Ubiquitination-specific protease 7 enhances stemness of hepatocellular carcinoma by stabilizing basic transcription factor 3
This study aims to explore the molecular regulation mechanism of ubiquitination-specific protease 7 (USP7) in facilitating the stemness properties of hepatocellular carcinoma (HCC). Gain-of-function and loss-of-function assays were conducted in SK-Hep1 and HepG2 cells transfected with USP7 overexpre...
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| creator | Hu, Mingchao Dai, Chengchen Sun, Xieyin Chen, Yinqi Xu, Nuo Lin, Zhaoyi Xu, Shiyu Cheng, Chun Tan, Zhonghua Bian, Saiyan Zheng, Wenjie |
| description | This study aims to explore the molecular regulation mechanism of ubiquitination-specific protease 7 (USP7) in facilitating the stemness properties of hepatocellular carcinoma (HCC). Gain-of-function and loss-of-function assays were conducted in SK-Hep1 and HepG2 cells transfected with USP7 overexpression/knockdown plasmids and USP7 inhibitor P22077. The proliferation, migration, invasion, and self-renewal capacity of hepatocellular carcinoma cells were detected by CCK-8, colony formation, Transwell, scratch, and tumor sphere formation, respectively. MS was performed to identify the potential substrate of USP7 following P22077 treatment. Co-IP assay was used to verify the interaction between USP7 and basic transcription factor 3 (BTF3) in HCC cells. The overexpression of USP7 could promote the proliferation, migration, invasion, and colony formation capacity of SK-Hep1 and HepG2 cells. Additionally, ectopic UPS7 enhanced the epithelial-mesenchymal transition (EMT) and stem-like characteristics of the HCC cells. In contrast, USP7 depletion by knockdown of USP7 or administrating inhibitor P22077 significantly inhibited these malignant phenotypes of SK-Hep1 and HepG2 cells. Following MS analysis, BTF3 was identified as a potential substrate for USP7. USP7 could interact with BTF3 and upregulate its protein level, while USP7 depletion significantly upregulated the ubiquitination levels. Overexpression of BTF3 partially rescue the inhibitory effects of USP7 depletion on the malignant phenotypes and stemness properties of SK-Hep1 and HepG2 cells. USP7 can promote the stemness and malignant phenotype of HCC by stabilizing BTF3. |
| doi_str_mv | 10.1007/s10142-024-01310-5 |
| format | Article |
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Gain-of-function and loss-of-function assays were conducted in SK-Hep1 and HepG2 cells transfected with USP7 overexpression/knockdown plasmids and USP7 inhibitor P22077. The proliferation, migration, invasion, and self-renewal capacity of hepatocellular carcinoma cells were detected by CCK-8, colony formation, Transwell, scratch, and tumor sphere formation, respectively. MS was performed to identify the potential substrate of USP7 following P22077 treatment. Co-IP assay was used to verify the interaction between USP7 and basic transcription factor 3 (BTF3) in HCC cells. The overexpression of USP7 could promote the proliferation, migration, invasion, and colony formation capacity of SK-Hep1 and HepG2 cells. Additionally, ectopic UPS7 enhanced the epithelial-mesenchymal transition (EMT) and stem-like characteristics of the HCC cells. In contrast, USP7 depletion by knockdown of USP7 or administrating inhibitor P22077 significantly inhibited these malignant phenotypes of SK-Hep1 and HepG2 cells. Following MS analysis, BTF3 was identified as a potential substrate for USP7. USP7 could interact with BTF3 and upregulate its protein level, while USP7 depletion significantly upregulated the ubiquitination levels. Overexpression of BTF3 partially rescue the inhibitory effects of USP7 depletion on the malignant phenotypes and stemness properties of SK-Hep1 and HepG2 cells. USP7 can promote the stemness and malignant phenotype of HCC by stabilizing BTF3.</description><identifier>ISSN: 1438-793X</identifier><identifier>EISSN: 1438-7948</identifier><identifier>DOI: 10.1007/s10142-024-01310-5</identifier><identifier>PMID: 38340226</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animal Genetics and Genomics ; Biochemistry ; Bioinformatics ; Biomedical and Life Sciences ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; Cell adhesion & migration ; Cell Biology ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - genetics ; Cell self-renewal ; Cholecystokinin ; gain-of-function mutation ; Gene Expression Regulation, Neoplastic ; genomics ; Genotype & phenotype ; Hepatocellular carcinoma ; hepatoma ; Humans ; Immunoassay ; Life Sciences ; Liver cancer ; Liver Neoplasms - genetics ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; loss-of-function mutation ; Microbial Genetics and Genomics ; Original Article ; phenotype ; Phenotypes ; Plant Genetics and Genomics ; Plasmids ; protein content ; proteinases ; Thiophenes ; Transcription factors ; Transcription Factors - metabolism ; Ubiquitin-Specific Peptidase 7 - genetics ; Ubiquitin-Specific Peptidase 7 - metabolism ; Ubiquitination</subject><ispartof>Functional & integrative genomics, 2024-02, Vol.24 (1), p.28-28, Article 28</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. 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Gain-of-function and loss-of-function assays were conducted in SK-Hep1 and HepG2 cells transfected with USP7 overexpression/knockdown plasmids and USP7 inhibitor P22077. The proliferation, migration, invasion, and self-renewal capacity of hepatocellular carcinoma cells were detected by CCK-8, colony formation, Transwell, scratch, and tumor sphere formation, respectively. MS was performed to identify the potential substrate of USP7 following P22077 treatment. Co-IP assay was used to verify the interaction between USP7 and basic transcription factor 3 (BTF3) in HCC cells. The overexpression of USP7 could promote the proliferation, migration, invasion, and colony formation capacity of SK-Hep1 and HepG2 cells. Additionally, ectopic UPS7 enhanced the epithelial-mesenchymal transition (EMT) and stem-like characteristics of the HCC cells. In contrast, USP7 depletion by knockdown of USP7 or administrating inhibitor P22077 significantly inhibited these malignant phenotypes of SK-Hep1 and HepG2 cells. Following MS analysis, BTF3 was identified as a potential substrate for USP7. USP7 could interact with BTF3 and upregulate its protein level, while USP7 depletion significantly upregulated the ubiquitination levels. Overexpression of BTF3 partially rescue the inhibitory effects of USP7 depletion on the malignant phenotypes and stemness properties of SK-Hep1 and HepG2 cells. USP7 can promote the stemness and malignant phenotype of HCC by stabilizing BTF3.</description><subject>Animal Genetics and Genomics</subject><subject>Biochemistry</subject><subject>Bioinformatics</subject><subject>Biomedical and Life Sciences</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell adhesion & migration</subject><subject>Cell Biology</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Cell self-renewal</subject><subject>Cholecystokinin</subject><subject>gain-of-function mutation</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>genomics</subject><subject>Genotype & phenotype</subject><subject>Hepatocellular carcinoma</subject><subject>hepatoma</subject><subject>Humans</subject><subject>Immunoassay</subject><subject>Life Sciences</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - pathology</subject><subject>loss-of-function mutation</subject><subject>Microbial Genetics and Genomics</subject><subject>Original Article</subject><subject>phenotype</subject><subject>Phenotypes</subject><subject>Plant Genetics and Genomics</subject><subject>Plasmids</subject><subject>protein content</subject><subject>proteinases</subject><subject>Thiophenes</subject><subject>Transcription factors</subject><subject>Transcription Factors - metabolism</subject><subject>Ubiquitin-Specific Peptidase 7 - genetics</subject><subject>Ubiquitin-Specific Peptidase 7 - metabolism</subject><subject>Ubiquitination</subject><issn>1438-793X</issn><issn>1438-7948</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1vFSEUhomxsbX6B1wYEjfdjD183TssTaPVpImbNnFHgHtoaWZgCjOLNv54md5aExe6AsJz3sPhIeQdg48MYHtaGTDJO-CyAyYYdOoFOWJS9N1Wy_7l8178OCSva70FAAVavCKHohcSON8ckZ9XLt4tcY7JzjGnrk7oY4ieTiXPaCvSLcV0Y5PHSuuMY8JaaQ70Bic7Z4_DsAy2UG-LjymPlrr7xlkXh_gQ0zV1tra0udhUfYnT2oQG6-dcqHhDDoIdKr59Wo_J1ZfPl2dfu4vv59_OPl10Xig9d6J3sOGWebcDF2DnHartDnvLgGPfzkFpG7QKPLgNIpdcIlMOpLIaEKU4Jif73DbU3YJ1NmOs69NtwrxUI5gSGyY0h_-iXHPV_pFJ3dAPf6G3eSmpDbJSUgnN2BrI95QvudaCwUwljrbcGwZm1Wj2Gk3TaB41GtWK3j9FL27E3XPJb28NEHugtqt0jeVP73_E_gL5yapG</recordid><startdate>20240201</startdate><enddate>20240201</enddate><creator>Hu, Mingchao</creator><creator>Dai, Chengchen</creator><creator>Sun, Xieyin</creator><creator>Chen, Yinqi</creator><creator>Xu, Nuo</creator><creator>Lin, Zhaoyi</creator><creator>Xu, Shiyu</creator><creator>Cheng, Chun</creator><creator>Tan, Zhonghua</creator><creator>Bian, Saiyan</creator><creator>Zheng, Wenjie</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope></search><sort><creationdate>20240201</creationdate><title>Ubiquitination-specific protease 7 enhances stemness of hepatocellular carcinoma by stabilizing basic transcription factor 3</title><author>Hu, Mingchao ; Dai, Chengchen ; Sun, Xieyin ; Chen, Yinqi ; Xu, Nuo ; Lin, Zhaoyi ; Xu, Shiyu ; Cheng, Chun ; Tan, Zhonghua ; Bian, Saiyan ; Zheng, Wenjie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c359t-38b062a1cbd0bf0dcbe57de8a102e80dcf59af95f2fb6ee2424e15b045a90ee43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animal Genetics and Genomics</topic><topic>Biochemistry</topic><topic>Bioinformatics</topic><topic>Biomedical and Life Sciences</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Cell adhesion & migration</topic><topic>Cell Biology</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Cell self-renewal</topic><topic>Cholecystokinin</topic><topic>gain-of-function mutation</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>genomics</topic><topic>Genotype & phenotype</topic><topic>Hepatocellular carcinoma</topic><topic>hepatoma</topic><topic>Humans</topic><topic>Immunoassay</topic><topic>Life Sciences</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - pathology</topic><topic>loss-of-function mutation</topic><topic>Microbial Genetics and Genomics</topic><topic>Original Article</topic><topic>phenotype</topic><topic>Phenotypes</topic><topic>Plant Genetics and Genomics</topic><topic>Plasmids</topic><topic>protein content</topic><topic>proteinases</topic><topic>Thiophenes</topic><topic>Transcription factors</topic><topic>Transcription Factors - metabolism</topic><topic>Ubiquitin-Specific Peptidase 7 - genetics</topic><topic>Ubiquitin-Specific Peptidase 7 - metabolism</topic><topic>Ubiquitination</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Mingchao</creatorcontrib><creatorcontrib>Dai, Chengchen</creatorcontrib><creatorcontrib>Sun, Xieyin</creatorcontrib><creatorcontrib>Chen, Yinqi</creatorcontrib><creatorcontrib>Xu, Nuo</creatorcontrib><creatorcontrib>Lin, Zhaoyi</creatorcontrib><creatorcontrib>Xu, Shiyu</creatorcontrib><creatorcontrib>Cheng, Chun</creatorcontrib><creatorcontrib>Tan, Zhonghua</creatorcontrib><creatorcontrib>Bian, Saiyan</creatorcontrib><creatorcontrib>Zheng, Wenjie</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Functional & integrative genomics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Mingchao</au><au>Dai, Chengchen</au><au>Sun, Xieyin</au><au>Chen, Yinqi</au><au>Xu, Nuo</au><au>Lin, Zhaoyi</au><au>Xu, Shiyu</au><au>Cheng, Chun</au><au>Tan, Zhonghua</au><au>Bian, Saiyan</au><au>Zheng, Wenjie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ubiquitination-specific protease 7 enhances stemness of hepatocellular carcinoma by stabilizing basic transcription factor 3</atitle><jtitle>Functional & integrative genomics</jtitle><stitle>Funct Integr Genomics</stitle><addtitle>Funct Integr Genomics</addtitle><date>2024-02-01</date><risdate>2024</risdate><volume>24</volume><issue>1</issue><spage>28</spage><epage>28</epage><pages>28-28</pages><artnum>28</artnum><issn>1438-793X</issn><eissn>1438-7948</eissn><abstract>This study aims to explore the molecular regulation mechanism of ubiquitination-specific protease 7 (USP7) in facilitating the stemness properties of hepatocellular carcinoma (HCC). Gain-of-function and loss-of-function assays were conducted in SK-Hep1 and HepG2 cells transfected with USP7 overexpression/knockdown plasmids and USP7 inhibitor P22077. The proliferation, migration, invasion, and self-renewal capacity of hepatocellular carcinoma cells were detected by CCK-8, colony formation, Transwell, scratch, and tumor sphere formation, respectively. MS was performed to identify the potential substrate of USP7 following P22077 treatment. Co-IP assay was used to verify the interaction between USP7 and basic transcription factor 3 (BTF3) in HCC cells. The overexpression of USP7 could promote the proliferation, migration, invasion, and colony formation capacity of SK-Hep1 and HepG2 cells. Additionally, ectopic UPS7 enhanced the epithelial-mesenchymal transition (EMT) and stem-like characteristics of the HCC cells. In contrast, USP7 depletion by knockdown of USP7 or administrating inhibitor P22077 significantly inhibited these malignant phenotypes of SK-Hep1 and HepG2 cells. Following MS analysis, BTF3 was identified as a potential substrate for USP7. USP7 could interact with BTF3 and upregulate its protein level, while USP7 depletion significantly upregulated the ubiquitination levels. Overexpression of BTF3 partially rescue the inhibitory effects of USP7 depletion on the malignant phenotypes and stemness properties of SK-Hep1 and HepG2 cells. USP7 can promote the stemness and malignant phenotype of HCC by stabilizing BTF3.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>38340226</pmid><doi>10.1007/s10142-024-01310-5</doi><tpages>1</tpages></addata></record> |
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| subjects | Animal Genetics and Genomics Biochemistry Bioinformatics Biomedical and Life Sciences Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology Cell adhesion & migration Cell Biology Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - genetics Cell self-renewal Cholecystokinin gain-of-function mutation Gene Expression Regulation, Neoplastic genomics Genotype & phenotype Hepatocellular carcinoma hepatoma Humans Immunoassay Life Sciences Liver cancer Liver Neoplasms - genetics Liver Neoplasms - metabolism Liver Neoplasms - pathology loss-of-function mutation Microbial Genetics and Genomics Original Article phenotype Phenotypes Plant Genetics and Genomics Plasmids protein content proteinases Thiophenes Transcription factors Transcription Factors - metabolism Ubiquitin-Specific Peptidase 7 - genetics Ubiquitin-Specific Peptidase 7 - metabolism Ubiquitination |
| title | Ubiquitination-specific protease 7 enhances stemness of hepatocellular carcinoma by stabilizing basic transcription factor 3 |
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