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FYN is required for ARHGEF16 to promote proliferation and migration in colon cancer cells
ARHGEF16 is a recently identified Rho-family guanine nucleotide exchange factor (GEF) that has been implicated in the activation of Rho-family GTPases such as Rho G, Rac, and Cdc42. However, its functions in colon cancer cell proliferation and migration are not well understood. In this study, we sho...
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Published in: | Cell death & disease 2020-08, Vol.11 (8), p.652-652, Article 652 |
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description | ARHGEF16 is a recently identified Rho-family guanine nucleotide exchange factor (GEF) that has been implicated in the activation of Rho-family GTPases such as Rho G, Rac, and Cdc42. However, its functions in colon cancer cell proliferation and migration are not well understood. In this study, we showed that ARHGEF16 was highly expressed in clinical specimens of colon cancer. In colon cancer cells, ARHGEF16-stimulated proliferation and migration in vitro and in vivo. Furthermore, we identified a nonreceptor tyrosine kinase, FYN, as a novel partner of ARHGEF16. Knocking down FYN expression decreased ARHGEF16 protein level in colon cancer cells. We further demonstrated that ARHGEF16-induced colon cancer cell proliferation and migration were dependent on FYN since knockdown FYN abolished the ARHGEF16-induced proliferation and migration of colon cancer cells. The FYN-ARHGEF16 axis mediates colon cancer progression and is a potential therapeutic target for colon cancer treatment. |
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However, its functions in colon cancer cell proliferation and migration are not well understood. In this study, we showed that ARHGEF16 was highly expressed in clinical specimens of colon cancer. In colon cancer cells, ARHGEF16-stimulated proliferation and migration in vitro and in vivo. Furthermore, we identified a nonreceptor tyrosine kinase, FYN, as a novel partner of ARHGEF16. Knocking down FYN expression decreased ARHGEF16 protein level in colon cancer cells. We further demonstrated that ARHGEF16-induced colon cancer cell proliferation and migration were dependent on FYN since knockdown FYN abolished the ARHGEF16-induced proliferation and migration of colon cancer cells. The FYN-ARHGEF16 axis mediates colon cancer progression and is a potential therapeutic target for colon cancer treatment.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-020-02830-1</identifier><identifier>PMID: 32811808</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/109 ; 13/51 ; 13/89 ; 13/95 ; 38/1 ; 38/111 ; 38/77 ; 38/90 ; 631/67/395 ; 692/699/1503 ; 82 ; 82/80 ; 96 ; 96/63 ; Adult ; Aged ; Antibodies ; Biochemistry ; Biomedical and Life Sciences ; cdc42 GTP-Binding Protein - metabolism ; Cdc42 protein ; Cell Biology ; Cell Culture ; Cell growth ; Cell migration ; Cell Movement - genetics ; Cell proliferation ; Cell Proliferation - genetics ; China ; Colon cancer ; Colonic Neoplasms - genetics ; Colonic Neoplasms - metabolism ; Colorectal cancer ; Female ; Fyn protein ; Guanine ; Guanine nucleotide exchange factor ; Guanine Nucleotide Exchange Factors - genetics ; Guanine Nucleotide Exchange Factors - metabolism ; Humans ; Immunology ; Kinases ; Life Sciences ; Male ; Middle Aged ; Protein Binding ; Protein-tyrosine kinase ; Proto-Oncogene Proteins c-fyn - genetics ; Proto-Oncogene Proteins c-fyn - metabolism ; rho GTP-Binding Proteins - metabolism ; Signal Transduction - genetics</subject><ispartof>Cell death & disease, 2020-08, Vol.11 (8), p.652-652, Article 652</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. 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However, its functions in colon cancer cell proliferation and migration are not well understood. In this study, we showed that ARHGEF16 was highly expressed in clinical specimens of colon cancer. In colon cancer cells, ARHGEF16-stimulated proliferation and migration in vitro and in vivo. Furthermore, we identified a nonreceptor tyrosine kinase, FYN, as a novel partner of ARHGEF16. Knocking down FYN expression decreased ARHGEF16 protein level in colon cancer cells. We further demonstrated that ARHGEF16-induced colon cancer cell proliferation and migration were dependent on FYN since knockdown FYN abolished the ARHGEF16-induced proliferation and migration of colon cancer cells. The FYN-ARHGEF16 axis mediates colon cancer progression and is a potential therapeutic target for colon cancer treatment.</description><subject>13</subject><subject>13/109</subject><subject>13/51</subject><subject>13/89</subject><subject>13/95</subject><subject>38/1</subject><subject>38/111</subject><subject>38/77</subject><subject>38/90</subject><subject>631/67/395</subject><subject>692/699/1503</subject><subject>82</subject><subject>82/80</subject><subject>96</subject><subject>96/63</subject><subject>Adult</subject><subject>Aged</subject><subject>Antibodies</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>cdc42 GTP-Binding Protein - metabolism</subject><subject>Cdc42 protein</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell Movement - genetics</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>China</subject><subject>Colon cancer</subject><subject>Colonic Neoplasms - 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metabolism</topic><topic>Signal Transduction - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Bei</creatorcontrib><creatorcontrib>Xu, Linlin</creatorcontrib><creatorcontrib>Chen, Limin</creatorcontrib><creatorcontrib>Wang, Yao</creatorcontrib><creatorcontrib>Jiang, Hongying</creatorcontrib><creatorcontrib>Wang, Yiting</creatorcontrib><creatorcontrib>Yan, Yehong</creatorcontrib><creatorcontrib>Luo, Shiwen</creatorcontrib><creatorcontrib>Zhai, Zhenyu</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</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 UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest Science Journals</collection><collection>ProQuest Biological Science Journals</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Bei</au><au>Xu, Linlin</au><au>Chen, Limin</au><au>Wang, Yao</au><au>Jiang, Hongying</au><au>Wang, Yiting</au><au>Yan, Yehong</au><au>Luo, Shiwen</au><au>Zhai, Zhenyu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>FYN is required for ARHGEF16 to promote proliferation and migration in colon cancer cells</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2020-08-07</date><risdate>2020</risdate><volume>11</volume><issue>8</issue><spage>652</spage><epage>652</epage><pages>652-652</pages><artnum>652</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>ARHGEF16 is a recently identified Rho-family guanine nucleotide exchange factor (GEF) that has been implicated in the activation of Rho-family GTPases such as Rho G, Rac, and Cdc42. However, its functions in colon cancer cell proliferation and migration are not well understood. In this study, we showed that ARHGEF16 was highly expressed in clinical specimens of colon cancer. In colon cancer cells, ARHGEF16-stimulated proliferation and migration in vitro and in vivo. Furthermore, we identified a nonreceptor tyrosine kinase, FYN, as a novel partner of ARHGEF16. Knocking down FYN expression decreased ARHGEF16 protein level in colon cancer cells. We further demonstrated that ARHGEF16-induced colon cancer cell proliferation and migration were dependent on FYN since knockdown FYN abolished the ARHGEF16-induced proliferation and migration of colon cancer cells. The FYN-ARHGEF16 axis mediates colon cancer progression and is a potential therapeutic target for colon cancer treatment.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32811808</pmid><doi>10.1038/s41419-020-02830-1</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-4215-6092</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | 13 13/109 13/51 13/89 13/95 38/1 38/111 38/77 38/90 631/67/395 692/699/1503 82 82/80 96 96/63 Adult Aged Antibodies Biochemistry Biomedical and Life Sciences cdc42 GTP-Binding Protein - metabolism Cdc42 protein Cell Biology Cell Culture Cell growth Cell migration Cell Movement - genetics Cell proliferation Cell Proliferation - genetics China Colon cancer Colonic Neoplasms - genetics Colonic Neoplasms - metabolism Colorectal cancer Female Fyn protein Guanine Guanine nucleotide exchange factor Guanine Nucleotide Exchange Factors - genetics Guanine Nucleotide Exchange Factors - metabolism Humans Immunology Kinases Life Sciences Male Middle Aged Protein Binding Protein-tyrosine kinase Proto-Oncogene Proteins c-fyn - genetics Proto-Oncogene Proteins c-fyn - metabolism rho GTP-Binding Proteins - metabolism Signal Transduction - genetics |
title | FYN is required for ARHGEF16 to promote proliferation and migration in colon cancer cells |
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