of the first-line chemotherapeutic agents for the treatment of gastric cancer. However, some patients with DGC do not benefit from OX therapy. Resibufogenin (RBF), one of the main active components of the Chinese medicine Huachansu, has demonstrated significant anti-cancer effects. Nevertheless, the potential of RBF to enhance the sensitivity of OX treatment in DGC and its underlying mechanisms have not been reported.</p><p><strong>Objective: </strong>The aim of this study is to investigate the sensitizing effect of RBF on OX therapy for DGC, as well as to elucidate the potential targets and mechanisms of action. This exploration is of significant importance for the development of sensitizers that can improve the therapeutic efficacy of OX and for the advancement of patentable innovations in this field.</p><p><strong>Methods: </strong>MTT assay, flow cytometry, Western blotting, and immunofluorescence assays were employed to assess the inhibitory effects of Resibufogenin (RBF) in combination with OX on DGC in vitro. Human DGC cell xenografts were established in a mouse model to evaluate the efficacy and safety of RBF and OX for treating DGC in vivo.</p><p><strong>Results and discussion: </strong>It was found that RBF inhibited the proliferation of DGC cells in a timeand dose-dependent manner. When RBF was used in combination with OX, the sensitivity of DGC cells to OX was improved. Significantly, the combination of OX and RBF acts synergistically to induce apoptosis and autophagy while inhibiting migration and invasion of DGC cells in vitro. In vivo, the combination of OX and RBF dramatically inhibited the progression of DGC in the subcutaneous xenograft model without observable toxicity. Mechanistically, RBF significantly inhibited the expression and activation of FAK. OX and RBF synergistically inhibited the phosphorylation of FAK, AKT, and GSK3β to abrogate the entry of β-catenin into the cell nucleus. RBF sensitizes DGC to oxaliplatin via FAK suppression.</p><p><strong>Conclusion: </strong>RBF exhibits a pronounced suppressive effect on FAK, and its combination with OX synergistically blocks the FAK/AKT/GSK3β/β-catenin signaling cascade, thereby inhibiting the growth and metastasis of DGC. This study provides a novel avenue for future research and patent development of FAK inhibitors, with the potential to enhance the therapeutic efficacy of DGC treatment and overcome drug resistance.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"14-30"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143702608","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":"Ubiquitination-related Gene UBTD1 Mediates Poor Prognosis of Colorectal Cancer and Affects Colorectal Cancer Cell Proliferation and Ferroptosis.","authors":"Yuzhao Jin, Luyu Liao, Lingjiao Guo, Qianping Chen, Bufu Tang, Jin Jiang, Ji Zhu, Minghua Bai","doi":"10.2174/0115748928323408241002131753","DOIUrl":"10.2174/0115748928323408241002131753","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is the third most common cancer worldwide, and its occurrence and progression are often regulated by genetic and hereditary factors. Ubiquitination and the associated ubiquitin-binding enzymes and ligases regulate the tumor microenvironment and antitumor immunity to mediate tumor pathogenesis and progression. In this study, we examined the molecular characteristics and immunomodulatory effects of ubiquitination-associated genes that mediate CRC prognosis.</p><p><strong>Methods: </strong>The ubiquitination-related gene ubiquitin domain-containing protein 1 (UBTD1) was identified using bioinformatics and single-cell analyses. Subsequently, the ability of UBTD1 to predict CRC prognosis and immune checkpoint correlation was analyzed, the potential drug telatinib targeting UBTD1 was explored, and the correlation between UBTD1 and ferroptosis was analyzed. The role of UBTD1 in CRC and ferroptosis was verified using immunohistochemistry, gene knockout, western blot, cell cloning, and immunofluorescence.</p><p><strong>Results: </strong>UBTD1 was identified as a significant prognostic and predictive gene for CRC and was involved in regulating immune checkpoint levels and immune cell function of CRC patients with CRC. High UBTD1 expression was found to enhance the presence of immune checkpoints that induce immune escape and inhibit ferroptosis onset. Telatinib may be a potential therapeutic drug targeting UBTD1.</p><p><strong>Discussion: </strong>This study first identifies UBTD1 as an independent prognostic marker for CRC, with high expression correlating with poor patient survival. Mechanistically, UBTD1 promotes tumor immune escape by upregulating key immune checkpoints and inhibits ferroptosis via regulating GPX4 and lipid peroxidation, thereby facilitating CRC progression. Telatinib shows strong binding affinity with UBTD1 and inhibits CRC cell viability, offering a potential targeted therapy for high UBTD1-expressing CRC. These findings link ubiquitination, immune escape, and ferroptosis in CRC, providing a novel molecular target for precision treatment.</p><p><strong>Conclusion: </strong>Our study demonstrated that UBTD1 is a prognostic marker for CRC in the regulation of ubiquitination and the tumor immune microenvironment and may serve as a modulator of ferroptosis.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"126-139"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13312376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143019150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ABC Transporter Protein-mediated Multidrug Resistance in Breast Cancer and Development of Targeting Strategies.","authors":"Xiaoyun Yu, Qihang Shang, Mengrui Yang, Jia Wang, Wenfeng Zhang, Xue Wang, Yan Yao, Jing Zhuang, Changgang Sun","doi":"10.2174/0115748928394153250731033624","DOIUrl":"10.2174/0115748928394153250731033624","url":null,"abstract":"<p><p>Drug resistance (MDR) poses a significant challenge in breast cancer (BrCa) treatment, resulting in reduced efficacy and increased tumor recurrence. Resolving MDR in BrCa is necessary for improving the clinical efficacy of antitumor therapy. However, the molecular mechanisms underlying MDR are complex and involve various biological processes, including ABC drug transporter-mediated drug efflux, abnormal drug metabolism, and the development of the tumor microenvironment. The abnormal expression of ABC transporter proteins constitutes a critical mechanism driving MDR in BrCa. Factors like breast cancer stem cells (BCSCs), epigenetic changes, cell membrane lipids, and microenvironmental components affect the expression and function of ABC transporter proteins in BrCa. Here, we focus on the roles of Pglycoprotein (P-gp), multidrug resistance protein 1 (MRP1), and breast cancer resistance protein (BCRP) in relation to MDR. Additionally, we review the factors affecting the expression and function of these transporters, emphasizing strategies such as gene modification, drug development, and modulation of cell membrane lipids.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"290-308"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144877686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"West African Medicinal Plant Substances and Molecules Activities Against Viral Hepatitis B and Hepatocellular Carcinoma.","authors":"Pengdwendé Fabienne Ingrid Zongo, Bagora Bayala, Jacques Simpore","doi":"10.2174/0115748928320670241011073848","DOIUrl":"10.2174/0115748928320670241011073848","url":null,"abstract":"<p><strong>Background: </strong>Chronic hepatitis B virus (HBV) infection remains a major global public health problem with devastating consequences, such as hepatocellular carcinoma. Currently, approved treatments are limited to interferon and nucleoside/nucleotide analogues for chronic hepatitis B and chemotherapy, radiotherapy, and surgery for cancer. Both treatments have their limitations, making complete cure an elusive goal. Therefore, the identification of new therapeutic targets using medicinal plants and the development of new antiviral and anticancer strategies are of utmost importance.</p><p><strong>Objective: </strong>The aim of this review is to identify from the literature the substances and molecules of West African flora involved in the fight against chronic hepatitis B and liver cancer and to provide a summary of their mechanisms of action.</p><p><strong>Methods: </strong>Pubmed, HAL open science, and Google Scholar literature search engines were used to identify medicinal plants and molecules from the West African flora.</p><p><strong>Results and discussions: </strong>Among West African countries, Gambia and Niger had the highest prevalence of hepatitis B virus infection, and 09 West African countries had high rates of liver cancer. A number of studies carried out in Mali, Benin, Senegal, and Burkina Faso enabled us to list anti-HBV and anticancer plants, as well as a number of molecules isolated from plants found in West African regions.</p><p><strong>Conclusion: </strong>By offering a glimpse into the world of anti-HBV and anticancer molecules from West Africa, this review provides valuable information to support the future development of herbal antiviral and anticancer drugs.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"1-13"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515621","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":"A Metastasis-competent CAF Subpopulation Defined by <i>MFAP5⁺THY1</i>⁺ Co-expression Drives Prostate Cancer Metastasis via EMT Activation.","authors":"Yongqiang Huang, Yu Wang, Wei Zhang, Wenfeng Wang, Leilei Du, Xingming Zhang, Wenhao Xu, Jianghua Zheng, Guohai Shi, Jianhua Wang","doi":"10.2174/0115748928439833251118072935","DOIUrl":"10.2174/0115748928439833251118072935","url":null,"abstract":"<p><strong>Background: </strong>The tumor microenvironment, particularly cancer-associated fibroblasts (CAFs), contributes to prostate cancer (PCa) metastasis, however, the role of CAF heterogeneity remains incompletely characterized. The study aims to identify and functionally characterize a metastasis-competent CAF subpopulation in PCa and evaluate its potential as a biomarker for predicting metastatic progression.</p><p><strong>Methods: </strong>We integrated single-cell RNA sequencing data from 1,214 CAFs across 14 PCa specimens. Metastasis-derived CAFs were functionally validated in vitro. Stromal marker expression was assessed by multiplex immunofluorescence in 78 PCa tissues samples.</p><p><strong>Results: </strong>A 20-gene signature stratified CAFs into three subsets, with the MFAP5-expressing subset (CAFa) enriched in metastatic patients. Co-expression of MFAP5 and THY1 specifically identified CAFa with 96.2% specificity. MFAP5 secretion was associated with AKT phosphorylation, Slug upregulation, and epithelial-mesenchymal transition (EMT). Stromal MFAP5⁺THY1⁺ colocalization predicted postoperative metastasis risk independently of Gleason score (multivariate HR = 5.69, p < 0.001).</p><p><strong>Discussion: </strong>Our findings establish stromal MFAP5⁺THY1⁺ co-localization as a potential prognostic biomarker that could complement Gleason scoring. Further validation in multi-center cohorts is required to confirm its clinical independence.</p><p><strong>Conclusion: </strong>We identified a metastasis-competent CAF subpopulation defined by MFAP5⁺THY1⁺ co-expression, where THY1 serves as a spatial anchor for MFAP5 detection and MFAP5 secretion is functionally linked to AKT/EMT pathway activation.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"224-243"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145656773","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":"The Prognostic Role of Interferon Gamma-inducible Protein 30 in Clear Cell Renal Cell Carcinoma with Immune Infiltrates.","authors":"Wu Xu, Taihong Wu, Yufeng Liu, Yang Luo, Dawei Liu, Lingfei Yan, Qing Li, Tao Wang","doi":"10.2174/0115748928367598250124123411","DOIUrl":"10.2174/0115748928367598250124123411","url":null,"abstract":"<p><strong>Background: </strong>Recent research has demonstrated the significance of Interferon Gamma- Inducible Protein 30 (IFI30), an interferon gamma-induced protein, in the immune response to cancerous growths. However, the relationship between IFI30 expression levels, patient prognosis, and tumor-infiltrating lymphocytes in clear cell renal cell carcinoma (ccRCC) remains inadequately defined.</p><p><strong>Methods: </strong>To ascertain the potential link between IFI30 expression, clinical data, and overall survival (OS) in ccRCC patients, we employed diverse databases, which include TCGA, Gene Expression Profiling Interaction Analysis (GEPIA), and UALCAN. Furthermore, an in-depth analysis of the link between tumor-infiltrating immune cells (TIIC) and IFI30 was carried out using the TIMER, GEPIA, and TISIDB databases. Immunohistochemistry (IHC) was utilized to identify the IFI30 and PD-1 expression levels in a tissue microarray. Patents about molecular classification and drugs in ccRCC were reviewed through Worldwide Espacenet®.</p><p><strong>Results: </strong>The expression of IFI30 demonstrated a strong association with sample type, lymph node stage, tumor grade, and cancer stage. Elevated IFI30 expression was linked to unfavorable Disease- Specific Survival (DSS) and Overall Survival (OS) outcomes (p <0.01). Furthermore, overexpression of IFI30 was strongly linked to immunomodulatory molecules, chemokines, and increased infiltration of regulatory T cells (Tregs), natural killer (NK) CD56 cells, T helper 1 (Th1) cells, cytotoxic T cells, and T helper cells. IHC analysis confirmed a robust correlation between IFI30 and PD-1 expression.</p><p><strong>Conclusion: </strong>IFI30 is a prognostic biomarker for ccRCC patients. Targeting IFI30 may provide new strategies for cancer therapy and improve the prognosis of ccRCC patients.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"140-160"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143401122","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":"Morusin Suppresses Pancreatic Cancer Cell Proliferation and Migration by Targeting SLC6A12 to Inhibit NF-κB and β-catenin Signaling Pathways.","authors":"Wenyan Yang, Wei Zhu, Zhiyang Yao, Zhao Wang, Shengzhi Liu, Xiaoqing Guan, Jiang-Jiang Qin","doi":"10.2174/0115748928376279250613051117","DOIUrl":"10.2174/0115748928376279250613051117","url":null,"abstract":"<p><strong>Introduction: </strong>Pancreatic cancer is characterized by a poor prognosis and low survival rate, underscoring the urgent need for the development and optimization of novel therapeutic interventions. Morusin has been reported to have anticancer activity in a variety of cancers. Therefore, the present study aimed to elucidate the anticancer effects and potential mechanisms of Morusin in pancreatic cancer.</p><p><strong>Methods: </strong>We evaluated the anticancer effect of Morusin in pancreatic cancer cells, including its impact on pancreatic cancer cell proliferation, colony formation potential, migration, invasion, cell cycle and apoptosis. RNA sequencing (RNA-seq) analysis was employed to identify potential genes involved in the anticancer activity of Morusin. Furthermore, RT-qPCR and Western blot analysis were utilized to verify the findings.</p><p><strong>Results: </strong>Our results demonstrated that Morusin administration significantly impaired cell proliferation, migration and invasive activity of pancreatic cancer cells. Additionally, Morusin induced apoptosis and disrupted cell cycle progression. Importantly, Morusin was found to co-regulate SLC6A12, HSPA2, P2RY6 and JPH2 in both cell lines by RNA-seq analysis, with the most significant decrease in mRNA levels of SLC6A12 following administration. Mechanistically, Morusin was found to regulate the expression of SLC6A12 and inhibit NF-κB and β-catenin signaling pathways, which may represent the underlying mechanisms of its antitumor activity.</p><p><strong>Conclusion: </strong>Our findings suggest that Morusin holds potential as an anti-pancreatic cancer agent by targeting SLC6A12 and modulating its associated signaling pathways.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"188-200"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546729","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}