Anti-cancer agents in medicinal chemistry最新文献

{"title":"Validating the Role of TRAF2 and Nck-Interacting Kinase as a Potential Target in Colorectal Cancer Progression: A Deeper Insight from Expression Profiling and Epigenetic Analysis.","authors":"Sherlin Rosita Arokiaraj, Ragothaman Prathiviraj, Daniel Andrew M Gideon, Jay Shree Mathivanan, Bala Sundar Muthukumar, Chaiyavat Chaiyasut, Bhagavathi Sundaram Sivamaruthi","doi":"10.2174/0118715206488572260812120229","DOIUrl":"https://doi.org/10.2174/0118715206488572260812120229","url":null,"abstract":"<p><strong>Introduction: </strong>Colorectal cancer (CRC) remains a significant global health burden; therefore, a better understanding of its molecular underpinnings is needed to develop more effective therapeutic methods. Traf2 and Nck-interacting kinase (TNIK) have emerged as key regulators in various malignancies, including CRC, but their exact roles and regulatory mechanisms remain only partially understood. The present study aimed to characterize TNIK expression in colorectal cancer through integrative analysis of two independent GEO microarray datasets (GSE9348 and GSE21510) comprising a total of 193 CRC and 37 normal tissue samples.</p><p><strong>Methods: </strong>Differential gene expression (DEG) analysis was conducted using GEO2R with the limma package, and protein-protein interaction network analysis was performed using STRING v12.0 and visualized in Cytoscape v3.8.2 to identify TNIK's functional partners within the Wnt signaling pathway. This work highlights genes that are up- and downregulated in CRC using a significance threshold of p < 0.05 and log FC > 1. Additionally, to investigate the epigenetic regulation of TNIK, an exploratory differential methylation analysis was performed on a murine CRC RRBS dataset (PRJNA589067) that models Wnt hyperactivation in APC-mutant CRC organoids. The data were processed through Bismark v0.24.2 for alignment and the Bioconductor package edgeR for DMR identification in the CpG context. Therefore, an epigenetic analysis of colorectal cancer was conducted to identify differentially methylated regions, using the thresholds p < 0.05 and logFC > 1.</p><p><strong>Results: </strong>DEG analysis reveals that TNIK is significantly upregulated in cancer samples. From DMR analysis, TNIK was observed to be relatively hypomethylated in the murine experimental model, while expression analysis of human CRC microarray data identified TNIK as an upregulated gene, an inverse relationship consistent with established epigenetic regulatory trends.</p><p><strong>Discussion: </strong>The data analyses and interpretations in this work provide a molecular basis for future pharmacological studies targeting TNIK kinase activity and aberrant DNA methylation in CRC, with potential implications for drug discovery efforts to restore normal Wnt pathway regulation. The study links changes in DNA methylation patterns to gene expression and provides important mechanistic definitions of how epigenetic modifications affect gene regulation.</p><p><strong>Conclusion: </strong>The overall contribution of TNIK overexpression to carcinogenesis and tumor progression through epigenetic modulation in CRC could be applied as a clinical biomarker or candidate for tumor suppressor genes in future studies.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Biomarkers in Personalized Treatment of Gastrointestinal Cancers.","authors":"Shima Mehrabadi","doi":"10.2174/0118715206400800251128055423","DOIUrl":"https://doi.org/10.2174/0118715206400800251128055423","url":null,"abstract":"<p><p>Gastrointestinal (GI) cancers-including colorectal, gastric, pancreatic, and esophageal malignancies- remain among the most prevalent and lethal cancers worldwide, largely due to their biological complexity and late-stage diagnosis. This narrative review examines the critical role of biomarkers in advancing personalized treatment strategies for GI cancers. Key diagnostic, prognostic, and predictive biomarkers, such as KRAS, HER2, PD-L1, microsatellite instability (MSI), and circulating tumor DNA (ctDNA), are discussed about their application in clinical decision-making. The review highlights biomarker-driven approaches across different GI cancer types, demonstrating how molecular profiling informs early detection, treatment selection, and monitoring of therapeutic response. Recent technological advances-including liquid biopsy, next-generation sequencing, and multi-omics integration- have expanded biomarker discovery and enhanced clinical utility. Challenges in implementing biomarker testing, such as variability in expression, lack of standardization, and limited accessibility, are also addressed. Overall, this article emphasizes the transformative potential of biomarkers to tailor therapy, improve patient outcomes, and shape the future of precision oncology in gastrointestinal cancers.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Metabolic Dysfunctions in Cancer through Nanoparticles: Advances in Therapeutic Delivery.","authors":"Pankaj Popli, Mehak Awasthi, Manish Kumar Jeengar, Indu Singh, Thakur Gurjeet Singh, Rajan Swami","doi":"10.2174/0118715206477003260729120837","DOIUrl":"https://doi.org/10.2174/0118715206477003260729120837","url":null,"abstract":"<p><strong>Introduction: </strong>Cancer progression is characterized by metabolic reprogramming, including the enhanced Warburg effect, hypoxia-driven adaptations, ferroptosis regulation, and altered lipid metabolism. These metabolic changes promote tumor growth, survival, metastasis, and therapeutic resistance. This review aims to analyze the recent advances in nanoparticle-based strategies designed to target metabolic vulnerabilities in cancer and ameliorate therapeutic outcomes.</p><p><strong>Methods: </strong>A comprehensive analysis of recent studies was performed to examine nanoparticle-based interventions targeting key metabolic pathways in cancer. Different nanocarrier platforms, including polymeric, lipidbased, metallic, and biomimetic nanoparticle was assessed regarding their design, targeting mechanisms, and metabolic dysregulation capabilities.</p><p><strong>Results: </strong>Various nanoparticle systems have demonstrated considerable potential for selectively disrupting tumor metabolism. Polymeric nanoparticles provide controlled drug release and structural flexibility for targeted delivery. Conversely, lipid-based nanocarriers offer high biocompatibility. At the same time, metallic nanoparticles exhibit strong oxidative stress induction. Several studies also reported enhanced therapeutic efficacy through codelivery approaches and stimulus-responsive drug release.</p><p><strong>Discussion: </strong>Targeting cancer metabolism through nanotechnology offers significant advantages over conventional therapies by improving drug stability, bioavailability, and tumor specificity. Nevertheless, major challenges remain, including metabolic adaptability, off-target toxicity, variability in nanoparticle accumulation, and manufacturing complexities. Addressing these barriers requires a deeper understanding of metabolic interactions within the tumor microenvironment and the development of more precise, safe, and scalable nanoparticles.</p><p><strong>Conclusion: </strong>Nanoparticle-mediated targeting of cancer metabolism represents a promising therapeutic strategy. However, successful clinical translation requires improved understanding of metabolic networks, optimized nanoparticle design, and standardized evaluation frameworks.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research Progress on the Antitumor Effects of Isorhamnetin (ISO) and Its Molecular Mechanisms.","authors":"Yanan Hua, Xinxu Shen, Shuqi Niu, Jinlin Guo","doi":"10.2174/0118715206493644260809171851","DOIUrl":"https://doi.org/10.2174/0118715206493644260809171851","url":null,"abstract":"<p><strong>Introduction: </strong>Cancer remains a leading contributor to global mortality, and current therapeutic interventions continue to grapple with significant limitations. The multi-target characteristics and low toxicity of natural products position them as promising sources of novel anti-tumor agents. Isorhamnetin (ISO), a naturally occurring O-methylated flavonol, exemplifies this potential, demonstrating diverse bioactivities such as cardiovascular protection, inflammation modulation, and cancer suppression.</p><p><strong>Method: </strong>This review systematically analyzed the latest advances in ISO mediated anti-tumor effects by searching databases such as PubMed and Web of Science, focusing on elucidating their molecular mechanisms, experimental evidence, and combination therapy strategies.</p><p><strong>Result: </strong>Research has shown that ISO has broad-spectrum anti-tumor activity against various malignant tumors. Mechanistically, ISO inhibits tumor cell proliferation, induces apoptosis, suppresses angiogenesis, and metastasis by regulating key signaling pathways. In addition, combining ISO with traditional chemotherapy drugs or autophagy inhibitors has a synergistic effect.</p><p><strong>Discussion: </strong>Although the multi-target anti-tumor potential of ISO has been validated, the direct molecular targets have not been fully identified, and pharmacokinetics, metabolic pathways, and bioavailability still need to be systematically evaluated. The optimal clinical dose and long-term toxicity also need to be considered to promote translational applications.</p><p><strong>Conclusion: </strong>ISO is a promising natural anti-tumor drug with multi-target regulatory ability. This review provides a theoretical basis for its anti-tumor mechanism and supports its clinical translational potential as a new strategy for cancer treatment.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Wogonoside Suppresses the Self-renewal Ability of Glioma Stem Cells via Down-regulating AKT/ZEB1 Signaling Pathway.","authors":"Biyun Zhang, Hong Lu, Yijun Wang, Di Zhao, Zhengyu Wu, Yuandong Cao","doi":"10.2174/0118715206476866260812050945","DOIUrl":"https://doi.org/10.2174/0118715206476866260812050945","url":null,"abstract":"<p><strong>Introduction: </strong>Glioma is the most prevalent primary central nervous system malignancy. Wogonoside, a flavonoid bioactive derived from Scutellaria baicalensis Georgi, has been reported to induce apoptosis in glioblastoma cells. However, the functional roles and molecular mechanisms in regulating glioma stem cell (GSC)-driven malignant progression remain poorly defined. The authors initially investigated the inhibitory effects of wogonoside on GSCs, as well as the intrinsic mechanisms responsible for these actions.</p><p><strong>Materials and methods: </strong>In vitro functional assays including extreme limiting dilution analysis, tumorsphere formation, tube formation, flow cytometry, immunofluorescence, and Western blotting were performed in primary human GSC lines (GSC#1 and GSC#2). RNA sequencing was applied to identify the key signaling pathways modulated by wogonoside. An orthotopic glioma mouse model was established to verify the in vivo antitumor efficacy of wogonoside.</p><p><strong>Results: </strong>Wogonoside significantly suppressed GSC self-renewal capacity, as evidenced by reduced tumor sphere number and size, decreased tumor-forming frequency, and downregulated the expression of GSC stemness markers SOX2 and CD133. Mechanistically, wogonoside inhibited the PI3K/AKT signaling pathway and enhanced ZEB1-mediated transcriptional repression in GSCs. Notably, ZEB1 rescue substantially reversed the inhibitory effects of wogonoside on GSC sphere formation and stemness marker expression, and restored the expression of ZEB1 target genes. Consistent with the in vitro findings, wogonoside markedly inhibited GSC-derived tumor growth and prolonged the survival of orthotopic glioma-bearing mice.</p><p><strong>Conclusion: </strong>This study reveals a novel antitumor mechanism of wogonoside in glioma, whereby it suppresses GSC stemness and malignant progression via PI3K/AKT inactivation and ZEB1-dependent transcriptional regulation. Wogonoside is a promising therapeutic candidate for the treatment of recurrent glioma.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Design of Receptor-Specific Anticancer Agents for Gallbladder Cancer: Integrating Immunomodulatory Strategies.","authors":"Deepika Verma, Parag Jain, Heena Rathod, Karan Kumar Dharme, Gyaneshwari Verma, Ajazuddin","doi":"10.2174/0118715206436002260402044851","DOIUrl":"https://doi.org/10.2174/0118715206436002260402044851","url":null,"abstract":"<p><strong>Introduction: </strong>Gallbladder Cancer (GBC) remains one of the most aggressive biliary tract malignancies, frequently diagnosed at an advanced stage due to its subtle early symptoms. This review examines receptor-mediated drug delivery as a promising approach to address the challenges of late diagnosis, limited treatment options, and chemoresistance in GBC.</p><p><strong>Methods: </strong>A structured literature review methodology was used to produce a comprehensive synthesis of evidence on available advances in receptor-targeted drug delivery and immunomodulatory strategies for Gallbladder Cancer (GBC).</p><p><strong>Results: </strong>Emphasis is placed on exploiting specific cancer cell receptors, such as EGFR, HER2, VEGFR, FGFR, and the estrogen-related receptor, as targets for nanoparticles, liposomes, and antibody-drug conjugates to enhance drug internalization while reducing off-target toxicity.</p><p><strong>Discussion: </strong>In parallel, the role of modern immunotherapies, including immune checkpoint inhibitors, cancer vaccines, and adoptive cell therapies such as CAR-T cells, is discussed with respect to their synergistic potential when combined with targeted drug-delivery systems. Additionally, emerging RNA- and gene-based therapies provide new avenues to modulate tumor biology and reverse treatment resistance.</p><p><strong>Conclusion: </strong>Collectively, integrating receptor-targeted nanomedicine with immunotherapeutic strategies could pave the way for personalized treatment regimens that improve therapeutic outcomes and survival in patients with gallbladder cancer.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Alterations Associated with Reduced 5-FU Sensitivity in mtDNA-Depleted HGC-27 Cells.","authors":"Ozlem Turksoy Terzioglu, Ayse Busranur Celik, Gokhan Terzioglu, Gamze Yeşilay, Yusuf Tutar","doi":"10.2174/0118715206480595260722072353","DOIUrl":"https://doi.org/10.2174/0118715206480595260722072353","url":null,"abstract":"<p><strong>Introduction: </strong>Mitochondrial DNA (mtDNA) depletion has been linked to cancer progression and chemoresistance. However, its involvement in the response of Gastric Cancer (GC) to 5-Fluorouracil (5-FU) is unknown. This study sought to investigate the effects of mtDNA depletion on cellular behavior and drug sensitivity of HGC-27 gastric cancer cells.</p><p><strong>Methods: </strong>mtDNA-depleted cells were established, and the effect of 5-FU on viability of the cells, mitochondrial activity, gene and protein expression, and biochemical and functional parameters was subsequently determined. Pathway involvement was further evaluated using pharmacological inhibition analyses.</p><p><strong>Results: </strong>mtDNA-depleted HGC-27 cells exhibited decreased sensitivity to 5-FU compared to parental cells. Various cancer-related pathways, including HIF-1, TNF, MAPK signaling pathways, and PI3K-Akt, as well as Rap1 signaling, were found to be affected. Metabolic analysis demonstrated a switch towards glycolysis and the pentose phosphate pathway. mtDNA-depleted cells were primarily arrested at G0/G1 phase. These cells displayed an increased clonogenic potential following 5-FU treatment and increased migratory ability. In addition, VEGF-A, IL-6, p21, HIF-1α levels, and the pERK/ERK ratio were significantly elevated in mtDNA-depleted cells. Pharmacological inhibition of HIF-1α and MAPK/ERK signaling reduced cell survival following 5-FU treatment, supporting the potential involvement of these pathways in the adaptive response associated with mtDNA depletion. Raman spectroscopy further indicated that the biochemical response to 5-FU was markedly attenuated in mtDNA-depleted cells.</p><p><strong>Discussion: </strong>The findings suggest that mtDNA depletion is associated with a metabolically reprogrammed, stress-adapted phenotype in HGC-27 cells. Mitochondrial genome loss was associated with alterations in multiple pathways, including HIF-1α signaling and the MAPK pathway, particularly its ERK-associated branch, which may contribute to the reduced sensitivity to 5-FU observed in these cells.</p><p><strong>Conclusion: </strong>These findings suggest a potential link between mitochondrial dysfunction and reduced sensitivity to 5-FU in HGC-27 gastric cancer cells. They also imply that targeting mitochondrial stress-associated signaling pathways may represent a potential strategy to overcome chemoresistance.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of Artemisia argyi in the Treatment of Pancreatic Ductal Adenocarcinoma Based on Network Pharmacology and Experimental Validation.","authors":"Yan Luo, Jisheng Hu, Jian Guan, Jiachen Shi, Linzhu Zou, Jiawen Wu, Yuncheng Han, Wei Liu, Ping Xuan, Guanqun Li, Le Li, Bei Sun, Rui Kong","doi":"10.2174/0118715206439346260326193041","DOIUrl":"https://doi.org/10.2174/0118715206439346260326193041","url":null,"abstract":"<p><strong>Introduction: </strong>Artemisia argyi (AA) demonstrates anti-cancer potential. However, its mechanisms against pancreatic ductal adenocarcinoma (PDAC) remain unclear. This study investigates the anti-tumor mechanisms of AA in PDAC.</p><p><strong>Methods: </strong>The Traditional Chinese Medicine Systems Pharmacology (TCMSP) database was used to identify potential bioactive compounds. The Analyze Network tool revealed that stigmasterol (SS) was a key bioactive compound of AA. Then, the corresponding targets of SS were predicted through SwissTargetPrediction and SuperPred. A compound-target interaction network was subsequently constructed with Cytoscape, followed by the generation of a protein-protein interaction (PPI) network using the STRING database. Molecular docking was performed to evaluate the binding affinity between SS and the targets. Finally, the specific mechanism of SS on PDAC was experimentally investigated.</p><p><strong>Results: </strong>SS was identified as a major bioactive component of AA. A total of 107 overlapping targets between SS and PDAC were collected. Molecular docking demonstrated favorable binding interactions between SS and its candidate protein targets. The experimental results suggested that SS could promote PDAC cell apoptosis through the AMPK/mTOR pathway.</p><p><strong>Discussion: </strong>Our findings demonstrate that SS, a primary bioactive component of AA, exerts significant antitumor effects in PDAC by inducing tumor cell apoptosis through the activation of the AMPK/mTOR signaling pathway. Furthermore, we reveal a novel immunomodulatory dimension whereby SS remodels the immunosuppressive PDAC microenvironment. This dual action on both tumor cells and the immune landscape positions SS as a promising multi-faceted therapeutic candidate for PDAC.</p><p><strong>Conclusion: </strong>SS was characterized as the key bioactive component of AA, supporting its potential role as a promising therapeutic agent for PDAC.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated Transcriptomic and Functional Profiling Reveals IL-7R/FOXO1 Axis as a Target of Momordicine I in Meningioma.","authors":"Ying Kao, Jia-Rong Hu, Fu-Chi Yang, Dueng-Yuan Hueng, Chia-Kuang Tsai","doi":"10.2174/0118715206436644260326051935","DOIUrl":"https://doi.org/10.2174/0118715206436644260326051935","url":null,"abstract":"<p><strong>Introduction: </strong>Meningiomas are common intracranial tumors lacking effective chemotherapeutic options. Momordicine I, a triterpenoid isolated from bitter melon, has demonstrated anticancer activity, but its effects on meningioma remain unclear. The effect of Momordicine I on meningiomas is studied in this research.</p><p><strong>Methods: </strong>Human meningioma cells (IOMM-Lee and patient-derived P9) were treated with momordicine I. Cell viability, colony formation, migration, apoptosis, and cell cycle progression were assessed. RNA sequencing, qRT-PCR, Western blotting, and Seahorse analysis were used to investigate molecular mechanisms.</p><p><strong>Results: </strong>Momordicine I inhibited cell proliferation, colony formation, and migration, while inducing apoptosis and G1/G2-M phase arrest. Transcriptomic analysis revealed downregulation of IL7R, FOXO1, and PLK2. Treatment also increased γ-H2AX and reduced Survivin and Bcl-xL expression, indicating apoptosis via DNA damage and survival signaling suppression. Furthermore, mitochondrial oxidative phosphorylation was impaired.</p><p><strong>Discussion: </strong>These findings suggest that Momordicine I exerts its antitumor activity through coordinated suppression of cell survival pathways, modulation of cell cycle regulators, and mitochondrial dysfunction. Downregulation of IL7R and FOXO1, both associated with tumor progression and survival, underscores the potential of Momordicine I as a multi-pathway therapeutic agent.</p><p><strong>Conclusion: </strong>Momordicine I demonstrates potent anti-meningioma effects by targeting the IL7R/FOXO1 axis, inducing apoptosis, and impairing mitochondrial metabolism. These results support its development as a novel therapeutic candidate for malignant meningioma treatment.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Combination of Atractylon and Magnolol Inhibits the Survival of Hepatocellular Carcinoma Cells through Promoting Autophagy.","authors":"Haojia Wu, Jing Bi, Qinglong Guo, Yaqi Gong, Tingzhi Cao, Fan Zhang, Guoliang Zhang, Hengfei Li","doi":"10.2174/0118715206428557251226060428","DOIUrl":"https://doi.org/10.2174/0118715206428557251226060428","url":null,"abstract":"<p><strong>Background: </strong>New medications and treatment approaches are needed due to the rising frequency of hepatocellular carcinoma; pharmacological combination therapy is one such approach that is being thoroughly studied.</p><p><strong>Methods: </strong>After co-treatment with atractylon and magnolol, cell viability and death were assessed using a CCK8 kit and an LDH kit, cell migration and invasion were assessed using a transwell assay, and related proteins were detected by western blotting after applying specific drug treatments or disturbances.</p><p><strong>Results: </strong>In both HepG2 and Hep3B cells, magnolol and atractylon demonstrated significant synergistic effects, including the inhibition of cell proliferation, migration, and invasion. This mechanism may be mediated by the mTOR/TFEB signaling pathway.</p><p><strong>Discussion: </strong>Based on our experimental findings and the existing literature, the combined application of atractylon and magnolol is considered to have promising therapeutic potential for suppressing the growth of hepatocellular carcinoma cells. This warrants further investigation to elucidate the underlying mechanisms and optimize this combinatorial approach.</p><p><strong>Conclusion: </strong>The synergistic effect of magnolol and atractylon was found to be superior to that of either compound alone, particularly in terms of cell viability, migration, and invasion. The use of both drugs leads to autophagy-associated cell death, and the mTOR/TFEB signal pathway is an important factor in this process.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}