{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen W"],"funding":["Shenzhen Basic Research Project (Natural Science Foundation)","National Natural Science Foundation of China","Shenzhen People&apos;s Hospital Clinical Scientist Training &quot;Five Three&quot; Plan Project","Shenzhen Basic Research Project","Shenzhen People's Hospital Clinical Scientist Training \"Five Three\" Plan Project"],"pagination":["100"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12487252"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20(1)"],"pubmed_abstract":["<h4>Background</h4>Hepatocellular carcinoma (HCC) is significantly influenced by hepatitis B virus (HBV) infection. However, the roles of ferroptosis and ubiquitination modifications in this context remain poorly understood.<h4>Methods</h4>In this study, we utilized immunoprecipitation, immunofluorescence, and analysis of ubiquitin modifications to explore the regulatory mechanisms of MINPP1 in ferroptosis and its effects on tumor progression. Further mechanistic studies revealed that ZRANB1 regulates the K33-linked ubiquitination of CTSB. Ultimately, the contribution of the MINPP1-CTSB axis to tumor progression was validated using in vivo experiments.<h4>Results</h4>Our study demonstrates that MINPP1 regulates ferroptosis in HBV-positive HCC cells via a glycolytic bypass mechanism. Bioinf"],"journal":["Biology direct"],"pubmed_title":["MINPP1 promotes ferroptosis in HBV-related hepatocellular carcinoma by regulating CTSB K33-linked deubiquitination via ZRANB1."],"pmcid":["PMC12487252"],"funding_grant_id":["82270625","SYWGSJCYJ202406","JCYJ20240813104108012"],"pubmed_authors":["Chen W","Zhang S","Xiong F","Song Y","Wang L"],"additional_accession":[]},"is_claimable":false,"name":"MINPP1 promotes ferroptosis in HBV-related hepatocellular carcinoma by regulating CTSB K33-linked deubiquitination via ZRANB1.","description":"<h4>Background</h4>Hepatocellular carcinoma (HCC) is significantly influenced by hepatitis B virus (HBV) infection. However, the roles of ferroptosis and ubiquitination modifications in this context remain poorly understood.<h4>Methods</h4>In this study, we utilized immunoprecipitation, immunofluorescence, and analysis of ubiquitin modifications to explore the regulatory mechanisms of MINPP1 in ferroptosis and its effects on tumor progression. Further mechanistic studies revealed that ZRANB1 regulates the K33-linked ubiquitination of CTSB. Ultimately, the contribution of the MINPP1-CTSB axis to tumor progression was validated using in vivo experiments.<h4>Results</h4>Our study demonstrates that MINPP1 regulates ferroptosis in HBV-positive HCC cells via a glycolytic bypass mechanism. Bioinf","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Oct","modification":"2026-06-04T02:23:41.177Z","creation":"2026-05-04T03:13:11.206Z"},"accession":"S-EPMC12487252","cross_references":{"pubmed":["41035046"],"doi":["10.1186/s13062-025-00686-z"]}}