Recent patents on anti-cancer drug discovery最新文献

{"title":"Integrated Proteomics and Metabolomics Analysis Provides Insights into Metformin Down-regulating GLUL and SP1 to Inhibit Esophageal Squamous Cell Carcinoma Migration and Invasion.","authors":"Huayu Luo, Tao Shen, Jing Zhang, Yang Cheng, Zhongyu Zhang, Yujie He, Hongzheng Ren","doi":"10.2174/0115748928436219260622061458","DOIUrl":"https://doi.org/10.2174/0115748928436219260622061458","url":null,"abstract":"<p><strong>Introduction: </strong>Esophageal Cancer (EC) is a prevalent gastrointestinal malignancy. Despite significant advances in diagnostic and therapeutic approaches, the prognosis of Esophageal Squamous Cell Carcinoma (ESCC) remains poor. The development of new therapeutic agents for ESCC would greatly benefit patients and their families. Metformin has been found to be useful in other tumours, but its role and mechanism in ESCC have not been investigated.</p><p><strong>Methods: </strong>The effect of metformin on inhibiting invasive metastasis in ESCC cells was explored by in vitro cytology experiments. 4D-DIA proteomics and untargeted LC-MS metabolomics provided critical technical support for this study. The roles and mechanisms of differential proteins, metabolites, and key metabolic pathways in ESCC migration and invasion were further explored by identifying differentially expressed proteins and metabolites in metformin-treated ESCC cells using proteomics and metabolomics. RT-qPCR and Western blot were used to confirm metformin's inhibitory effects on key proteins in metabolic pathways associated with ESCC cell migration and invasion. Using the ESCC tissue microarray (TMA) to detect the expression levels of GLUL and SP1.</p><p><strong>Results: </strong>This study demonstrated that metformin significantly reduced ESCC cells' viability, proliferation, migration, and invasion, while enhancing apoptosis. Integrated multi-omics pathway analysis revealed the activation of several metabolic pathways following metformin treatment in ESCC cells. In vitro experiments confirmed that metformin significantly downregulated the key proteins GLUL and SP1, as identified in the differential proteomics analysis. Immunohistochemistry (IHC) showed that GLUL and SP1 expression were significantly lower in ESCC tumor tissues from patients with a history of preoperative metformin administration than in those without.</p><p><strong>Discussion: </strong>Enhanced glutamine metabolism in tumors promotes cancer progression. Downregulation of GLUL reduces glutamine production from the alanine, aspartate, and glutamate metabolic pathways, thereby inhibiting tumor progression. SP1 is an oncogenic factor in esophageal cancer and an unfavorable prognostic factor. Metformin downregulates both GLUL and SP1, affecting the alanine, aspartate, and glutamate metabolic pathways, as well as the choline metabolic pathway in cancer.</p><p><strong>Conclusion: </strong>In summary, metformin may inhibit the migration and invasion of ESCC cells through downregulation of GLUL and SP1, which play important roles in the mechanism of metformin's anti-tumor effects. These findings provide new insights into the therapeutic potential of metformin in the treatment of ESCC.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148364598","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":"SEZ6L2 Promotes Cervical Carcinogenesis by Activating the Wnt Signaling Pathway.","authors":"Min Hu, Rengong Zhuo, Yaling Tang, Jing-Ying Xu, Ke Liu, San-Gang Wu, Juan Zhou","doi":"10.2174/0115748928446227260226041957","DOIUrl":"https://doi.org/10.2174/0115748928446227260226041957","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to investigate the biological function and molecular mechanisms of seizure-related 6 homolog-like 2 (SEZ6L2) in Cervical Cancer (CC) progression and evaluated its potential as a therapeutic target.</p><p><strong>Methods: </strong>SEZ6L2 expression was analyzed in CC tissues and cells using online tools and experimental validation. Functional experiments, including cell-counting Kit-8, colony formation, wound-healing, transwell, and flow cytometry, together with in vivo models, were performed to assess the effects of SEZ6L2 on proliferation, migration, and metastasis. GSEA and Metascape enrichment were used to identify associated pathways. TargetScan was used to predict upstream miRNAs, followed by validation with dual-luciferase assays.</p><p><strong>Results: </strong>SEZ6L2 was significantly overexpressed in CC and correlated with poor prognosis. Knockdown of SEZ6L2 inhibited CC proliferation, migration, and invasion while inducing cell cycle arrest. In vivo, SEZ6L2 silencing reduced tumor growth and metastasis. Mechanistically, SEZ6L2 was found to activate the Wnt/β-catenin pathway, leading to upregulating β-catenin and driving Epithelial-Mesenchymal Transition (EMT). GSEA confirmed the involvement of the Wnt pathway. Moreover, hsa-miR1271-5p was identified as a direct upstream regulator of SEZ6L2.</p><p><strong>Discussion: </strong>Our findings identified SEZ6L2 as a novel oncoprotein in CC, contributing to tumor pathogenesis by activating the Wnt/β-catenin signaling and promoting EMT-driven metastasis. We further demonstrated that hsa-miR-1271-5p acts as a direct upstream repressor, providing mechanistic insight into the regulatory network governing SEZ6L2 expression. Collectively, these results position SEZ6L2 as a robust prognostic biomarker and illuminate its potential as a therapeutic target.</p><p><strong>Conclusion: </strong>SEZ6L2 promotes CC progression via Wnt/β-catenin signaling and EMT, serving as a prognostic biomarker and therapeutic target. Hsa-miR1271-5p may suppress SEZ6L2 expression, offering novel insights for CC treatment strategies.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148348103","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":"Shengma Biejia Decoction Suppresses Acute Myeloid Leukemia by Regulating Mitochondrial Dynamics through the PI3K/AKT Signaling Pathway.","authors":"Siyuan Cui, Wenjian Wei, Yuping Si, Lulu Li, Yaru Wang, Jingbo Shi, Changnian Li, Yan Wang, Ruirong Xu, Chenchen Ma","doi":"10.2174/0115748928469932260520054457","DOIUrl":"https://doi.org/10.2174/0115748928469932260520054457","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to identify the principal bioactive compounds of Shengma Biejia Decoction (SMBJD), evaluate its anti-acute myeloid leukemia (AML) activity in vivo, and clarify the underlying molecular mechanisms.</p><p><strong>Methods: </strong>Thirty NSG female mice were randomly assigned to the normal control (NC), AML model, and SMBJD treatment groups (low, medium, and high dose). After AML model establishment, SMBJD was administered by gavage, and anti-AML efficacy was evaluated by histopathology, bone marrow cytology, immunohistochemistry, flow cytometry, immunofluorescence, Western blotting, and transmission electron microscopy. UHPLC-MS/MS was used to characterize the chemical constituents of SMBJD. Network pharmacology was used to predict potential targets and pathways, and molecular docking was performed to assess the interactions between representative active compounds and key targets.</p><p><strong>Results: </strong>SMBJD showed significant anti-AML activity in vivo, and 51 major active constituents were identified. Network pharmacology analysis yielded 662 overlapping targets and 153 enriched pathways, among which the PI3K/AKT signaling pathway was prioritized. In vivo validation showed that SMBJD inhibited PI3K/AKT signaling, decreased mitochondrial fusion, increased mitochondrial fission, and promoted apoptosis in AML-bearing mice.</p><p><strong>Discussion: </strong>These findings suggest that SMBJD exerts anti-AML effects by suppressing PI3K/AKT signaling and shifting mitochondrial dynamics toward fission, thereby promoting apoptosis.</p><p><strong>Conclusion: </strong>In conclusion, SMBJD inhibited AML progression in vivo, at least in part, by regulating mitochondrial dynamics through suppression of the PI3K/AKT signaling pathway.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148280567","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":"Spatial and Single-cell Multi-omics Approaches Unravel the Genetic and Immunological Landscape of SIRPB1 in Kidney Renal Clear Cell Carcinoma.","authors":"Chien-Wei Huang, Chen-Yueh Wen, Tzu-Hung Hsiao, Yu-Ting Kang, Jin-Shuen Chen, Zhi-Hong Wen, Po-Hung Chen, Chia-Jung Li","doi":"10.2174/0115748928433346260131000542","DOIUrl":"https://doi.org/10.2174/0115748928433346260131000542","url":null,"abstract":"<p><strong>Introduction: </strong>Signal regulatory protein beta 1 (SIRPB1) is a member of the signal regulatory protein family and functions as a receptor-type glycoprotein. It participates in immune modulation through pathways connected with receptor tyrosine kinases. While its role in immunity has been reported, the relevance of SIRPB1 to the development and progression of kidney renal clear cell carcinoma (KIRC) has not been well established.</p><p><strong>Methods: </strong>We integrated multi-omics datasets, including TCGA KIRC (n ≈ 530) and GEO cohorts, to evaluate SIRPB1 expression, prognostic value, mutational associations, and immune infiltration patterns. Spatial transcriptomics and single-cell RNA sequencing were used to characterize the tumor microenvironment. Experimental validation was performed using immunohistochemistry and triple immunofluorescence on a tissue microarray containing 59 human renal tumor specimens. Pharmacogenomic profiling and drug response analyses were conducted using CRISPR-based perturbation data from RCC cell lines (predominantly ccRCC/KIRC-derived).</p><p><strong>Results: </strong>SIRPB1 expression was significantly elevated in advanced-stage tumors and correlated with poor overall survival. High SIRPB1 levels were associated with increased tumor grade, macrophage infiltration, and immune-related gene networks. Spatial and single-cell analyses identified macrophages as the dominant SIRPB1-expressing population within the tumor microenvironment. Loss of SIRPB1 sensitized RCC cell lines to several small-molecule compounds, revealing potential therapeutic vulnerabilities.</p><p><strong>Discussion: </strong>The data suggest that SIRPB1 not only reflects tumor aggressiveness but may also indicate responsiveness to therapeutic interventions. Its expression profile could therefore provide a basis for stratifying patients and optimizing treatment approaches.</p><p><strong>Conclusion: </strong>SIRPB1 emerges as a candidate biomarker with diagnostic, prognostic, and therapeutic relevance in KIRC. A patent application has been filed in relation to SIRPB1-based diagnostic and therapeutic strategies.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148280602","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 Active Components and Mechanisms of Schisandra Chinensis for Treatment of Non-small Cell Lung Cancer Based on Network Pharmacology and Experimental Validation.","authors":"Wenyue Zhuang, Jing Fang, Chenghe Zhao, Zhengyi Li, Haiming Song","doi":"10.2174/0115748928462748260531111950","DOIUrl":"https://doi.org/10.2174/0115748928462748260531111950","url":null,"abstract":"<p><strong>Introduction: </strong>Schisandra chinensis has been reported to exhibit antitumor activity; however, its active components and molecular mechanisms in non-small cell lung cancer (NSCLC) remain unclear.</p><p><strong>Methods: </strong>Network pharmacology was employed to identify active compounds and potential targets of Schisandra chinensis against NSCLC, followed by protein-protein interaction analysis, GO and KEGG enrichment analyses, and molecular docking. A549 cells were used for experimental validation. Cell viability was assessed by MTT assay, oxidative stress markers (GSH, SOD, MDA) were quantified, and the expression of PTGS2, inflammatory factors, and apoptosis-related genes was examined by qRT-PCR and Western blot.</p><p><strong>Results: </strong>Eight active components of Schisandra chinensis were identified, with seven overlapping targets related to NSCLC. Molecular docking revealed that Gomisin R exhibited the strongest binding affinity to PTGS2, with a docking score of -7.3 kcal/mol. In vitro experiments demonstrated that Gomisin R significantly inhibited A549 cell proliferation in a dose- and time-dependent manner, with a pronounced effect observed at 25 µM (p < 0.01). Gomisin R markedly downregulated PTGS2 expression at both mRNA and protein levels (p < 0.001), accompanied by reduced expression of inflammatory cytokines IL-1β and IL-6, increased antioxidant capacity (elevated GSH and SOD levels and decreased MDA content), and modulation of apoptosis-related genes, characterized by decreased Bcl-2 and increased Caspase 9 expression (p < 0.05-0.001). These effects were partially reversed by the PTGS2 agonist rebamipide.</p><p><strong>Discussion: </strong>These findings suggest that Gomisin R may modulate PTGS2-associated inflammatory and redox pathways in NSCLC cells. The integration of network pharmacology with experimental validation provides a mechanistic framework for understanding the potential role of Gomisin R in NSCLC-related research, although further in vivo studies are required to confirm its translational relevance.</p><p><strong>Conclusion: </strong>Gomisin R exerts anti-NSCLC effects, in part, by regulating PTGS2 expression, leading to suppression of cell proliferation, attenuation of oxidative stress and inflammatory responses, and induction of apoptosis in A549 cells. This study provides quantitative evidence supporting Gomisin R as a key active component of Schisandra chinensis for the treatment of NSCLC.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148274111","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":"Patent Landscape and Technological Trajectory of Drug Delivery Systems for Overcoming Drug Resistance in Non-small Cell Lung Cancer.","authors":"Feiyan Wu, Xinglinzi Tang, Xinyi Luo, Caizhi Li, Xin Lai, Danyang Li, Hang Li","doi":"10.2174/0115748928434923260422093655","DOIUrl":"https://doi.org/10.2174/0115748928434923260422093655","url":null,"abstract":"<p><p>Widespread drug resistance in the treatment of non-small cell lung cancer (NSCLC) seriously restricts clinical efficacy, so the development of new drug delivery systems to overcome drug resistance has become a key area of research. Currently, no systematic study has been conducted on anti-drug resistance drug delivery systems for NSCLC. This study systematically analyzed patent application trends and delivery system types for drug resistance in NSCLC over the past two decades using the WIPO, Espacenet, and Incopat global patent databases. The analysis focused on the evolution of delivery technology and the value and effectiveness of related technologies. The results showed that the number of patent applications has grown continuously, reflecting progressive innovation in this field of technology from basic research and development to breakthrough applications. The main technology types are nano delivery (56.6% of total patents) and coupled delivery (28.3%). Additionally, emerging technologies such as exosomes, vesicles, and siRNA have emerged. There has been a leap in technology evolution from single-carrier development to intelligent, responsive delivery. In recent years, research has focused on the synergistic application of stimuli-responsive nano systems and combination therapy. High-value patents typically offer the combined benefits of various technologies and mechanisms, particularly in terms of overcoming drug resistance, achieving precise delivery, and reducing toxic side effects. This study provides an important theoretical basis and practical guidance for optimizing the research and development (R&D) strategy and patent portfolio for anti-drug-resistance drug delivery technology in NSCLC.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147984094","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 Comprehensive Review of Genistein and Chitosan: Mechanistic Foundations, Regulatory Roadmap, and Future Research Directions.","authors":"Bishop Adhikari, D Nagasamy Venkatesh, Vivek Puri, Ameya Sharma, Prashant Nayak, Syed Suhaib Ahmed","doi":"10.2174/0115748928438838260406215239","DOIUrl":"https://doi.org/10.2174/0115748928438838260406215239","url":null,"abstract":"<p><strong>Introduction: </strong>Genistein, a phytoestrogen with multi-target anticancer activity, and chitosan, a biocompatible polymer with versatile drug carrier properties, are increasingly investigated for use in advanced drug delivery systems. Cancer remains a leading cause of mortality globally, with current therapeutic approaches like systemic toxicity, non-specific drug delivery, multidrug resistance, and limited bioavailability of therapeutic compounds.</p><p><strong>Methods: </strong>This review synthesized evidence from PubMed, Scopus, Web of Science, Science Direct, and Google Patents. Most of the studies involving genistein, chitosan, nano-formulations, pharmacokinetics, regulatory guidelines, and patents were screened. Some of the recent patents from 2020 to 2025 on drug delivery have been analyzed to map translation development.</p><p><strong>Results: </strong>Moreover, the genistein chitosan systems are positioned as a synergistic co-therapy platform. Composite systems such as nanoparticles, liposomes, hydrogels, and micelles show significant improvements in bioavailability (5-10-fold), tumor retention, and reduced systemic toxicity in preclinical models. The clinical implications of this integrated system are profound.</p><p><strong>Discussion: </strong>Despite strong preclinical data, regulatory challenges persist, including variability in the molecular weight of genistein and chitosan, limited nanotoxicology standards, and classification inconsistencies for natural products. The regulatory landscapes of the developing and non-developing countries, which evolved across key pharmaceutical jurisdictions including the FDA, EMA, CDSCO, PMDA, AND NMPA.</p><p><strong>Conclusion: </strong>Genistein and chitosan drug delivery systems represent a promising approach for precision oncology, offering improved pharmacokinetics, targeted delivery, and reduced toxicity. This review also critically addresses the regulatory gaps, biocompatibility, and modular delivery systems.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147984925","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":"CAIX-HIF-1α Inhibition by 2-(4-Chlorophenyl)-3-(4-Ethoxyphenyl) Thiazolidin-4-one (BCS12) Activates Caspase Cascade and PARP Cleavage, Driving Mitochondrial Apoptosis in Hypoxic Breast Cancer.","authors":"Gaurav Ranjan, Shakti Prasad Pattanayak, Priyashree Sunita","doi":"10.2174/0115748928441521260224055625","DOIUrl":"https://doi.org/10.2174/0115748928441521260224055625","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Hypoxia is a hallmark of aggressive breast cancers, particularly Triple- Negative Breast Cancer (TNBC), where stabilization of Hypoxia-Inducible Factor-1α (HIF-1α) upregulates Carbonic Anhydrase IX (CAIX), thereby enabling tumor pH homeostasis, proliferation, and resistance to therapy. Selective CAIX inhibition, therefore, offers a promising therapeutic strategy. In this study, a thiazolidine derivative was identified as a selective inhibitor of CAIX with the use of integrated computational, in vitro, and in vivo studies to develop targeted therapy against TNBC.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A series of thiazolidinone derivatives was subjected to in silico molecular docking against human carbonic anhydrase isoforms. The most active compound, 2-(4-chlorophenyl)-3- (4-ethoxyphenyl)thiazolidin-4-one (BCS12), was tested and analyzed using 200 ns MD simulations to evaluate the stability of the complexes. Pharmacokinetic parameters were predicted using ADME profiling. Cytotoxicity was evaluated in MDA-MB-231 and MDA-MB-468 breast cancer cells, with IC50 values of 15.49 μM and 18.81 μM, compared to 121.6 μM in noncancerous MCF-10A cells (n = 3, p &lt; 0.05). Free Radical generation, mitochondrial membrane depolarization, and expression of apoptosis markers (Bax, Bcl-2, caspase 9, caspase 7, and caspase 3, and PARP) were quantified using mechanistic studies in hypoxia-adapted MDA-MB- 231 cells by RT-qPCR, western blotting, and immunofluorescence. The number of apoptotic cells was also determined by flow cytometry. The in vivo activity was assessed against DMBAinduced breast tumor-bearing rats by histopathology and TUNEL staining.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;BCS12 showed strong docking affinity as well as stable binding with active-site residues of CAIX in simulations. It preferentially suppressed TNBC cell viability, promoted oxidative stress, impaired the integrity of mitochondria, and activated an intracellular apoptosis pathway. In vivo, BCS12 treatment induces an increase of TUNEL-positive nuclei in a dosedependent manner compared with the control, with significantly higher contrast index values at 20 mg/kg and 40 mg/kg (p &lt; 0.0001). The apoptotic response was strongest in the 40 mg/kg group, and was associated with a marked decrease in tumor burden and restoration of tissue architecture. The lead compound reduced tumor mass, improved histological parameters, and increased TUNEL-positive apoptotic nuclei with an associated decrease in expression of CAIX and activation of pro-apoptotic proteins.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;Our findings suggest that BCS12 disrupts hypoxia-induced survival pathways through inhibition of CAIX to enhance TNBC cell sensitivity to apoptosis. These data reveal a therapeutic benefit of selective CAIX inhibition to counteract hypoxia-induced therapy resistance and further insights into the mechanism underlying hypoxia-targeted therapies for aggressive breast cancer.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Con","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147984973","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":"Melanoma Metastasizing to the Breast: A Case Report.","authors":"Xiaocheng Pan, Zichang Chen, Junhong Chen, Jiaxu Huang, Ruipei Chen, Gengcong Luo, Junbing He, Hongpeng Chen","doi":"10.2174/0115748928449521260410075051","DOIUrl":"https://doi.org/10.2174/0115748928449521260410075051","url":null,"abstract":"<p><strong>Background: </strong>Melanoma metastasizing to the breast is a rare event, accounting for only 1.3%-2.7% of reported cases. Due to its overlapping clinical and imaging features, it is frequently misdiagnosed as primary breast cancer.</p><p><strong>Case presentation: </strong>This study presents a rare case of metastatic malignant melanoma involving the breast. A 49-year-old female was admitted with a palpable mass in the right breast. The breast lesion was classified as BI-RADS 4b. Core needle biopsy initially suggested primary breast malignancy. However, postoperative histopathological examination of the resected specimen revealed positivity for S-100, SOX10, and Ki-67 on immunohistochemical staining, supporting the diagnosis of malignant melanoma. Subsequent physical examination identified a pigmented nevus on the right abdominal wall as the primary lesion.</p><p><strong>Conclusion: </strong>Metastasis of malignant melanoma to the breast is uncommon. This case highlights the potential for cutaneous malignant melanoma to metastasize to the breast and underscores the importance of immunohistochemical staining in distinguishing metastatic melanoma from primary breast malignancies.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147978070","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":"Multi-omics Analysis Uncovers TFRC/HMOX1-dependent Ferroptosis Mediating Celastrol's Anti-invasive/Metastatic Effects on Esophageal Squamous Cell Carcinoma.","authors":"Yulong Zha, Tao Shen, Huayu Luo, Yu Zhang, Hongzheng Ren","doi":"10.2174/0115748928434600260226051559","DOIUrl":"https://doi.org/10.2174/0115748928434600260226051559","url":null,"abstract":"<p><strong>Background: </strong>Esophageal squamous cell carcinoma (ESCC) is an aggressive malignancy with high incidence, low survival rates, and poor prognosis. Current treatments are unsatisfactory, highlighting the need for novel agents. Celastrol (Cela), from Tripterygium wilfordii, shows anti-ESCC potential, but its direct inhibitory mechanisms remain unclear.</p><p><strong>Objective: </strong>This study explores Cela's effects on ESCC cell proliferation, migration, and invasion, utilises metabolomics and proteomics to identify its anti-ESCC mechanisms, and validates these findings via molecular techniques and ferroptosis inhibitor tests.</p><p><strong>Methods: </strong>ESCC lines EC109 and KYSE520 were treated with different Cela concentrations. Proliferation (CCK-8), migration (wound healing), and invasion (Transwell) were assessed. Metabolomics, proteomics, Western blot/RT-qPCR, and Fe²⁷/MDA/GSH measurements were conducted. Rescue experiments used 1 µM Ferrostatin-1 [1].</p><p><strong>Results: </strong>Cela inhibited ESCC functions dose-dependently, inducing ferroptotic phenotypes (elevated Fe²⁷/MDA, reduced GSH). Multi-omics analysis revealed ferroptosis pathway enrichment; the specific ferroptosis inhibitor Fer-1 reversed these Cela-induced ferroptotic phenotypes and restored ESCC functions, confirming ferroptosis as the key mediating pathway.</p><p><strong>Discussion: </strong>Cela's anti-tumor potential is supported by existing patents [2-4]; this study adds a novel mechanism: ferroptosis-mediated inhibition of ESCC invasion and metastasis.</p><p><strong>Conclusion: </strong>Cela inhibits ESCC invasion and metastasis via TFRC/HMOX1-mediated ferroptosis, with multi-omics providing systematic mechanistic insights. This study uncovers a novel ferroptosis-centred anti-ESCC mechanism, supporting Cela's therapeutic potential.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848059","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}