Down regulation of N-acetylglucosaminyltransferase V facilitates all-transretinoic acid to induce apoptosis of human hepatocarcinoma cells
After N-acetylglucosaminyltransferase V (GnT-V) activity was down-regulated by the transfection of its antisense cDNA(GnTV-AS), apoptosis of H7721 cells was appeared and the apoptosis induced by 80μM all-transretinoic acid (ATRA) was facilitated, while ATRA itself could not induce apparent apoptosis...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2006-03, Vol.284 (1-2), p.103-110 |
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| creator | Guo, Peng Chen, Hai-jiao Wang, Qiu-yan Chen, Hui-Li |
| description | After N-acetylglucosaminyltransferase V (GnT-V) activity was down-regulated by the transfection of its antisense cDNA(GnTV-AS), apoptosis of H7721 cells was appeared and the apoptosis induced by 80μM all-transretinoic acid (ATRA) was facilitated, while ATRA itself could not induce apparent apoptosis in mock cells transfected with the vector. In the study of the molecular mechanism of this phenomenon, it was found that GnTV-AS reduced the expressions of anti-apoptotic proteins, such as phosphorylated protein kinase B and phosphorylated Bad as well as Bcl-2 and Bcl-X L, and elevated those of pro-apoptotic proteins, including Bax, full length caspase-3 and its activated fragments as well as anti-oncoprotein p53. In the contrast, ATRA up regulated the expressions of Bax and activated caspase-3 fragments only. After the GnTV-AS transfected cells were treated with ATRA, phosphorylated PKB and Bad were further decreased, while Bax and activated caspase-3 fragment were further increased, leading to the enhanced apoptosis in flow-cytometry analysis when compared with GnTV-AS cells not treated with ATRA. It was speculated that the decreased phospho-Bad resulted from the reduced phospho-PKB and the up regulation of p53 caused the elevated activity of Bax. The increased active caspase-3 was the consequence of the elevated Bax/ Bcl-2(Bcl-X L) activity ratio in the cells. |
| doi_str_mv | 10.1007/s11010-005-9022-5 |
| format | Article |
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In the study of the molecular mechanism of this phenomenon, it was found that GnTV-AS reduced the expressions of anti-apoptotic proteins, such as phosphorylated protein kinase B and phosphorylated Bad as well as Bcl-2 and Bcl-X L, and elevated those of pro-apoptotic proteins, including Bax, full length caspase-3 and its activated fragments as well as anti-oncoprotein p53. In the contrast, ATRA up regulated the expressions of Bax and activated caspase-3 fragments only. After the GnTV-AS transfected cells were treated with ATRA, phosphorylated PKB and Bad were further decreased, while Bax and activated caspase-3 fragment were further increased, leading to the enhanced apoptosis in flow-cytometry analysis when compared with GnTV-AS cells not treated with ATRA. It was speculated that the decreased phospho-Bad resulted from the reduced phospho-PKB and the up regulation of p53 caused the elevated activity of Bax. The increased active caspase-3 was the consequence of the elevated Bax/ Bcl-2(Bcl-X L) activity ratio in the cells.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-005-9022-5</identifier><identifier>PMID: 16411021</identifier><language>eng</language><publisher>Netherlands: Boston : Springer US</publisher><subject>all-transretinoic acid (ATRA) ; Apoptosis ; Bcl-2 family ; bcl-2-Associated X Protein - metabolism ; bcl-Associated Death Protein - metabolism ; bcl-X Protein - metabolism ; Carcinoma, Hepatocellular ; caspase ; Caspase 3 ; Caspases - metabolism ; Cell Line, Tumor ; Down-Regulation ; Humans ; I-kappa B Proteins - metabolism ; Kinases ; N-acetylglucosaminyltransferase V (GnT-V) ; N-Acetylglucosaminyltransferases - biosynthesis ; N-Acetylglucosaminyltransferases - genetics ; NF-KappaB Inhibitor alpha ; Phosphorylation ; protein kinase B (PKB/Akt) ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Tretinoin - pharmacology ; Tretinoin - physiology ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Molecular and cellular biochemistry, 2006-03, Vol.284 (1-2), p.103-110</ispartof><rights>Springer Science+Business Media, Inc. 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1951-a474a56796a65cff44fbfcdc98832cdcc64fef0d71c5aa2f8b1f8c61cad4f8e93</citedby><cites>FETCH-LOGICAL-c1951-a474a56796a65cff44fbfcdc98832cdcc64fef0d71c5aa2f8b1f8c61cad4f8e93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16411021$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Peng</creatorcontrib><creatorcontrib>Chen, Hai-jiao</creatorcontrib><creatorcontrib>Wang, Qiu-yan</creatorcontrib><creatorcontrib>Chen, Hui-Li</creatorcontrib><title>Down regulation of N-acetylglucosaminyltransferase V facilitates all-transretinoic acid to induce apoptosis of human hepatocarcinoma cells</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><description>After N-acetylglucosaminyltransferase V (GnT-V) activity was down-regulated by the transfection of its antisense cDNA(GnTV-AS), apoptosis of H7721 cells was appeared and the apoptosis induced by 80μM all-transretinoic acid (ATRA) was facilitated, while ATRA itself could not induce apparent apoptosis in mock cells transfected with the vector. In the study of the molecular mechanism of this phenomenon, it was found that GnTV-AS reduced the expressions of anti-apoptotic proteins, such as phosphorylated protein kinase B and phosphorylated Bad as well as Bcl-2 and Bcl-X L, and elevated those of pro-apoptotic proteins, including Bax, full length caspase-3 and its activated fragments as well as anti-oncoprotein p53. In the contrast, ATRA up regulated the expressions of Bax and activated caspase-3 fragments only. After the GnTV-AS transfected cells were treated with ATRA, phosphorylated PKB and Bad were further decreased, while Bax and activated caspase-3 fragment were further increased, leading to the enhanced apoptosis in flow-cytometry analysis when compared with GnTV-AS cells not treated with ATRA. It was speculated that the decreased phospho-Bad resulted from the reduced phospho-PKB and the up regulation of p53 caused the elevated activity of Bax. The increased active caspase-3 was the consequence of the elevated Bax/ Bcl-2(Bcl-X L) activity ratio in the cells.</description><subject>all-transretinoic acid (ATRA)</subject><subject>Apoptosis</subject><subject>Bcl-2 family</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>bcl-Associated Death Protein - metabolism</subject><subject>bcl-X Protein - metabolism</subject><subject>Carcinoma, Hepatocellular</subject><subject>caspase</subject><subject>Caspase 3</subject><subject>Caspases - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Down-Regulation</subject><subject>Humans</subject><subject>I-kappa B Proteins - metabolism</subject><subject>Kinases</subject><subject>N-acetylglucosaminyltransferase V (GnT-V)</subject><subject>N-Acetylglucosaminyltransferases - biosynthesis</subject><subject>N-Acetylglucosaminyltransferases - genetics</subject><subject>NF-KappaB Inhibitor alpha</subject><subject>Phosphorylation</subject><subject>protein kinase B (PKB/Akt)</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Tretinoin - pharmacology</subject><subject>Tretinoin - physiology</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkc2OFCEURonROO3oA7hR4sIdyq0qiqqlmfEvmehCxy25TUEPEwpKoGL6FXxqKbsTE1d3cc_3ccMh5DnwN8C5fJsBOHDGuWAjbxomHpAdCNmyboTxIdnxlnM2gJQX5EnO97zCHOAxuYC-q9EGduT3dfwVaDKH1WNxMdBo6ReG2pSjP_hVx4yzC0dfEoZsTcJs6A9qUTvvChaTKXrP_m6TKS5Ep2ldTrRE6sK0akNxiUuJ2eWt-26dMdA7s2CJGpOuiRmpNt7np-SRRZ_Ns_O8JLcf3n-_-sRuvn78fPXuhmkYBTDsZIeil2OPvdDWdp3dWz3pcRjapk7dd9ZYPknQArGxwx7soHvQOHV2MGN7SV6fepcUf64mFzW7vF2AwcQ1q616hEZU8NV_4H1cU6i3KSn6hkMvZYXgBOkUc_0Dq5bkZkxHBVxtltTJkqqW1GZJbcUvzsXrfjbTv8RZSwVengCLUeEhuaxuv9UHq88BxkFA-wfe_5p_</recordid><startdate>200603</startdate><enddate>200603</enddate><creator>Guo, Peng</creator><creator>Chen, Hai-jiao</creator><creator>Wang, Qiu-yan</creator><creator>Chen, Hui-Li</creator><general>Boston : Springer US</general><general>Springer Nature B.V</general><scope>FBQ</scope><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>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>200603</creationdate><title>Down regulation of N-acetylglucosaminyltransferase V facilitates all-transretinoic acid to induce apoptosis of human hepatocarcinoma cells</title><author>Guo, Peng ; Chen, Hai-jiao ; Wang, Qiu-yan ; Chen, Hui-Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1951-a474a56796a65cff44fbfcdc98832cdcc64fef0d71c5aa2f8b1f8c61cad4f8e93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>all-transretinoic acid (ATRA)</topic><topic>Apoptosis</topic><topic>Bcl-2 family</topic><topic>bcl-2-Associated X Protein - 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Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Peng</au><au>Chen, Hai-jiao</au><au>Wang, Qiu-yan</au><au>Chen, Hui-Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Down regulation of N-acetylglucosaminyltransferase V facilitates all-transretinoic acid to induce apoptosis of human hepatocarcinoma cells</atitle><jtitle>Molecular and cellular biochemistry</jtitle><addtitle>Mol Cell Biochem</addtitle><date>2006-03</date><risdate>2006</risdate><volume>284</volume><issue>1-2</issue><spage>103</spage><epage>110</epage><pages>103-110</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>After N-acetylglucosaminyltransferase V (GnT-V) activity was down-regulated by the transfection of its antisense cDNA(GnTV-AS), apoptosis of H7721 cells was appeared and the apoptosis induced by 80μM all-transretinoic acid (ATRA) was facilitated, while ATRA itself could not induce apparent apoptosis in mock cells transfected with the vector. In the study of the molecular mechanism of this phenomenon, it was found that GnTV-AS reduced the expressions of anti-apoptotic proteins, such as phosphorylated protein kinase B and phosphorylated Bad as well as Bcl-2 and Bcl-X L, and elevated those of pro-apoptotic proteins, including Bax, full length caspase-3 and its activated fragments as well as anti-oncoprotein p53. In the contrast, ATRA up regulated the expressions of Bax and activated caspase-3 fragments only. After the GnTV-AS transfected cells were treated with ATRA, phosphorylated PKB and Bad were further decreased, while Bax and activated caspase-3 fragment were further increased, leading to the enhanced apoptosis in flow-cytometry analysis when compared with GnTV-AS cells not treated with ATRA. It was speculated that the decreased phospho-Bad resulted from the reduced phospho-PKB and the up regulation of p53 caused the elevated activity of Bax. The increased active caspase-3 was the consequence of the elevated Bax/ Bcl-2(Bcl-X L) activity ratio in the cells.</abstract><cop>Netherlands</cop><pub>Boston : Springer US</pub><pmid>16411021</pmid><doi>10.1007/s11010-005-9022-5</doi><tpages>8</tpages></addata></record> |
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| subjects | all-transretinoic acid (ATRA) Apoptosis Bcl-2 family bcl-2-Associated X Protein - metabolism bcl-Associated Death Protein - metabolism bcl-X Protein - metabolism Carcinoma, Hepatocellular caspase Caspase 3 Caspases - metabolism Cell Line, Tumor Down-Regulation Humans I-kappa B Proteins - metabolism Kinases N-acetylglucosaminyltransferase V (GnT-V) N-Acetylglucosaminyltransferases - biosynthesis N-Acetylglucosaminyltransferases - genetics NF-KappaB Inhibitor alpha Phosphorylation protein kinase B (PKB/Akt) Proteins Proto-Oncogene Proteins c-akt - metabolism Tretinoin - pharmacology Tretinoin - physiology Tumor Suppressor Protein p53 - metabolism |
| title | Down regulation of N-acetylglucosaminyltransferase V facilitates all-transretinoic acid to induce apoptosis of human hepatocarcinoma cells |
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