STAT1 inhibits human hepatocellular carcinoma cell growth through induction of p53 and Fbxw7
Aberrant STAT1 signaling is observed in human hepatocellular carcinoma (HCC) and has been associated with the modulation of cell proliferation and survival. However, the role of STAT1 signaling in HCC and its underlying mechanism remain elusive. We transiently transfected pcDNA3.1-STAT1 and STAT1 si...
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| Veröffentlicht in: | Cancer Cell International 2015-11, Vol.15 (1), p.111-111, Article 111 |
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| creator | Chen, Jiayu Wang, Haihe Wang, Jing Huang, Shishun Zhang, Wei |
| description | Aberrant STAT1 signaling is observed in human hepatocellular carcinoma (HCC) and has been associated with the modulation of cell proliferation and survival. However, the role of STAT1 signaling in HCC and its underlying mechanism remain elusive.
We transiently transfected pcDNA3.1-STAT1 and STAT1 siRNA into SMMC7721 and HepG2 cells. Western blot and qRT-PCR examined the expression of protein and RNA of target genes. Cell viability was assessed using MTT assay, and cell cycle and apoptosis were analyzed by flow cytometry.
We found that STAT1 overexpression increased protein expression of p53 and Fbxw7, and downregulated the expression of cyclin A, cyclin D1, cyclin E, CDK2, Hes-1 and NF-κB p65. These changes led to growth inhibition and induced G0/G1 cell cycle arrest and apoptosis in SMMC7721 and HepG2 cells. Conversely, ablation of STAT1 had the opposite effect on p53, Fbxw7, Hes-1, NF-κB p65, cyclin A, cyclin D1, cyclin E and CDK2, and improved the viability of SMMC7721 and HepG2 cells.
Our data indicate that STAT1 exerts tumor-suppressive effects in hepatocarcinogenesis through induction of G0/G1 cell cycle arrest and apoptosis, and may provide a basis for the design of new therapies for the intervention of HCC in the clinic. |
| doi_str_mv | 10.1186/s12935-015-0253-6 |
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We transiently transfected pcDNA3.1-STAT1 and STAT1 siRNA into SMMC7721 and HepG2 cells. Western blot and qRT-PCR examined the expression of protein and RNA of target genes. Cell viability was assessed using MTT assay, and cell cycle and apoptosis were analyzed by flow cytometry.
We found that STAT1 overexpression increased protein expression of p53 and Fbxw7, and downregulated the expression of cyclin A, cyclin D1, cyclin E, CDK2, Hes-1 and NF-κB p65. These changes led to growth inhibition and induced G0/G1 cell cycle arrest and apoptosis in SMMC7721 and HepG2 cells. Conversely, ablation of STAT1 had the opposite effect on p53, Fbxw7, Hes-1, NF-κB p65, cyclin A, cyclin D1, cyclin E and CDK2, and improved the viability of SMMC7721 and HepG2 cells.
Our data indicate that STAT1 exerts tumor-suppressive effects in hepatocarcinogenesis through induction of G0/G1 cell cycle arrest and apoptosis, and may provide a basis for the design of new therapies for the intervention of HCC in the clinic.</description><identifier>ISSN: 1475-2867</identifier><identifier>EISSN: 1475-2867</identifier><identifier>DOI: 10.1186/s12935-015-0253-6</identifier><identifier>PMID: 26617467</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Apoptosis ; Growth ; Hepatoma ; Primary Research ; RNA ; Tumor proteins</subject><ispartof>Cancer Cell International, 2015-11, Vol.15 (1), p.111-111, Article 111</ispartof><rights>COPYRIGHT 2015 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2015</rights><rights>Chen et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c598t-79c364d9a1e61ecb3b511b88eea6e5db24bba15daa9a1cda02f745d16f6c520a3</citedby><cites>FETCH-LOGICAL-c598t-79c364d9a1e61ecb3b511b88eea6e5db24bba15daa9a1cda02f745d16f6c520a3</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/PMC4661940/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4661940/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26617467$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Jiayu</creatorcontrib><creatorcontrib>Wang, Haihe</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Huang, Shishun</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><title>STAT1 inhibits human hepatocellular carcinoma cell growth through induction of p53 and Fbxw7</title><title>Cancer Cell International</title><addtitle>Cancer Cell Int</addtitle><description>Aberrant STAT1 signaling is observed in human hepatocellular carcinoma (HCC) and has been associated with the modulation of cell proliferation and survival. However, the role of STAT1 signaling in HCC and its underlying mechanism remain elusive.
We transiently transfected pcDNA3.1-STAT1 and STAT1 siRNA into SMMC7721 and HepG2 cells. Western blot and qRT-PCR examined the expression of protein and RNA of target genes. Cell viability was assessed using MTT assay, and cell cycle and apoptosis were analyzed by flow cytometry.
We found that STAT1 overexpression increased protein expression of p53 and Fbxw7, and downregulated the expression of cyclin A, cyclin D1, cyclin E, CDK2, Hes-1 and NF-κB p65. These changes led to growth inhibition and induced G0/G1 cell cycle arrest and apoptosis in SMMC7721 and HepG2 cells. Conversely, ablation of STAT1 had the opposite effect on p53, Fbxw7, Hes-1, NF-κB p65, cyclin A, cyclin D1, cyclin E and CDK2, and improved the viability of SMMC7721 and HepG2 cells.
Our data indicate that STAT1 exerts tumor-suppressive effects in hepatocarcinogenesis through induction of G0/G1 cell cycle arrest and apoptosis, and may provide a basis for the design of new therapies for the intervention of HCC in the clinic.</description><subject>Analysis</subject><subject>Apoptosis</subject><subject>Growth</subject><subject>Hepatoma</subject><subject>Primary Research</subject><subject>RNA</subject><subject>Tumor proteins</subject><issn>1475-2867</issn><issn>1475-2867</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNpdUcFqHSEUldLQpGk_oJsidNPNpOqMOm4Kj9CkhUAXedkF5Oo4bwwz-qozSfv38TFpSIuIl-s5R889CH2g5IzSVnzJlKmaV4SWzXhdiVfohDaSV6wV8vWL-hi9zfmOECpbQd6gYyYElY2QJ-j2ervZUuzD4I2fMx6WCQIe3B7maN04LiMkbCFZH-IE-NDCuxQf5gHPQ4rLbijcbrGzjwHHHu95jSF0-ML8fpDv0FEPY3bvn85TdHPxbXv-vbr6efnjfHNVWa7auZLK1qLpFFAnqLOmNpxS07bOgXC8M6wxBijvAArEdkBYLxveUdELyxmB-hR9XXX3i5lcZ12YE4x6n_wE6Y-O4PW_N8EPehfvdVPmoBpSBD4_CaT4a3F51pPPB68QXFyyLsNSXCkleYF--g96F5cUir2CkkooUkZbUGcragej0z70sbxry-rc5G0Mrvelv2mEooytsnQl2BRzTq5__j0l-hC2XsPWJWx9CFuLwvn40vYz42-69SPh26YN</recordid><startdate>20151126</startdate><enddate>20151126</enddate><creator>Chen, Jiayu</creator><creator>Wang, Haihe</creator><creator>Wang, Jing</creator><creator>Huang, Shishun</creator><creator>Zhang, Wei</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IAO</scope><scope>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20151126</creationdate><title>STAT1 inhibits human hepatocellular carcinoma cell growth through induction of p53 and Fbxw7</title><author>Chen, Jiayu ; Wang, Haihe ; Wang, Jing ; Huang, Shishun ; Zhang, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c598t-79c364d9a1e61ecb3b511b88eea6e5db24bba15daa9a1cda02f745d16f6c520a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Analysis</topic><topic>Apoptosis</topic><topic>Growth</topic><topic>Hepatoma</topic><topic>Primary Research</topic><topic>RNA</topic><topic>Tumor proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Jiayu</creatorcontrib><creatorcontrib>Wang, Haihe</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Huang, Shishun</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer Cell International</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Jiayu</au><au>Wang, Haihe</au><au>Wang, Jing</au><au>Huang, Shishun</au><au>Zhang, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>STAT1 inhibits human hepatocellular carcinoma cell growth through induction of p53 and Fbxw7</atitle><jtitle>Cancer Cell International</jtitle><addtitle>Cancer Cell Int</addtitle><date>2015-11-26</date><risdate>2015</risdate><volume>15</volume><issue>1</issue><spage>111</spage><epage>111</epage><pages>111-111</pages><artnum>111</artnum><issn>1475-2867</issn><eissn>1475-2867</eissn><abstract>Aberrant STAT1 signaling is observed in human hepatocellular carcinoma (HCC) and has been associated with the modulation of cell proliferation and survival. However, the role of STAT1 signaling in HCC and its underlying mechanism remain elusive.
We transiently transfected pcDNA3.1-STAT1 and STAT1 siRNA into SMMC7721 and HepG2 cells. Western blot and qRT-PCR examined the expression of protein and RNA of target genes. Cell viability was assessed using MTT assay, and cell cycle and apoptosis were analyzed by flow cytometry.
We found that STAT1 overexpression increased protein expression of p53 and Fbxw7, and downregulated the expression of cyclin A, cyclin D1, cyclin E, CDK2, Hes-1 and NF-κB p65. These changes led to growth inhibition and induced G0/G1 cell cycle arrest and apoptosis in SMMC7721 and HepG2 cells. Conversely, ablation of STAT1 had the opposite effect on p53, Fbxw7, Hes-1, NF-κB p65, cyclin A, cyclin D1, cyclin E and CDK2, and improved the viability of SMMC7721 and HepG2 cells.
Our data indicate that STAT1 exerts tumor-suppressive effects in hepatocarcinogenesis through induction of G0/G1 cell cycle arrest and apoptosis, and may provide a basis for the design of new therapies for the intervention of HCC in the clinic.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>26617467</pmid><doi>10.1186/s12935-015-0253-6</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Apoptosis Growth Hepatoma Primary Research RNA Tumor proteins |
| title | STAT1 inhibits human hepatocellular carcinoma cell growth through induction of p53 and Fbxw7 |
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