Loss of PIG3 increases HIF-1α level by promoting protein synthesis via mTOR pathway in renal cell carcinoma cells
PIG3 is a target of the tumor suppressor p53 and is thought to be involved in p53-mediated cell apoptosis. Although PIG3 is similar to oxidoreductases involved in generating ROS, whether PIG3 would regulate HIF-1α was never characterized directly. Here we demonstrated that knockdown of PIG3 by trans...
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| creator | Chen, Guang Xu, Jin-Ye Chen, Jie Zhang, Jian-Xin Zhou, Jun Liang, Yong Ding, Xiao-Fei |
| description | PIG3 is a target of the tumor suppressor p53 and is thought to be involved in p53-mediated cell apoptosis. Although PIG3 is similar to oxidoreductases involved in generating ROS, whether PIG3 would regulate HIF-1α was never characterized directly. Here we demonstrated that knockdown of PIG3 by transfecting with specific siRNA could increase the expression of HIF-1α in several human cancer cell lines, including CAKI, FTC-133 and A549. It indicates that PIG3 may be involved in the regulation of HIF-1α. Furthermore, we revealed that PIG3-siliencing increased HIF-1α protein level through promoting its protein biosynthesis via mTOR pathway. In addition, the effect of PIG3 on the production of HIF-1α was further related to VEGF secretion and cell migration. PIG3-downregulation increased the secretion of VEGF and promoted the migration of renal cancer cells obviously. Taken together, these data suggest that PIG3 was involved in HIF-1α regulation, and reveal a novel signaling pathway of PIG3/HIF-1α in the regulation of cell migration in renal cell carcinoma. |
| doi_str_mv | 10.18632/oncotarget.8401 |
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Although PIG3 is similar to oxidoreductases involved in generating ROS, whether PIG3 would regulate HIF-1α was never characterized directly. Here we demonstrated that knockdown of PIG3 by transfecting with specific siRNA could increase the expression of HIF-1α in several human cancer cell lines, including CAKI, FTC-133 and A549. It indicates that PIG3 may be involved in the regulation of HIF-1α. Furthermore, we revealed that PIG3-siliencing increased HIF-1α protein level through promoting its protein biosynthesis via mTOR pathway. In addition, the effect of PIG3 on the production of HIF-1α was further related to VEGF secretion and cell migration. PIG3-downregulation increased the secretion of VEGF and promoted the migration of renal cancer cells obviously. Taken together, these data suggest that PIG3 was involved in HIF-1α regulation, and reveal a novel signaling pathway of PIG3/HIF-1α in the regulation of cell migration in renal cell carcinoma.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.8401</identifier><identifier>PMID: 27029070</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>A549 Cells ; Carcinoma, Renal Cell - genetics ; Carcinoma, Renal Cell - metabolism ; Carcinoma, Renal Cell - pathology ; Cell Line, Tumor ; Cell Movement - genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit - genetics ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Immunoblotting ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - metabolism ; Kidney Neoplasms - genetics ; Kidney Neoplasms - metabolism ; Kidney Neoplasms - pathology ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - metabolism ; Research Paper ; RNA Interference ; Signal Transduction ; TOR Serine-Threonine Kinases - metabolism ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>Oncotarget, 2016-05, Vol.7 (19), p.27176-27184</ispartof><rights>Copyright: © 2016 Chen et al. 2016</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c354t-9793c6cf629738fe6627c6f82c0f52cdc6cbeecefccaeac6b77f9823ade0a0853</citedby><cites>FETCH-LOGICAL-c354t-9793c6cf629738fe6627c6f82c0f52cdc6cbeecefccaeac6b77f9823ade0a0853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5053640/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5053640/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27029070$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Guang</creatorcontrib><creatorcontrib>Xu, Jin-Ye</creatorcontrib><creatorcontrib>Chen, Jie</creatorcontrib><creatorcontrib>Zhang, Jian-Xin</creatorcontrib><creatorcontrib>Zhou, Jun</creatorcontrib><creatorcontrib>Liang, Yong</creatorcontrib><creatorcontrib>Ding, Xiao-Fei</creatorcontrib><title>Loss of PIG3 increases HIF-1α level by promoting protein synthesis via mTOR pathway in renal cell carcinoma cells</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>PIG3 is a target of the tumor suppressor p53 and is thought to be involved in p53-mediated cell apoptosis. Although PIG3 is similar to oxidoreductases involved in generating ROS, whether PIG3 would regulate HIF-1α was never characterized directly. Here we demonstrated that knockdown of PIG3 by transfecting with specific siRNA could increase the expression of HIF-1α in several human cancer cell lines, including CAKI, FTC-133 and A549. It indicates that PIG3 may be involved in the regulation of HIF-1α. Furthermore, we revealed that PIG3-siliencing increased HIF-1α protein level through promoting its protein biosynthesis via mTOR pathway. In addition, the effect of PIG3 on the production of HIF-1α was further related to VEGF secretion and cell migration. PIG3-downregulation increased the secretion of VEGF and promoted the migration of renal cancer cells obviously. Taken together, these data suggest that PIG3 was involved in HIF-1α regulation, and reveal a novel signaling pathway of PIG3/HIF-1α in the regulation of cell migration in renal cell carcinoma.</description><subject>A549 Cells</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Carcinoma, Renal Cell - metabolism</subject><subject>Carcinoma, Renal Cell - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>Immunoblotting</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - metabolism</subject><subject>Kidney Neoplasms - pathology</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Research Paper</subject><subject>RNA Interference</subject><subject>Signal Transduction</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>1949-2553</issn><issn>1949-2553</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUctOWzEQtVBRQZR9V8hLNpf6cR_2phJCBSJFAlWwtibOOHF1r53aTlA-ix_hm7gBSmEW89DMnHkcQr5zdsZVK8WPGGwskBZYzlTN-B455LrWlWga-eWDf0COc_7DRmnqTgn9lRyIjgnNOnZI0jTmTKOjt5MrSX2wCSFjpteTy4o_PdIeN9jT2ZauUhxi8WGx8wr6QPM2lCVmn-nGAx3ubn7TFZTlA2xHHJowQE8t9qOCZH2IA7yE-RvZd9BnPH6zR-T-8tfdxXU1vbmaXJxPKyubulS609K21rVCd1I5bFvR2dYpYZlrhJ2PuRmiRWctINh21nVOKyFhjgyYauQR-fmKu1rPBpxbDCVBb1bJD5C2JoI3nzPBL80ibkzDGtnWbAQ4fQNI8e8aczGDz7sTIGBcZ8MVF0pzVYuxlL2W2jT-M6F7H8OZeWHL_GfL7NgaW04-rvfe8I8b-Qy2iZa5</recordid><startdate>20160510</startdate><enddate>20160510</enddate><creator>Chen, Guang</creator><creator>Xu, Jin-Ye</creator><creator>Chen, Jie</creator><creator>Zhang, Jian-Xin</creator><creator>Zhou, Jun</creator><creator>Liang, Yong</creator><creator>Ding, Xiao-Fei</creator><general>Impact Journals LLC</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160510</creationdate><title>Loss of PIG3 increases HIF-1α level by promoting protein synthesis via mTOR pathway in renal cell carcinoma cells</title><author>Chen, Guang ; Xu, Jin-Ye ; Chen, Jie ; Zhang, Jian-Xin ; Zhou, Jun ; Liang, Yong ; Ding, Xiao-Fei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c354t-9793c6cf629738fe6627c6f82c0f52cdc6cbeecefccaeac6b77f9823ade0a0853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>A549 Cells</topic><topic>Carcinoma, Renal Cell - genetics</topic><topic>Carcinoma, Renal Cell - metabolism</topic><topic>Carcinoma, Renal Cell - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</topic><topic>Immunoblotting</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - metabolism</topic><topic>Kidney Neoplasms - pathology</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Research Paper</topic><topic>RNA Interference</topic><topic>Signal Transduction</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><toplevel>online_resources</toplevel><creatorcontrib>Chen, Guang</creatorcontrib><creatorcontrib>Xu, Jin-Ye</creatorcontrib><creatorcontrib>Chen, Jie</creatorcontrib><creatorcontrib>Zhang, Jian-Xin</creatorcontrib><creatorcontrib>Zhou, Jun</creatorcontrib><creatorcontrib>Liang, Yong</creatorcontrib><creatorcontrib>Ding, Xiao-Fei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncotarget</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Guang</au><au>Xu, Jin-Ye</au><au>Chen, Jie</au><au>Zhang, Jian-Xin</au><au>Zhou, Jun</au><au>Liang, Yong</au><au>Ding, Xiao-Fei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of PIG3 increases HIF-1α level by promoting protein synthesis via mTOR pathway in renal cell carcinoma cells</atitle><jtitle>Oncotarget</jtitle><addtitle>Oncotarget</addtitle><date>2016-05-10</date><risdate>2016</risdate><volume>7</volume><issue>19</issue><spage>27176</spage><epage>27184</epage><pages>27176-27184</pages><issn>1949-2553</issn><eissn>1949-2553</eissn><abstract>PIG3 is a target of the tumor suppressor p53 and is thought to be involved in p53-mediated cell apoptosis. Although PIG3 is similar to oxidoreductases involved in generating ROS, whether PIG3 would regulate HIF-1α was never characterized directly. Here we demonstrated that knockdown of PIG3 by transfecting with specific siRNA could increase the expression of HIF-1α in several human cancer cell lines, including CAKI, FTC-133 and A549. It indicates that PIG3 may be involved in the regulation of HIF-1α. Furthermore, we revealed that PIG3-siliencing increased HIF-1α protein level through promoting its protein biosynthesis via mTOR pathway. In addition, the effect of PIG3 on the production of HIF-1α was further related to VEGF secretion and cell migration. PIG3-downregulation increased the secretion of VEGF and promoted the migration of renal cancer cells obviously. 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| subjects | A549 Cells Carcinoma, Renal Cell - genetics Carcinoma, Renal Cell - metabolism Carcinoma, Renal Cell - pathology Cell Line, Tumor Cell Movement - genetics Gene Expression Regulation, Neoplastic Humans Hypoxia-Inducible Factor 1, alpha Subunit - genetics Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Immunoblotting Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Kidney Neoplasms - genetics Kidney Neoplasms - metabolism Kidney Neoplasms - pathology Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Research Paper RNA Interference Signal Transduction TOR Serine-Threonine Kinases - metabolism Vascular Endothelial Growth Factor A - metabolism |
| title | Loss of PIG3 increases HIF-1α level by promoting protein synthesis via mTOR pathway in renal cell carcinoma cells |
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