Demonstration and biological significance of a gastrin‐P21‐activated kinase 1 feedback loop in colorectal cancer cells
Gastrins, including amidated gastrin17 and glycine‐extended gastrin17, are important growth factors in colorectal cancer (CRC). The p21‐activated kinase 1 (PAK1) plays key roles in cellular processes including proliferation, survival, and motility, and in cell transformation and tumor progression. P...
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| description | Gastrins, including amidated gastrin17 and glycine‐extended gastrin17, are important growth factors in colorectal cancer (CRC). The p21‐activated kinase 1 (PAK1) plays key roles in cellular processes including proliferation, survival, and motility, and in cell transformation and tumor progression. PAK1 expression increases with the progression of CRC, and knockdown of PAK1 blocks CRC cell growth and metastasis both in vitro and in vivo. The aim of this study was to determine the interaction between PAK1 and gastrins in CRC cells. PAK1 expression and activation were assayed by Western blots, and concentrations of gastrin mRNA and peptides by real‐time PCR and radioimmunoassay, respectively. Proliferation of CRC cells was measured by 3H‐thymidine incorporation, and vascular endothelial growth factor (VEGF) secretion was measured by ELISA. Gastrins activated PAK1 via PI3K‐dependent pathways. Activated PAK1 in turn mediated gastrin‐stimulated activation of β‐catenin and VEGF secretion in CRC cells, as knockdown of PAK1 blocked stimulation of these cellular processes by gastrins. Downregulation of gastrin reduced the expression and activity of PAK1, but in contrast there was a compensatory increase in gastrins either when PAK1 was downregulated, or after treatment with a PAK inhibitor. Our results indicate that PAK1 is required for the stimulation of CRC cells by gastrins, and suggest the existence of an inhibitory feedback loop by which PAK1 downregulates gastrin production in CRC cells.
e12048
The results in this study indicate that PAK1 is required for the stimulation of CRC cells by gastrins, and suggest the existence of an inhibitory feedback loop by which PAK1 downregulates gastrin production in CRC cells. |
| doi_str_mv | 10.14814/phy2.12048 |
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The results in this study indicate that PAK1 is required for the stimulation of CRC cells by gastrins, and suggest the existence of an inhibitory feedback loop by which PAK1 downregulates gastrin production in CRC cells.</description><identifier>ISSN: 2051-817X</identifier><identifier>EISSN: 2051-817X</identifier><identifier>DOI: 10.14814/phy2.12048</identifier><identifier>PMID: 24963032</identifier><language>eng</language><publisher>United States: John Wiley & Sons, Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; Apoptosis ; Cell activation ; Cell adhesion & migration ; Cell growth ; Cell proliferation ; Colon cancer ; Colorectal cancer ; Colorectal carcinoma ; Cyclin-dependent kinase inhibitor p21 ; Enzyme-linked immunosorbent assay ; Feedback ; Gamide ; Gastrin ; Gene expression ; Glycine ; glycine extended ; Growth factors ; Kinases ; Metastases ; Metastasis ; mRNA ; Mutation ; Original Research ; p21‐activated kinase 1 ; Peptides ; Physiology ; Proteins ; Radioimmunoassay ; Secretion ; Thymidine ; Tumors ; Vascular endothelial growth factor ; Western blotting</subject><ispartof>Physiological reports, 2014-06, Vol.2 (6), p.e12048-n/a</ispartof><rights>2014 The Authors. published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.</rights><rights>2014 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.</rights><rights>2014. This work is published under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 The Authors. published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4858-6a621efc7ff30ccc3d269c93fd3b50fa11854ef861fef5dc219136be7b6980e43</citedby><cites>FETCH-LOGICAL-c4858-6a621efc7ff30ccc3d269c93fd3b50fa11854ef861fef5dc219136be7b6980e43</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/PMC4208650/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4208650/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1416,11561,27923,27924,45573,45574,46051,46475,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24963032$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huynh, Nhi</creatorcontrib><creatorcontrib>Liu, Kevin H.</creatorcontrib><creatorcontrib>Yim, Mildred</creatorcontrib><creatorcontrib>Shulkes, Arthur</creatorcontrib><creatorcontrib>Baldwin, Graham S.</creatorcontrib><creatorcontrib>He, Hong</creatorcontrib><title>Demonstration and biological significance of a gastrin‐P21‐activated kinase 1 feedback loop in colorectal cancer cells</title><title>Physiological reports</title><addtitle>Physiol Rep</addtitle><description>Gastrins, including amidated gastrin17 and glycine‐extended gastrin17, are important growth factors in colorectal cancer (CRC). The p21‐activated kinase 1 (PAK1) plays key roles in cellular processes including proliferation, survival, and motility, and in cell transformation and tumor progression. PAK1 expression increases with the progression of CRC, and knockdown of PAK1 blocks CRC cell growth and metastasis both in vitro and in vivo. The aim of this study was to determine the interaction between PAK1 and gastrins in CRC cells. PAK1 expression and activation were assayed by Western blots, and concentrations of gastrin mRNA and peptides by real‐time PCR and radioimmunoassay, respectively. Proliferation of CRC cells was measured by 3H‐thymidine incorporation, and vascular endothelial growth factor (VEGF) secretion was measured by ELISA. Gastrins activated PAK1 via PI3K‐dependent pathways. Activated PAK1 in turn mediated gastrin‐stimulated activation of β‐catenin and VEGF secretion in CRC cells, as knockdown of PAK1 blocked stimulation of these cellular processes by gastrins. Downregulation of gastrin reduced the expression and activity of PAK1, but in contrast there was a compensatory increase in gastrins either when PAK1 was downregulated, or after treatment with a PAK inhibitor. Our results indicate that PAK1 is required for the stimulation of CRC cells by gastrins, and suggest the existence of an inhibitory feedback loop by which PAK1 downregulates gastrin production in CRC cells.
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The results in this study indicate that PAK1 is required for the stimulation of CRC cells by gastrins, and suggest the existence of an inhibitory feedback loop by which PAK1 downregulates gastrin production in CRC cells.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Apoptosis</subject><subject>Cell activation</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Cyclin-dependent kinase inhibitor p21</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Feedback</subject><subject>Gamide</subject><subject>Gastrin</subject><subject>Gene expression</subject><subject>Glycine</subject><subject>glycine extended</subject><subject>Growth factors</subject><subject>Kinases</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>mRNA</subject><subject>Mutation</subject><subject>Original Research</subject><subject>p21‐activated kinase 1</subject><subject>Peptides</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Radioimmunoassay</subject><subject>Secretion</subject><subject>Thymidine</subject><subject>Tumors</subject><subject>Vascular endothelial growth factor</subject><subject>Western blotting</subject><issn>2051-817X</issn><issn>2051-817X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkkFrFDEYhgdRbKk9eZeAF0G2fl-SmclcBGmtFQr2oKCnkMl82aadTdZktrKe-hP8jf4S091aqge9JB_k4SFv8lbVU4QDlArlq-X5mh8gB6keVLscapwpbD8_vDfvVPs5XwAAghAdyMfVDpddI0Dw3er7ES1iyFMyk4-BmTCw3scxzr01I8t-HrwrY7DEomOGzU1hffh5_eOMY1mNnfyVmWhglz6YTAyZIxp6Yy_ZGOOS-cBs8SWyUxFuTIlZGsf8pHrkzJhp_3bfqz4dv_14eDI7_fDu_eGb05mVqlazxjQcydnWOQHWWjHwprOdcIPoa3AGUdWSnGrQkasHy7FD0fTU9k2ngKTYq15vvctVv6DBUihpR71MfmHSWkfj9Z8nwZ_rebzSkoNqaiiCF7eCFL-uKE964fNNBBMorrLGFlupVMvx_2gtoUXBhSro87_Qi7hKobyE5rwDUAJVW6iXW8qmmHMid3dvBL1pgL5pgN40oNDP7ke9Y3__dwH4FvjmR1r_y6XPTr7wrfUXlZe-ww</recordid><startdate>201406</startdate><enddate>201406</enddate><creator>Huynh, Nhi</creator><creator>Liu, Kevin H.</creator><creator>Yim, Mildred</creator><creator>Shulkes, Arthur</creator><creator>Baldwin, Graham S.</creator><creator>He, Hong</creator><general>John Wiley & Sons, Inc</general><general>Wiley Periodicals, Inc</general><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</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>CCPQU</scope><scope>DWQXO</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>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7TO</scope><scope>5PM</scope></search><sort><creationdate>201406</creationdate><title>Demonstration and biological significance of a gastrin‐P21‐activated kinase 1 feedback loop in colorectal cancer cells</title><author>Huynh, Nhi ; Liu, Kevin H. ; Yim, Mildred ; Shulkes, Arthur ; Baldwin, Graham S. ; He, Hong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4858-6a621efc7ff30ccc3d269c93fd3b50fa11854ef861fef5dc219136be7b6980e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Apoptosis</topic><topic>Cell activation</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Colon cancer</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Cyclin-dependent kinase inhibitor p21</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Feedback</topic><topic>Gamide</topic><topic>Gastrin</topic><topic>Gene expression</topic><topic>Glycine</topic><topic>glycine extended</topic><topic>Growth factors</topic><topic>Kinases</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>mRNA</topic><topic>Mutation</topic><topic>Original Research</topic><topic>p21‐activated kinase 1</topic><topic>Peptides</topic><topic>Physiology</topic><topic>Proteins</topic><topic>Radioimmunoassay</topic><topic>Secretion</topic><topic>Thymidine</topic><topic>Tumors</topic><topic>Vascular endothelial growth factor</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huynh, Nhi</creatorcontrib><creatorcontrib>Liu, Kevin H.</creatorcontrib><creatorcontrib>Yim, Mildred</creatorcontrib><creatorcontrib>Shulkes, Arthur</creatorcontrib><creatorcontrib>Baldwin, Graham S.</creatorcontrib><creatorcontrib>He, Hong</creatorcontrib><collection>Wiley Open Access</collection><collection>Wiley Free Archive</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Biological Science Database</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>Oncogenes and Growth Factors Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Physiological reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huynh, Nhi</au><au>Liu, Kevin H.</au><au>Yim, Mildred</au><au>Shulkes, Arthur</au><au>Baldwin, Graham S.</au><au>He, Hong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Demonstration and biological significance of a gastrin‐P21‐activated kinase 1 feedback loop in colorectal cancer cells</atitle><jtitle>Physiological reports</jtitle><addtitle>Physiol Rep</addtitle><date>2014-06</date><risdate>2014</risdate><volume>2</volume><issue>6</issue><spage>e12048</spage><epage>n/a</epage><pages>e12048-n/a</pages><issn>2051-817X</issn><eissn>2051-817X</eissn><abstract>Gastrins, including amidated gastrin17 and glycine‐extended gastrin17, are important growth factors in colorectal cancer (CRC). The p21‐activated kinase 1 (PAK1) plays key roles in cellular processes including proliferation, survival, and motility, and in cell transformation and tumor progression. PAK1 expression increases with the progression of CRC, and knockdown of PAK1 blocks CRC cell growth and metastasis both in vitro and in vivo. The aim of this study was to determine the interaction between PAK1 and gastrins in CRC cells. PAK1 expression and activation were assayed by Western blots, and concentrations of gastrin mRNA and peptides by real‐time PCR and radioimmunoassay, respectively. Proliferation of CRC cells was measured by 3H‐thymidine incorporation, and vascular endothelial growth factor (VEGF) secretion was measured by ELISA. Gastrins activated PAK1 via PI3K‐dependent pathways. Activated PAK1 in turn mediated gastrin‐stimulated activation of β‐catenin and VEGF secretion in CRC cells, as knockdown of PAK1 blocked stimulation of these cellular processes by gastrins. Downregulation of gastrin reduced the expression and activity of PAK1, but in contrast there was a compensatory increase in gastrins either when PAK1 was downregulated, or after treatment with a PAK inhibitor. Our results indicate that PAK1 is required for the stimulation of CRC cells by gastrins, and suggest the existence of an inhibitory feedback loop by which PAK1 downregulates gastrin production in CRC cells.
e12048
The results in this study indicate that PAK1 is required for the stimulation of CRC cells by gastrins, and suggest the existence of an inhibitory feedback loop by which PAK1 downregulates gastrin production in CRC cells.</abstract><cop>United States</cop><pub>John Wiley & Sons, Inc</pub><pmid>24963032</pmid><doi>10.14814/phy2.12048</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase Apoptosis Cell activation Cell adhesion & migration Cell growth Cell proliferation Colon cancer Colorectal cancer Colorectal carcinoma Cyclin-dependent kinase inhibitor p21 Enzyme-linked immunosorbent assay Feedback Gamide Gastrin Gene expression Glycine glycine extended Growth factors Kinases Metastases Metastasis mRNA Mutation Original Research p21‐activated kinase 1 Peptides Physiology Proteins Radioimmunoassay Secretion Thymidine Tumors Vascular endothelial growth factor Western blotting |
| title | Demonstration and biological significance of a gastrin‐P21‐activated kinase 1 feedback loop in colorectal cancer cells |
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