USP19 Negatively Regulates p53 and Promotes Cervical Cancer Progression
p53 is a tumor suppressor gene activated in response to cellular stressors that inhibits cell cycle progression and induces pro-apoptotic signaling. The protein level of p53 is well balanced by the action of several E3 ligases and deubiquitinating enzymes (DUBs). Several DUBs have been reported to n...
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| Veröffentlicht in: | Molecular biotechnology 2024-08, Vol.66 (8), p.2032-2045 |
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| creator | Tyagi, Apoorvi Karapurkar, Janardhan Keshav Colaco, Jencia Carminha Sarodaya, Neha Antao, Ainsley Mike Kaushal, Kamini Haq, Saba Chandrasekaran, Arun Pandian Das, Soumyadip Singh, Vijai Hong, Seok-Ho Suresh, Bharathi Kim, Kye-Seong Ramakrishna, Suresh |
| description | p53 is a tumor suppressor gene activated in response to cellular stressors that inhibits cell cycle progression and induces pro-apoptotic signaling. The protein level of p53 is well balanced by the action of several E3 ligases and deubiquitinating enzymes (DUBs). Several DUBs have been reported to negatively regulate and promote p53 degradation in tumors. In this study, we identified USP19 as a negative regulator of p53 protein level. We demonstrate a direct interaction between USP19 and p53 by pull down assay. The overexpression of USP19 promoted ubiquitination of p53 and reduced its protein half-life. We also demonstrate that CRISPR/Cas9-mediated knockout of
USP19
in cervical cancer cells elevates p53 protein levels, resulting in reduced colony formation, cell migration, and cell invasion. Overall, our results indicate that USP19 negatively regulates p53 protein levels in cervical cancer progression. |
| doi_str_mv | 10.1007/s12033-023-00814-y |
| format | Article |
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USP19
in cervical cancer cells elevates p53 protein levels, resulting in reduced colony formation, cell migration, and cell invasion. Overall, our results indicate that USP19 negatively regulates p53 protein levels in cervical cancer progression.</description><identifier>ISSN: 1073-6085</identifier><identifier>ISSN: 1559-0305</identifier><identifier>EISSN: 1559-0305</identifier><identifier>DOI: 10.1007/s12033-023-00814-y</identifier><identifier>PMID: 37572221</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Antibodies ; Apoptosis ; Biochemistry ; Biological Techniques ; Biotechnology ; Cancer ; Cell Biology ; Cell cycle ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Cell Proliferation ; Cellular stress response ; Cervical cancer ; Chemistry ; Chemistry and Materials Science ; Cloning ; CRISPR ; CRISPR-Cas Systems ; Density ; Disease Progression ; Endopeptidases - genetics ; Endopeptidases - metabolism ; Enzymes ; Female ; Gene Expression Regulation, Neoplastic ; Genes ; Glycerol ; HeLa Cells ; Human Genetics ; Humans ; Kinases ; Life sciences ; Metastasis ; Mutation ; Original Paper ; p53 Protein ; Plasmids ; Protein Science ; Proteins ; Tumor suppressor genes ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism ; Tumors ; Ubiquitination ; Uterine Cervical Neoplasms - genetics ; Uterine Cervical Neoplasms - metabolism ; Uterine Cervical Neoplasms - pathology ; Yeast</subject><ispartof>Molecular biotechnology, 2024-08, Vol.66 (8), p.2032-2045</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. 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>2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c326t-bd06f949dd9587a239be84079d1e537d94469b9f980ec356275051dbfc976c323</cites><orcidid>0000-0002-4038-1085</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12033-023-00814-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12033-023-00814-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37572221$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tyagi, Apoorvi</creatorcontrib><creatorcontrib>Karapurkar, Janardhan Keshav</creatorcontrib><creatorcontrib>Colaco, Jencia Carminha</creatorcontrib><creatorcontrib>Sarodaya, Neha</creatorcontrib><creatorcontrib>Antao, Ainsley Mike</creatorcontrib><creatorcontrib>Kaushal, Kamini</creatorcontrib><creatorcontrib>Haq, Saba</creatorcontrib><creatorcontrib>Chandrasekaran, Arun Pandian</creatorcontrib><creatorcontrib>Das, Soumyadip</creatorcontrib><creatorcontrib>Singh, Vijai</creatorcontrib><creatorcontrib>Hong, Seok-Ho</creatorcontrib><creatorcontrib>Suresh, Bharathi</creatorcontrib><creatorcontrib>Kim, Kye-Seong</creatorcontrib><creatorcontrib>Ramakrishna, Suresh</creatorcontrib><title>USP19 Negatively Regulates p53 and Promotes Cervical Cancer Progression</title><title>Molecular biotechnology</title><addtitle>Mol Biotechnol</addtitle><addtitle>Mol Biotechnol</addtitle><description>p53 is a tumor suppressor gene activated in response to cellular stressors that inhibits cell cycle progression and induces pro-apoptotic signaling. The protein level of p53 is well balanced by the action of several E3 ligases and deubiquitinating enzymes (DUBs). Several DUBs have been reported to negatively regulate and promote p53 degradation in tumors. In this study, we identified USP19 as a negative regulator of p53 protein level. We demonstrate a direct interaction between USP19 and p53 by pull down assay. The overexpression of USP19 promoted ubiquitination of p53 and reduced its protein half-life. We also demonstrate that CRISPR/Cas9-mediated knockout of
USP19
in cervical cancer cells elevates p53 protein levels, resulting in reduced colony formation, cell migration, and cell invasion. Overall, our results indicate that USP19 negatively regulates p53 protein levels in cervical cancer progression.</description><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biological Techniques</subject><subject>Biotechnology</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cellular stress response</subject><subject>Cervical cancer</subject><subject>Chemistry</subject><subject>Chemistry and Materials Science</subject><subject>Cloning</subject><subject>CRISPR</subject><subject>CRISPR-Cas Systems</subject><subject>Density</subject><subject>Disease Progression</subject><subject>Endopeptidases - genetics</subject><subject>Endopeptidases - metabolism</subject><subject>Enzymes</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Glycerol</subject><subject>HeLa Cells</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Kinases</subject><subject>Life sciences</subject><subject>Metastasis</subject><subject>Mutation</subject><subject>Original Paper</subject><subject>p53 Protein</subject><subject>Plasmids</subject><subject>Protein Science</subject><subject>Proteins</subject><subject>Tumor suppressor genes</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumors</subject><subject>Ubiquitination</subject><subject>Uterine Cervical Neoplasms - genetics</subject><subject>Uterine Cervical Neoplasms - metabolism</subject><subject>Uterine Cervical Neoplasms - pathology</subject><subject>Yeast</subject><issn>1073-6085</issn><issn>1559-0305</issn><issn>1559-0305</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM9LwzAUx4MoTqf_gAcpePFSfUmapjnK0CkMHerOIW1fS0d_zGQd9L83c1PBg4fwQt7nffP4EHJB4YYCyFtHGXAeAvMHEhqFwwE5oUKoEDiIQ38HycMYEjEip84tARgVET8mIy6FZIzREzJdvM2pCp6xNOtqg_UQvGLZ12aNLlgJHpg2D-a2a7rtwwTtpspMHUxMm6HdNkqLzlVde0aOClM7PN_XMVk83L9PHsPZy_RpcjcLM87idZjmEBcqUnmuRCIN4yrFJAKpcoqCy1xFUaxSVagEMOMiZlKAoHlaZErGPoKPyfUud2W7jx7dWjeVy7CuTYtd7zRLBHBKlRIevfqDLrvetn47zSGJlJRUgqfYjsps55zFQq9s1Rg7aAp6q1nvNGuvWX9p1oMfutxH92mD-c_It1cP8B3gfKst0f7-_U_sJ3hPhcY</recordid><startdate>20240801</startdate><enddate>20240801</enddate><creator>Tyagi, Apoorvi</creator><creator>Karapurkar, Janardhan Keshav</creator><creator>Colaco, Jencia Carminha</creator><creator>Sarodaya, Neha</creator><creator>Antao, Ainsley Mike</creator><creator>Kaushal, Kamini</creator><creator>Haq, Saba</creator><creator>Chandrasekaran, Arun Pandian</creator><creator>Das, Soumyadip</creator><creator>Singh, Vijai</creator><creator>Hong, Seok-Ho</creator><creator>Suresh, Bharathi</creator><creator>Kim, Kye-Seong</creator><creator>Ramakrishna, Suresh</creator><general>Springer US</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>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4038-1085</orcidid></search><sort><creationdate>20240801</creationdate><title>USP19 Negatively Regulates p53 and Promotes Cervical Cancer Progression</title><author>Tyagi, Apoorvi ; Karapurkar, Janardhan Keshav ; Colaco, Jencia Carminha ; Sarodaya, Neha ; Antao, Ainsley Mike ; Kaushal, Kamini ; Haq, Saba ; Chandrasekaran, Arun Pandian ; Das, Soumyadip ; Singh, Vijai ; Hong, Seok-Ho ; Suresh, Bharathi ; Kim, Kye-Seong ; Ramakrishna, Suresh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c326t-bd06f949dd9587a239be84079d1e537d94469b9f980ec356275051dbfc976c323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biological Techniques</topic><topic>Biotechnology</topic><topic>Cancer</topic><topic>Cell Biology</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cellular stress response</topic><topic>Cervical cancer</topic><topic>Chemistry</topic><topic>Chemistry and Materials Science</topic><topic>Cloning</topic><topic>CRISPR</topic><topic>CRISPR-Cas Systems</topic><topic>Density</topic><topic>Disease Progression</topic><topic>Endopeptidases - genetics</topic><topic>Endopeptidases - metabolism</topic><topic>Enzymes</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Glycerol</topic><topic>HeLa Cells</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Kinases</topic><topic>Life sciences</topic><topic>Metastasis</topic><topic>Mutation</topic><topic>Original Paper</topic><topic>p53 Protein</topic><topic>Plasmids</topic><topic>Protein Science</topic><topic>Proteins</topic><topic>Tumor suppressor genes</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumors</topic><topic>Ubiquitination</topic><topic>Uterine Cervical Neoplasms - genetics</topic><topic>Uterine Cervical Neoplasms - metabolism</topic><topic>Uterine Cervical Neoplasms - pathology</topic><topic>Yeast</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tyagi, Apoorvi</creatorcontrib><creatorcontrib>Karapurkar, Janardhan Keshav</creatorcontrib><creatorcontrib>Colaco, Jencia Carminha</creatorcontrib><creatorcontrib>Sarodaya, Neha</creatorcontrib><creatorcontrib>Antao, Ainsley Mike</creatorcontrib><creatorcontrib>Kaushal, Kamini</creatorcontrib><creatorcontrib>Haq, Saba</creatorcontrib><creatorcontrib>Chandrasekaran, Arun Pandian</creatorcontrib><creatorcontrib>Das, Soumyadip</creatorcontrib><creatorcontrib>Singh, Vijai</creatorcontrib><creatorcontrib>Hong, Seok-Ho</creatorcontrib><creatorcontrib>Suresh, Bharathi</creatorcontrib><creatorcontrib>Kim, Kye-Seong</creatorcontrib><creatorcontrib>Ramakrishna, Suresh</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular biotechnology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tyagi, Apoorvi</au><au>Karapurkar, Janardhan Keshav</au><au>Colaco, Jencia Carminha</au><au>Sarodaya, Neha</au><au>Antao, Ainsley Mike</au><au>Kaushal, Kamini</au><au>Haq, Saba</au><au>Chandrasekaran, Arun Pandian</au><au>Das, Soumyadip</au><au>Singh, Vijai</au><au>Hong, Seok-Ho</au><au>Suresh, Bharathi</au><au>Kim, Kye-Seong</au><au>Ramakrishna, Suresh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>USP19 Negatively Regulates p53 and Promotes Cervical Cancer Progression</atitle><jtitle>Molecular biotechnology</jtitle><stitle>Mol Biotechnol</stitle><addtitle>Mol Biotechnol</addtitle><date>2024-08-01</date><risdate>2024</risdate><volume>66</volume><issue>8</issue><spage>2032</spage><epage>2045</epage><pages>2032-2045</pages><issn>1073-6085</issn><issn>1559-0305</issn><eissn>1559-0305</eissn><abstract>p53 is a tumor suppressor gene activated in response to cellular stressors that inhibits cell cycle progression and induces pro-apoptotic signaling. The protein level of p53 is well balanced by the action of several E3 ligases and deubiquitinating enzymes (DUBs). Several DUBs have been reported to negatively regulate and promote p53 degradation in tumors. In this study, we identified USP19 as a negative regulator of p53 protein level. We demonstrate a direct interaction between USP19 and p53 by pull down assay. The overexpression of USP19 promoted ubiquitination of p53 and reduced its protein half-life. We also demonstrate that CRISPR/Cas9-mediated knockout of
USP19
in cervical cancer cells elevates p53 protein levels, resulting in reduced colony formation, cell migration, and cell invasion. Overall, our results indicate that USP19 negatively regulates p53 protein levels in cervical cancer progression.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>37572221</pmid><doi>10.1007/s12033-023-00814-y</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-4038-1085</orcidid></addata></record> |
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| subjects | Antibodies Apoptosis Biochemistry Biological Techniques Biotechnology Cancer Cell Biology Cell cycle Cell Line, Tumor Cell migration Cell Movement Cell Proliferation Cellular stress response Cervical cancer Chemistry Chemistry and Materials Science Cloning CRISPR CRISPR-Cas Systems Density Disease Progression Endopeptidases - genetics Endopeptidases - metabolism Enzymes Female Gene Expression Regulation, Neoplastic Genes Glycerol HeLa Cells Human Genetics Humans Kinases Life sciences Metastasis Mutation Original Paper p53 Protein Plasmids Protein Science Proteins Tumor suppressor genes Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Tumors Ubiquitination Uterine Cervical Neoplasms - genetics Uterine Cervical Neoplasms - metabolism Uterine Cervical Neoplasms - pathology Yeast |
| title | USP19 Negatively Regulates p53 and Promotes Cervical Cancer Progression |
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