Flap endonuclease 1 Facilitated Hepatocellular Carcinoma Progression by Enhancing USP7/MDM2-mediated P53 Inactivation
Overexpression of Flap endonuclease 1 (FEN1) has been previously implicated in hepatocellular carcinoma (HCC), while its expression features and mechanisms remain unclear. In the current study, differential expression genes (DEGs) were screened in HCC tissues and normal liver tissues in 4 Gene Expre...
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| Veröffentlicht in: | International journal of biological sciences 2022, Vol.18 (3), p.1022-1038 |
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| creator | Bian, Saiyan Ni, Wenkai Zhu, Mengqi Zhang, Xue Qiang, Yuwei Zhang, Jianping Ni, Zhiyu Shen, Yiping Qiu, Shi Song, Qianqian Xiao, Mingbing Zheng, Wenjie |
| description | Overexpression of Flap endonuclease 1 (FEN1) has been previously implicated in hepatocellular carcinoma (HCC), while its expression features and mechanisms remain unclear. In the current study, differential expression genes (DEGs) were screened in HCC tissues and normal liver tissues in 4 Gene Expression Omnibus (GEO) datasets. FEN1, one of the hub co-overexpressed genes, was further determined overexpressed in HCC tissues in TCGA, local HCC cohorts, and hepatocarcinogenesis model. In addition, high expression of FEN1 indicated poor prognosis of HCC patients. Loss-of-function and gain-of-function assays demonstrated that FEN1 enhanced the proliferation, cell cycle phage transition, migration/ invasion, therapy resistance, xenograft growth, and epithelial-mesenchymal transition (EMT) process of HCC cells. Mechanically, FEN1 could inactivate P53 signaling by preventing the ubiquitination and degradation of mouse double minute 2 (MDM2) via recruiting ubiquitin-specific protease 7 (USP7). Interfering USP7 with P22077 significantly reversed the malignant phenotypes activated by FEN1. In conclusion, this study suggests FEN1 as a robust prognostic biomarker and potential target for HCC. |
| doi_str_mv | 10.7150/ijbs.68179 |
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| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8771828</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2629872269</sourcerecordid><originalsourceid>FETCH-LOGICAL-c406t-b033395904c1f2f970b220b8daec327e23f475ef63c74abede8ff3778a9884923</originalsourceid><addsrcrecordid>eNpdkVtr3DAQhUVoya196Q8ogr6UgBNdbEt6CZRtNgkkZKHNsxjL440Wr7SR7ED-fb25keZpBuabw5k5hHzj7Fjxip34VZOPa82V2SH7vCxNIYTWn971e-Qg5xVjsq402yV7suJKVrLcJ-O8hw3F0MYwuh4hI-V0Ds73foABW3qBGxiiw74fe0h0Bsn5ENdAFykuE-bsY6DNIz0LdxCm0ZLe_lmok-vf16JYY-ufRBaVpJcB3OAfYJgWvpDPHfQZv77UQ3I7P_s7uyiubs4vZ7-uCleyeigaJqU0lWGl453ojGKNEKzRLaCTQqGQXakq7GrpVAkNtqi7TiqlwWhdGiEPyemz7mZsJjMOw5Cgt5vk15AebQRv_58Ef2eX8cFqpbgWehL4-SKQ4v2IebBrn7fPgIBxzFbUwmglRG0m9McHdBXHFKbzthTjgrFKTtTRM-VSzDlh92aGM7tN027TtE9pTvD39_bf0Nf45D9zlpug</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2620120053</pqid></control><display><type>article</type><title>Flap endonuclease 1 Facilitated Hepatocellular Carcinoma Progression by Enhancing USP7/MDM2-mediated P53 Inactivation</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>PubMed Central Open Access</source><creator>Bian, Saiyan ; Ni, Wenkai ; Zhu, Mengqi ; Zhang, Xue ; Qiang, Yuwei ; Zhang, Jianping ; Ni, Zhiyu ; Shen, Yiping ; Qiu, Shi ; Song, Qianqian ; Xiao, Mingbing ; Zheng, Wenjie</creator><creatorcontrib>Bian, Saiyan ; Ni, Wenkai ; Zhu, Mengqi ; Zhang, Xue ; Qiang, Yuwei ; Zhang, Jianping ; Ni, Zhiyu ; Shen, Yiping ; Qiu, Shi ; Song, Qianqian ; Xiao, Mingbing ; Zheng, Wenjie</creatorcontrib><description>Overexpression of Flap endonuclease 1 (FEN1) has been previously implicated in hepatocellular carcinoma (HCC), while its expression features and mechanisms remain unclear. In the current study, differential expression genes (DEGs) were screened in HCC tissues and normal liver tissues in 4 Gene Expression Omnibus (GEO) datasets. FEN1, one of the hub co-overexpressed genes, was further determined overexpressed in HCC tissues in TCGA, local HCC cohorts, and hepatocarcinogenesis model. In addition, high expression of FEN1 indicated poor prognosis of HCC patients. Loss-of-function and gain-of-function assays demonstrated that FEN1 enhanced the proliferation, cell cycle phage transition, migration/ invasion, therapy resistance, xenograft growth, and epithelial-mesenchymal transition (EMT) process of HCC cells. Mechanically, FEN1 could inactivate P53 signaling by preventing the ubiquitination and degradation of mouse double minute 2 (MDM2) via recruiting ubiquitin-specific protease 7 (USP7). Interfering USP7 with P22077 significantly reversed the malignant phenotypes activated by FEN1. In conclusion, this study suggests FEN1 as a robust prognostic biomarker and potential target for HCC.</description><identifier>ISSN: 1449-2288</identifier><identifier>EISSN: 1449-2288</identifier><identifier>DOI: 10.7150/ijbs.68179</identifier><identifier>PMID: 35173534</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>Animals ; Apoptosis ; Biomarkers ; Breast cancer ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - pathology ; Cell cycle ; Cell Line, Tumor ; Cell migration ; Cell Proliferation - genetics ; Deactivation ; Endonuclease ; Epithelial-Mesenchymal Transition - genetics ; FEN1 protein ; Flap Endonucleases - genetics ; Flap Endonucleases - metabolism ; Flow cytometry ; Gene expression ; Gene Expression Regulation, Neoplastic - genetics ; Genes ; Hepatitis B ; Hepatocellular carcinoma ; Humans ; Inactivation ; Liver cancer ; Liver Neoplasms - genetics ; Liver Neoplasms - pathology ; MDM2 protein ; Medical prognosis ; Mesenchyme ; Mice ; p53 Protein ; Phages ; Phenotypes ; Plasmids ; Proteins ; Proto-Oncogene Proteins c-mdm2 - metabolism ; Research Paper ; Spheroids ; Tissues ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism ; Ubiquitin ; Ubiquitin-Specific Peptidase 7 - genetics ; Ubiquitin-Specific Peptidase 7 - metabolism ; Ubiquitin-specific proteinase ; Ubiquitination ; Wound healing ; Xenografts ; Xenotransplantation</subject><ispartof>International journal of biological sciences, 2022, Vol.18 (3), p.1022-1038</ispartof><rights>The author(s).</rights><rights>2022. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The author(s) 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-b033395904c1f2f970b220b8daec327e23f475ef63c74abede8ff3778a9884923</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8771828/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8771828/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35173534$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bian, Saiyan</creatorcontrib><creatorcontrib>Ni, Wenkai</creatorcontrib><creatorcontrib>Zhu, Mengqi</creatorcontrib><creatorcontrib>Zhang, Xue</creatorcontrib><creatorcontrib>Qiang, Yuwei</creatorcontrib><creatorcontrib>Zhang, Jianping</creatorcontrib><creatorcontrib>Ni, Zhiyu</creatorcontrib><creatorcontrib>Shen, Yiping</creatorcontrib><creatorcontrib>Qiu, Shi</creatorcontrib><creatorcontrib>Song, Qianqian</creatorcontrib><creatorcontrib>Xiao, Mingbing</creatorcontrib><creatorcontrib>Zheng, Wenjie</creatorcontrib><title>Flap endonuclease 1 Facilitated Hepatocellular Carcinoma Progression by Enhancing USP7/MDM2-mediated P53 Inactivation</title><title>International journal of biological sciences</title><addtitle>Int J Biol Sci</addtitle><description>Overexpression of Flap endonuclease 1 (FEN1) has been previously implicated in hepatocellular carcinoma (HCC), while its expression features and mechanisms remain unclear. In the current study, differential expression genes (DEGs) were screened in HCC tissues and normal liver tissues in 4 Gene Expression Omnibus (GEO) datasets. FEN1, one of the hub co-overexpressed genes, was further determined overexpressed in HCC tissues in TCGA, local HCC cohorts, and hepatocarcinogenesis model. In addition, high expression of FEN1 indicated poor prognosis of HCC patients. Loss-of-function and gain-of-function assays demonstrated that FEN1 enhanced the proliferation, cell cycle phage transition, migration/ invasion, therapy resistance, xenograft growth, and epithelial-mesenchymal transition (EMT) process of HCC cells. Mechanically, FEN1 could inactivate P53 signaling by preventing the ubiquitination and degradation of mouse double minute 2 (MDM2) via recruiting ubiquitin-specific protease 7 (USP7). Interfering USP7 with P22077 significantly reversed the malignant phenotypes activated by FEN1. In conclusion, this study suggests FEN1 as a robust prognostic biomarker and potential target for HCC.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomarkers</subject><subject>Breast cancer</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Proliferation - genetics</subject><subject>Deactivation</subject><subject>Endonuclease</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>FEN1 protein</subject><subject>Flap Endonucleases - genetics</subject><subject>Flap Endonucleases - metabolism</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Genes</subject><subject>Hepatitis B</subject><subject>Hepatocellular carcinoma</subject><subject>Humans</subject><subject>Inactivation</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - pathology</subject><subject>MDM2 protein</subject><subject>Medical prognosis</subject><subject>Mesenchyme</subject><subject>Mice</subject><subject>p53 Protein</subject><subject>Phages</subject><subject>Phenotypes</subject><subject>Plasmids</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-mdm2 - metabolism</subject><subject>Research Paper</subject><subject>Spheroids</subject><subject>Tissues</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Ubiquitin</subject><subject>Ubiquitin-Specific Peptidase 7 - genetics</subject><subject>Ubiquitin-Specific Peptidase 7 - metabolism</subject><subject>Ubiquitin-specific proteinase</subject><subject>Ubiquitination</subject><subject>Wound healing</subject><subject>Xenografts</subject><subject>Xenotransplantation</subject><issn>1449-2288</issn><issn>1449-2288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkVtr3DAQhUVoya196Q8ogr6UgBNdbEt6CZRtNgkkZKHNsxjL440Wr7SR7ED-fb25keZpBuabw5k5hHzj7Fjxip34VZOPa82V2SH7vCxNIYTWn971e-Qg5xVjsq402yV7suJKVrLcJ-O8hw3F0MYwuh4hI-V0Ds73foABW3qBGxiiw74fe0h0Bsn5ENdAFykuE-bsY6DNIz0LdxCm0ZLe_lmok-vf16JYY-ufRBaVpJcB3OAfYJgWvpDPHfQZv77UQ3I7P_s7uyiubs4vZ7-uCleyeigaJqU0lWGl453ojGKNEKzRLaCTQqGQXakq7GrpVAkNtqi7TiqlwWhdGiEPyemz7mZsJjMOw5Cgt5vk15AebQRv_58Ef2eX8cFqpbgWehL4-SKQ4v2IebBrn7fPgIBxzFbUwmglRG0m9McHdBXHFKbzthTjgrFKTtTRM-VSzDlh92aGM7tN027TtE9pTvD39_bf0Nf45D9zlpug</recordid><startdate>2022</startdate><enddate>2022</enddate><creator>Bian, Saiyan</creator><creator>Ni, Wenkai</creator><creator>Zhu, Mengqi</creator><creator>Zhang, Xue</creator><creator>Qiang, Yuwei</creator><creator>Zhang, Jianping</creator><creator>Ni, Zhiyu</creator><creator>Shen, Yiping</creator><creator>Qiu, Shi</creator><creator>Song, Qianqian</creator><creator>Xiao, Mingbing</creator><creator>Zheng, Wenjie</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</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>7U9</scope><scope>8FD</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>2022</creationdate><title>Flap endonuclease 1 Facilitated Hepatocellular Carcinoma Progression by Enhancing USP7/MDM2-mediated P53 Inactivation</title><author>Bian, Saiyan ; Ni, Wenkai ; Zhu, Mengqi ; Zhang, Xue ; Qiang, Yuwei ; Zhang, Jianping ; Ni, Zhiyu ; Shen, Yiping ; Qiu, Shi ; Song, Qianqian ; Xiao, Mingbing ; Zheng, Wenjie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c406t-b033395904c1f2f970b220b8daec327e23f475ef63c74abede8ff3778a9884923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Biomarkers</topic><topic>Breast cancer</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Proliferation - genetics</topic><topic>Deactivation</topic><topic>Endonuclease</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>FEN1 protein</topic><topic>Flap Endonucleases - genetics</topic><topic>Flap Endonucleases - metabolism</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Genes</topic><topic>Hepatitis B</topic><topic>Hepatocellular carcinoma</topic><topic>Humans</topic><topic>Inactivation</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - pathology</topic><topic>MDM2 protein</topic><topic>Medical prognosis</topic><topic>Mesenchyme</topic><topic>Mice</topic><topic>p53 Protein</topic><topic>Phages</topic><topic>Phenotypes</topic><topic>Plasmids</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-mdm2 - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of biological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bian, Saiyan</au><au>Ni, Wenkai</au><au>Zhu, Mengqi</au><au>Zhang, Xue</au><au>Qiang, Yuwei</au><au>Zhang, Jianping</au><au>Ni, Zhiyu</au><au>Shen, Yiping</au><au>Qiu, Shi</au><au>Song, Qianqian</au><au>Xiao, Mingbing</au><au>Zheng, Wenjie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Flap endonuclease 1 Facilitated Hepatocellular Carcinoma Progression by Enhancing USP7/MDM2-mediated P53 Inactivation</atitle><jtitle>International journal of biological sciences</jtitle><addtitle>Int J Biol Sci</addtitle><date>2022</date><risdate>2022</risdate><volume>18</volume><issue>3</issue><spage>1022</spage><epage>1038</epage><pages>1022-1038</pages><issn>1449-2288</issn><eissn>1449-2288</eissn><abstract>Overexpression of Flap endonuclease 1 (FEN1) has been previously implicated in hepatocellular carcinoma (HCC), while its expression features and mechanisms remain unclear. In the current study, differential expression genes (DEGs) were screened in HCC tissues and normal liver tissues in 4 Gene Expression Omnibus (GEO) datasets. FEN1, one of the hub co-overexpressed genes, was further determined overexpressed in HCC tissues in TCGA, local HCC cohorts, and hepatocarcinogenesis model. In addition, high expression of FEN1 indicated poor prognosis of HCC patients. Loss-of-function and gain-of-function assays demonstrated that FEN1 enhanced the proliferation, cell cycle phage transition, migration/ invasion, therapy resistance, xenograft growth, and epithelial-mesenchymal transition (EMT) process of HCC cells. Mechanically, FEN1 could inactivate P53 signaling by preventing the ubiquitination and degradation of mouse double minute 2 (MDM2) via recruiting ubiquitin-specific protease 7 (USP7). Interfering USP7 with P22077 significantly reversed the malignant phenotypes activated by FEN1. In conclusion, this study suggests FEN1 as a robust prognostic biomarker and potential target for HCC.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>35173534</pmid><doi>10.7150/ijbs.68179</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis Biomarkers Breast cancer Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - pathology Cell cycle Cell Line, Tumor Cell migration Cell Proliferation - genetics Deactivation Endonuclease Epithelial-Mesenchymal Transition - genetics FEN1 protein Flap Endonucleases - genetics Flap Endonucleases - metabolism Flow cytometry Gene expression Gene Expression Regulation, Neoplastic - genetics Genes Hepatitis B Hepatocellular carcinoma Humans Inactivation Liver cancer Liver Neoplasms - genetics Liver Neoplasms - pathology MDM2 protein Medical prognosis Mesenchyme Mice p53 Protein Phages Phenotypes Plasmids Proteins Proto-Oncogene Proteins c-mdm2 - metabolism Research Paper Spheroids Tissues Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Ubiquitin Ubiquitin-Specific Peptidase 7 - genetics Ubiquitin-Specific Peptidase 7 - metabolism Ubiquitin-specific proteinase Ubiquitination Wound healing Xenografts Xenotransplantation |
| title | Flap endonuclease 1 Facilitated Hepatocellular Carcinoma Progression by Enhancing USP7/MDM2-mediated P53 Inactivation |
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