Pyruvate kinase M2 promotes the growth of gastric cancer cells via regulation of Bcl-xL expression at transcriptional level
► PKM2 is associated with poor survival of gastric cancer patients. ► PKM2 affects cell survival by regulating Bcl-xL at the transcriptional level. ► PKM2 affects stabilization of p65 protein. ► PKM2/NF-κB/Bcl-xL may be a potential cascade in cancer progression. PKM2 is an isoenzyme of the glycolyti...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2012-06, Vol.423 (1), p.38-44 |
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| creator | Kwon, Oh-Hyung Kang, Tae-Wook Kim, Jeong-Hwan Kim, Mirang Noh, Seung-Moo Song, Kyu-Sang Yoo, Hyang-Sook Kim, Woo-Ho Xie, Zhi Pocalyko, David Kim, Seon-Young Kim, Yong Sung |
| description | ► PKM2 is associated with poor survival of gastric cancer patients. ► PKM2 affects cell survival by regulating Bcl-xL at the transcriptional level. ► PKM2 affects stabilization of p65 protein. ► PKM2/NF-κB/Bcl-xL may be a potential cascade in cancer progression.
PKM2 is an isoenzyme of the glycolytic enzyme pyruvate kinase that promotes aerobic glycolysis. Here, we describe an important role for PKM2 in regulating the survival of gastric cancer (GC) cells. We showed that PKM2 was overexpressed in gastric tumor tissues compared to normal tissues and its expression level was associated with poor survival of gastric cancer patients. We also showed that PKM2 affected cell survival by regulating Bcl-xL at the transcriptional level. PKM2 knockdown partially affected the stability of NF-kB subunit p65, suggesting that post-translational regulation of p65 by PKM2 is one of plausible mechanisms for the increased cell growth. Therefore, PKM2 may function as an upstream molecule that regulates p65 function and thus enhances the growth of tumor cells. |
| doi_str_mv | 10.1016/j.bbrc.2012.05.063 |
| format | Article |
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PKM2 is an isoenzyme of the glycolytic enzyme pyruvate kinase that promotes aerobic glycolysis. Here, we describe an important role for PKM2 in regulating the survival of gastric cancer (GC) cells. We showed that PKM2 was overexpressed in gastric tumor tissues compared to normal tissues and its expression level was associated with poor survival of gastric cancer patients. We also showed that PKM2 affected cell survival by regulating Bcl-xL at the transcriptional level. PKM2 knockdown partially affected the stability of NF-kB subunit p65, suggesting that post-translational regulation of p65 by PKM2 is one of plausible mechanisms for the increased cell growth. Therefore, PKM2 may function as an upstream molecule that regulates p65 function and thus enhances the growth of tumor cells.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2012.05.063</identifier><identifier>PMID: 22627140</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>bcl-X Protein - genetics ; Bcl-xL ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Cell Line, Tumor ; Cell Proliferation ; Gastric cancer ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; NF-κB ; PKM2 ; Prognosis ; Pyruvate Kinase - genetics ; Pyruvate Kinase - metabolism ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology ; Transcription Factor RelA - metabolism ; Transcription, Genetic</subject><ispartof>Biochemical and biophysical research communications, 2012-06, Vol.423 (1), p.38-44</ispartof><rights>2012 Elsevier Inc.</rights><rights>Copyright © 2012 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c422t-7d440ef5825f72f9acfd9aa705bc73d0ae8e540f0069949fef1a37da67799d383</citedby><cites>FETCH-LOGICAL-c422t-7d440ef5825f72f9acfd9aa705bc73d0ae8e540f0069949fef1a37da67799d383</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X12009400$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22627140$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kwon, Oh-Hyung</creatorcontrib><creatorcontrib>Kang, Tae-Wook</creatorcontrib><creatorcontrib>Kim, Jeong-Hwan</creatorcontrib><creatorcontrib>Kim, Mirang</creatorcontrib><creatorcontrib>Noh, Seung-Moo</creatorcontrib><creatorcontrib>Song, Kyu-Sang</creatorcontrib><creatorcontrib>Yoo, Hyang-Sook</creatorcontrib><creatorcontrib>Kim, Woo-Ho</creatorcontrib><creatorcontrib>Xie, Zhi</creatorcontrib><creatorcontrib>Pocalyko, David</creatorcontrib><creatorcontrib>Kim, Seon-Young</creatorcontrib><creatorcontrib>Kim, Yong Sung</creatorcontrib><title>Pyruvate kinase M2 promotes the growth of gastric cancer cells via regulation of Bcl-xL expression at transcriptional level</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>► PKM2 is associated with poor survival of gastric cancer patients. ► PKM2 affects cell survival by regulating Bcl-xL at the transcriptional level. ► PKM2 affects stabilization of p65 protein. ► PKM2/NF-κB/Bcl-xL may be a potential cascade in cancer progression.
PKM2 is an isoenzyme of the glycolytic enzyme pyruvate kinase that promotes aerobic glycolysis. Here, we describe an important role for PKM2 in regulating the survival of gastric cancer (GC) cells. We showed that PKM2 was overexpressed in gastric tumor tissues compared to normal tissues and its expression level was associated with poor survival of gastric cancer patients. We also showed that PKM2 affected cell survival by regulating Bcl-xL at the transcriptional level. PKM2 knockdown partially affected the stability of NF-kB subunit p65, suggesting that post-translational regulation of p65 by PKM2 is one of plausible mechanisms for the increased cell growth. Therefore, PKM2 may function as an upstream molecule that regulates p65 function and thus enhances the growth of tumor cells.</description><subject>bcl-X Protein - genetics</subject><subject>Bcl-xL</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Gastric cancer</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Knockdown Techniques</subject><subject>Humans</subject><subject>NF-κB</subject><subject>PKM2</subject><subject>Prognosis</subject><subject>Pyruvate Kinase - genetics</subject><subject>Pyruvate Kinase - metabolism</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><subject>Transcription Factor RelA - metabolism</subject><subject>Transcription, Genetic</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1vEzEQhi0EoqHwBzggH7nsMvZ-OJZ6aasWkILooUjcrIl3nDpsdlPbG1r1z-NVCkdOI42eeTXvw9h7AaUA0X7alut1sKUEIUtoSmirF2whQEMhBdQv2QIA2kJq8fOEvYlxCyBE3erX7ETKVipRw4I93TyG6YCJ-C8_YCT-TfJ9GHdjosjTHfFNGH-nOz46vsGYgrfc4mApcEt9H_nBIw-0mXpMfhxm7ML2xcOK08M-UIzzEhNPAYdog9_PFPa8pwP1b9krh32kd8_zlP24vrq9_FKsvn_-enm-KmwtZSpUV9dArlnKxinpNFrXaUQFzdqqqgOkJTU1uFxW61o7cgIr1WGrlNZdtaxO2cdjbi52P1FMZufj_D4ONE7RCJBZCIhKZVQeURvGGAM5sw9-h-ExQ2aWbrZmlm5m6QYak6Xnow_P-dN6R92_k7-WM3B2BCi3PHgKJlpP2WLnA9lkutH_L_8PLvSU2g</recordid><startdate>20120622</startdate><enddate>20120622</enddate><creator>Kwon, Oh-Hyung</creator><creator>Kang, Tae-Wook</creator><creator>Kim, Jeong-Hwan</creator><creator>Kim, Mirang</creator><creator>Noh, Seung-Moo</creator><creator>Song, Kyu-Sang</creator><creator>Yoo, Hyang-Sook</creator><creator>Kim, Woo-Ho</creator><creator>Xie, Zhi</creator><creator>Pocalyko, David</creator><creator>Kim, Seon-Young</creator><creator>Kim, Yong Sung</creator><general>Elsevier Inc</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></search><sort><creationdate>20120622</creationdate><title>Pyruvate kinase M2 promotes the growth of gastric cancer cells via regulation of Bcl-xL expression at transcriptional level</title><author>Kwon, Oh-Hyung ; Kang, Tae-Wook ; Kim, Jeong-Hwan ; Kim, Mirang ; Noh, Seung-Moo ; Song, Kyu-Sang ; Yoo, Hyang-Sook ; Kim, Woo-Ho ; Xie, Zhi ; Pocalyko, David ; Kim, Seon-Young ; Kim, Yong Sung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c422t-7d440ef5825f72f9acfd9aa705bc73d0ae8e540f0069949fef1a37da67799d383</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>bcl-X Protein - genetics</topic><topic>Bcl-xL</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Gastric cancer</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Knockdown Techniques</topic><topic>Humans</topic><topic>NF-κB</topic><topic>PKM2</topic><topic>Prognosis</topic><topic>Pyruvate Kinase - genetics</topic><topic>Pyruvate Kinase - metabolism</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - pathology</topic><topic>Transcription Factor RelA - metabolism</topic><topic>Transcription, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kwon, Oh-Hyung</creatorcontrib><creatorcontrib>Kang, Tae-Wook</creatorcontrib><creatorcontrib>Kim, Jeong-Hwan</creatorcontrib><creatorcontrib>Kim, Mirang</creatorcontrib><creatorcontrib>Noh, Seung-Moo</creatorcontrib><creatorcontrib>Song, Kyu-Sang</creatorcontrib><creatorcontrib>Yoo, Hyang-Sook</creatorcontrib><creatorcontrib>Kim, Woo-Ho</creatorcontrib><creatorcontrib>Xie, Zhi</creatorcontrib><creatorcontrib>Pocalyko, David</creatorcontrib><creatorcontrib>Kim, Seon-Young</creatorcontrib><creatorcontrib>Kim, Yong Sung</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><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kwon, Oh-Hyung</au><au>Kang, Tae-Wook</au><au>Kim, Jeong-Hwan</au><au>Kim, Mirang</au><au>Noh, Seung-Moo</au><au>Song, Kyu-Sang</au><au>Yoo, Hyang-Sook</au><au>Kim, Woo-Ho</au><au>Xie, Zhi</au><au>Pocalyko, David</au><au>Kim, Seon-Young</au><au>Kim, Yong Sung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pyruvate kinase M2 promotes the growth of gastric cancer cells via regulation of Bcl-xL expression at transcriptional level</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2012-06-22</date><risdate>2012</risdate><volume>423</volume><issue>1</issue><spage>38</spage><epage>44</epage><pages>38-44</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>► PKM2 is associated with poor survival of gastric cancer patients. ► PKM2 affects cell survival by regulating Bcl-xL at the transcriptional level. ► PKM2 affects stabilization of p65 protein. ► PKM2/NF-κB/Bcl-xL may be a potential cascade in cancer progression.
PKM2 is an isoenzyme of the glycolytic enzyme pyruvate kinase that promotes aerobic glycolysis. Here, we describe an important role for PKM2 in regulating the survival of gastric cancer (GC) cells. We showed that PKM2 was overexpressed in gastric tumor tissues compared to normal tissues and its expression level was associated with poor survival of gastric cancer patients. We also showed that PKM2 affected cell survival by regulating Bcl-xL at the transcriptional level. PKM2 knockdown partially affected the stability of NF-kB subunit p65, suggesting that post-translational regulation of p65 by PKM2 is one of plausible mechanisms for the increased cell growth. Therefore, PKM2 may function as an upstream molecule that regulates p65 function and thus enhances the growth of tumor cells.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22627140</pmid><doi>10.1016/j.bbrc.2012.05.063</doi><tpages>7</tpages></addata></record> |
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| subjects | bcl-X Protein - genetics Bcl-xL Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Cell Line, Tumor Cell Proliferation Gastric cancer Gene Expression Regulation, Neoplastic Gene Knockdown Techniques Humans NF-κB PKM2 Prognosis Pyruvate Kinase - genetics Pyruvate Kinase - metabolism Stomach Neoplasms - genetics Stomach Neoplasms - pathology Transcription Factor RelA - metabolism Transcription, Genetic |
| title | Pyruvate kinase M2 promotes the growth of gastric cancer cells via regulation of Bcl-xL expression at transcriptional level |
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