Biological Procedures Online最新文献

{"title":"ALKBH5 promotes ovarian cancer progression by activating Notch2 signaling.","authors":"Yanying Liu, Huafeng Luo, Luhong Li, Ziao Gao, Qian Wang, Hao Liu, Ruiyun Wu, Cong Peng","doi":"10.1186/s12575-026-00330-8","DOIUrl":"10.1186/s12575-026-00330-8","url":null,"abstract":"<p><strong>Background: </strong>ALKBH5, one of the RNA N6-methyladenosine (m6A) demethyltransferases, has been suggested to be involved in the progression of several cancers. The aim of this study was to investigate clinical significance and biological functions of ALKBH5 in promoting ovarian cancer progression.</p><p><strong>Results: </strong>We found a significant upregulation of ALKBH5 expression in ovarian cancer tissues compared with normal tissues. Correlation analyses indicated an association between heightened ALKBH5 expression and FIGO stage, as well as lymph node metastasis. Importantly, increased ALKBH5 expression indicated shorter progression-free survival and overall survival. Moreover, we found that hypoxia induced an increase in ALKBH5 expression in ovarian cancer via an HIF-1α-dependent mechanism. Loss-of-function assays demonstrated that ALKBH5 knockdown inhibited ovarian cancer cell progression both in vitro and in vivo. Furthermore, we found that knockdown of ALKBH5-meidated m6A demethylation decreased Notch2 mRNA stability and expression, resulting in the inhibition of cell proliferation, invasion and metastasis in OC cells.</p><p><strong>Conclusion: </strong>In summary, our findings demonstrated that ALKBH5 promotes the progression of ovarian cancer by activating Notch2 signaling, and suggested that ALKBH5 functions as an oncogene and may serve as a prognostic biomarker and therapeutic target in ovarian cancer.</p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13063600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147347114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Key molecular mechanisms and regulatory networks in colorectal cancer liver metastasis.","authors":"Zhipeng Zhang, Yuchun Ni, Jie Wang, Jianhui Tian, Likun Liu, Shulan Hao","doi":"10.1186/s12575-026-00332-6","DOIUrl":"10.1186/s12575-026-00332-6","url":null,"abstract":"","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13059156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147324490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TSZAF Monomer Combination Inhibits the Progression of Ovarian Cancer Via Regulating the AKT/FOXO3A-mediated Glycolysis Pathway.","authors":"Long Zhang, Jialiang Yao, Ziqi Chen, Pan Yu, Xinyi Lu, Jiajun Liu, Bin Luo, Jiwei Liu, Zujun Que, Yan Wu, Jianhui Tian","doi":"10.1186/s12575-025-00323-z","DOIUrl":"https://doi.org/10.1186/s12575-025-00323-z","url":null,"abstract":"<p><strong>Background: </strong>Tiao-Shen-Zhi-Ai Formula (TSZAF) is a compound prescription of traditional Chinese medicine used clinically for the treatment of ovarian cancer. In this study, we selected three main active ingredients from TSZAF and combined them into a new TSZAF monomer combination (TSZAF mc) to investigate its effects and mechanisms on inhibiting ovarian cancer proliferation and inducing apoptosis.</p><p><strong>Methods: </strong>The effects of TSZAF mc on proliferative activity and apoptosis in ovarian cancer HEY and SKOV3.IP1 cells were assessed in vitro using CCK-8 assay, colony formation assay, and apoptosis assay. Micromethods, flow cytometry, and immunofluorescence were employed to evaluate the impact of TSZAF mc on aerobic glycolytic metabolites and mitochondrial membrane potential. The mRNA and protein expression of key glycolytic genes were detected by quantitative real-time PCR (RT-PCR) and Western blot (WB). An ovarian cancer subcutaneous tumor model was established in NOD-SCID mice using SKOV3.IP1 cells. TSZAF mc was administered via continuous intraperitoneal injection, and its antitumor efficacy in vivo was assessed through anatomical observation, hematoxylin and eosin (H&E) staining, and immunohistochemistry (IHC). Further RT-PCR, WB, and IHC were performed to validate the expression of key upstream glycolytic genes at mRNA and protein levels. Drug affinity responsive target stability (DARTS) and cellular thermal shift assay (CETSA) were used to confirm binding targets. Molecular docking was performed to predict the binding interactions between the monomers and AKT. Finally, the regulatory relationships within signaling pathways were elucidated based on functional assays.</p><p><strong>Results: </strong>TSZAF mc effectively inhibited ovarian cancer proliferation and induced apoptosis. It reduced lactate and ATP production, downregulated mitochondrial membrane potential, and decreased the mRNA and protein expression of key glycolytic genes, including HK2, PKM2, PFKM, GLUT1, and LDHA. In vivo, TSZAF mc suppressed ovarian cancer growth. Moreover, TSZAF mc downregulated the expression of phosphorylated AKT (p-AKT) and phosphorylated FOXO3A (p-FOXO3A) at both protein and tissue levels. CETSA and DARTS demonstrated that TSZAF mc binds AKT. The AKT activator SC79 reversed the inhibitory effects of TSZAF mc on ovarian cancer proliferation and the downregulation of glycolytic proteins.</p><p><strong>Conclusion: </strong>TSZAF mc inhibits ovarian cancer progression by regulating the AKT/ FOXO3A-mediated glycolysis pathway, which may represent one of the mechanisms underlying the clinical efficacy of TSZAF in ovarian cancer treatment.</p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146206415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leishmania Infection: A Bioorganic Model Under the Light of Benchtop Low Field Nuclear Magnetic Resonance.","authors":"Jairo Mendoza-Roldan, Paola Albanese, Carmela Di Spiridione, Mirco Vacca, Matteo Spagnuolo, Mario Alves, Mariaelisa Carbonara, Maria De Angelis, Danilo Vona, Domenico Otranto","doi":"10.1186/s12575-026-00328-2","DOIUrl":"10.1186/s12575-026-00328-2","url":null,"abstract":"","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13005448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146194084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Piperlongumine Inhibits Lung Cancer Growth by Inducing Endoplasmic Reticulum Stress Leading To Suppression of M2 Macrophage Polarization.","authors":"Yixin Zhou, Wenjing Teng, Jianchun Wu, Yingbin Luo, Yuli Wang, Yan Li","doi":"10.1186/s12575-026-00324-6","DOIUrl":"10.1186/s12575-026-00324-6","url":null,"abstract":"","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":"28 1","pages":"5"},"PeriodicalIF":4.3,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12833924/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New Candidate Reference Measurement Procedures for MET CNV Detection and Quantification Using Digital PCR.","authors":"Jessica Petiti, Sabrina Caria, Laura Revel, Marika Fava, Giovanna Carrà, Raffaella Albano, Sara Gilardi, Tiziana Venesio, Carla Divieto","doi":"10.1186/s12575-026-00325-5","DOIUrl":"10.1186/s12575-026-00325-5","url":null,"abstract":"","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":"10"},"PeriodicalIF":4.3,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12895716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146002880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Multi-Center Cohort-Based circRNA Diagnostic Model for Detection of Gastric Cancer.","authors":"Xiaoyu Gu, Shuo Ma, Xun Gao, Chenyan Yuan, Wei Gao, Fengfeng Zhao, Yonghui Liu, Chen Zhang, Guoqiu Wu, Shuang Liu","doi":"10.1186/s12575-026-00326-4","DOIUrl":"10.1186/s12575-026-00326-4","url":null,"abstract":"","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13045110/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145988013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated Bioinformatics and Experimental Validation Reveal Fuzheng Yi'ai Formula Induces Immunogenic Cell Death Via the PERK-eIF2α-ATF4 Pathway for Prostate Cancer Treatment.","authors":"Xiaopeng Yu, Lian Peng, Wen Sheng, Renyi Yang, Qinghu He","doi":"10.1186/s12575-025-00321-1","DOIUrl":"10.1186/s12575-025-00321-1","url":null,"abstract":"","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":"9"},"PeriodicalIF":4.3,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12870246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Clinically Derived TCM Decoction (WD-3) Attenuates Malignant Phenotypes of Gastric Cancer through the PPARγ-AMPK Pathway.","authors":"Hengzhou Zhu, Wenyue Zhao, Jingyi Qian, Xiaodan Zhu, Chencen Zhang, Yuqing Geng, Yun Yuan, Yuetong Xia, Lei Huang, Jiejie Fan, Liang Ma, Valeriy Smirnov, Chunhui Jin","doi":"10.1186/s12575-025-00320-2","DOIUrl":"10.1186/s12575-025-00320-2","url":null,"abstract":"<p><strong>Background & objective: </strong>Weitiao No. 3 decoction (WD-3), a clinically used adjuvant therapy for advanced gastrointestinal tumors, lacks clarified mechanisms in gastric cancer (GC).</p><p><strong>Methods: </strong>We profiled chemical constituents by liquid chromatography-mass spectrometry (LC-MS), predicted putative targets and pathways via network pharmacology, evaluated binding by molecular docking, and validated pharmacological effects in MGC-803 cells and mouse xenograft models.</p><p><strong>Results: </strong>LC-MS identified 344 constituents; network analyses yielded 188 putative targets and highlighted core nodes (e.g., AKT1, EGFR, PIK3CA, PPARG). Pathway enrichment and docking converged on the PPARγ (PPARG)/AMPK axis. Experimentally, WD-3 suppressed proliferation and migration, induced G1-phase arrest, and increased PPARγ and phospho-AMPK; perturbation of PPARγ modulated AMPK activation and anti-tumor effects. In vivo, high-dose WD-3 reduced xenograft tumor growth in a dose-dependent manner without overt hepato-renal histopathologic toxicity.</p><p><strong>Conclusions: </strong>Using LC-MS, network pharmacology, docking, and in vitro/in vivo assays, we found that WD-3 suppresses GC cell proliferation/migration and xenograft growth, accompanied by increased total PPARγ and AMPK Thr172 phosphorylation, supporting involvement of the PPARγ/AMPK axis.</p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":"8"},"PeriodicalIF":4.3,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12870326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145916665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ribosomal Protein RPL29 Promotes Hepatocellular Carcinoma Progression Through Regulation the Expression of Exosome Component 4.","authors":"Xiaoxue Wang, Zexin Zhu","doi":"10.1186/s12575-025-00322-0","DOIUrl":"10.1186/s12575-025-00322-0","url":null,"abstract":"<p><strong>Background: </strong>There are notable challenges in the development of effective therapeutic interventions for primary liver cancer (PLC). The role of ribosomal protein (RP) RPL29 in cancer has been rarely reported and the underlying mechanisms of RPL29 in the progression of Hepatocellular carcinoma (HCC) remain unclear.</p><p><strong>Methods: </strong>In the present study, the expression level and prognostic value of RPL29 in patients with HCC was evaluated by bioinformatics and immunohistochemistry. Moreover, gene expression was suppressed using targeted siRNAs and enhanced through plasmids containing specific gene cDNA sequences. Subsequently, assessments of cell viability and invasive capacity were conducted. Additionally, Western blot analyses and subcutaneous xenograft models in nude mice were utilized to elucidate the potential function of RPL29 in regulating the malignant phenotype of HCC.</p><p><strong>Results: </strong>The expression of RPL29 was found to be significantly elevated in HCC tissues. Further investigation demonstrated that RPL29 actively promotes the proliferation and metastatic potential of HCC cells. Moreover, RPL29 was shown to enhance the expression of Exosome Component 4 (EXOSC4), thereby contributing to the progression and metastasis of HCC. Both RPL29 and EXOSC4 were markedly overexpressed in HCC tissues and were associated with poorer overall survival and disease-free survival outcomes. Notably, the overexpression of RPL29 was able to restore cell viability and invasive capabilities in HCC cells in EXOSC4 silenced cells. In addition, we conducted a screening of two small molecule drugs that specifically target EXOSC4.</p><p><strong>Conclusion: </strong>The present study demonstrated that RPL29 facilitates HCC progression by regulating the expression of EXOSC4, which provides a novel therapeutic option for patients with HCC.</p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":"7"},"PeriodicalIF":4.3,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12866049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145896034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}