Silencing ARAF Suppresses the Malignant Phenotypes of Gallbladder Cancer Cells
ARAF is a member of the RAF kinase family that is necessary for mitogen-activated protein kinase (MAPK) activation in various malignancies, including lung, colorectal, pancreatic, and breast cancers. As the most common biliary tract tumor, gallbladder cancer (GBC) seriously harms human health while...
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| Veröffentlicht in: | BioMed research international 2020, Vol.2020 (2020), p.1-8 |
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| creator | Lu, Baochun Yu, Jianhua Li, Jiandong Wang, Yali Cen, Wenda Zhang, Weiguang Tong, Chenhao Lin, Weiguo Zhu, Zhiyang |
| description | ARAF is a member of the RAF kinase family that is necessary for mitogen-activated protein kinase (MAPK) activation in various malignancies, including lung, colorectal, pancreatic, and breast cancers. As the most common biliary tract tumor, gallbladder cancer (GBC) seriously harms human health while the function of ARAF in GBC remains elusive. Here, we found that ARAF expression was upregulated in gallbladder cancer tissues. In vitro, ARAF silencing mediated by RNA interference effectively inhibited cell proliferation, colony formation, migration, and invasion of GBC cells. Moreover, knocking down ARAF suppressed tumor growth in vivo. Our results indicated that ARAF functions as an oncogene in GBC and, thus, could be a potential therapeutic target for GBC. |
| doi_str_mv | 10.1155/2020/3235786 |
| format | Article |
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As the most common biliary tract tumor, gallbladder cancer (GBC) seriously harms human health while the function of ARAF in GBC remains elusive. Here, we found that ARAF expression was upregulated in gallbladder cancer tissues. In vitro, ARAF silencing mediated by RNA interference effectively inhibited cell proliferation, colony formation, migration, and invasion of GBC cells. Moreover, knocking down ARAF suppressed tumor growth in vivo. Our results indicated that ARAF functions as an oncogene in GBC and, thus, could be a potential therapeutic target for GBC.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2020/3235786</identifier><identifier>PMID: 32923479</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Antibodies ; Biliary tract ; Biotechnology ; Bladder cancer ; Breast cancer ; Cancer ; Cancer cells ; Cell growth ; Cell Line, Tumor ; Cell migration ; Cell Movement - genetics ; Cell proliferation ; Cell Proliferation - genetics ; Female ; Fluorides ; Gallbladder ; Gallbladder - pathology ; Gallbladder cancer ; Gallbladder Neoplasms - genetics ; Gallbladder Neoplasms - pathology ; Gene Expression Regulation, Neoplastic - genetics ; Genetic aspects ; Health aspects ; Hospitals ; Humans ; Kinases ; Laboratory animals ; Lung cancer ; Male ; MAP kinase ; MAP Kinase Signaling System - genetics ; Medical prognosis ; Metastasis ; Mice ; Mice, Nude ; Mutation ; Pancreas ; Phenotype ; Phenotypes ; Phosphotransferases ; Protein kinase ; Proteins ; raf Kinases - genetics ; Raf protein ; RNA-mediated interference ; Tumorigenesis ; Tumors ; Up-Regulation - genetics ; Wound healing</subject><ispartof>BioMed research international, 2020, Vol.2020 (2020), p.1-8</ispartof><rights>Copyright © 2020 Weiguo Lin et al.</rights><rights>COPYRIGHT 2020 John Wiley & Sons, Inc.</rights><rights>Copyright © 2020 Weiguo Lin et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Weiguo Lin et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-7eaa3e1314dd392cb2465859b3c591ce659cdfefc8a0e8214596b68a2b1fb54a3</citedby><cites>FETCH-LOGICAL-c499t-7eaa3e1314dd392cb2465859b3c591ce659cdfefc8a0e8214596b68a2b1fb54a3</cites><orcidid>0000-0002-6661-6647 ; 0000-0001-8350-0227</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7453270/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7453270/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32923479$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Li, Kui</contributor><contributor>Kui Li</contributor><creatorcontrib>Lu, Baochun</creatorcontrib><creatorcontrib>Yu, Jianhua</creatorcontrib><creatorcontrib>Li, Jiandong</creatorcontrib><creatorcontrib>Wang, Yali</creatorcontrib><creatorcontrib>Cen, Wenda</creatorcontrib><creatorcontrib>Zhang, Weiguang</creatorcontrib><creatorcontrib>Tong, Chenhao</creatorcontrib><creatorcontrib>Lin, Weiguo</creatorcontrib><creatorcontrib>Zhu, Zhiyang</creatorcontrib><title>Silencing ARAF Suppresses the Malignant Phenotypes of Gallbladder Cancer Cells</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>ARAF is a member of the RAF kinase family that is necessary for mitogen-activated protein kinase (MAPK) activation in various malignancies, including lung, colorectal, pancreatic, and breast cancers. As the most common biliary tract tumor, gallbladder cancer (GBC) seriously harms human health while the function of ARAF in GBC remains elusive. Here, we found that ARAF expression was upregulated in gallbladder cancer tissues. In vitro, ARAF silencing mediated by RNA interference effectively inhibited cell proliferation, colony formation, migration, and invasion of GBC cells. Moreover, knocking down ARAF suppressed tumor growth in vivo. Our results indicated that ARAF functions as an oncogene in GBC and, thus, could be a potential therapeutic target for GBC.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Biliary tract</subject><subject>Biotechnology</subject><subject>Bladder cancer</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - genetics</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Female</subject><subject>Fluorides</subject><subject>Gallbladder</subject><subject>Gallbladder - pathology</subject><subject>Gallbladder cancer</subject><subject>Gallbladder Neoplasms - genetics</subject><subject>Gallbladder Neoplasms - pathology</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Lung cancer</subject><subject>Male</subject><subject>MAP kinase</subject><subject>MAP Kinase Signaling System - genetics</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Mutation</subject><subject>Pancreas</subject><subject>Phenotype</subject><subject>Phenotypes</subject><subject>Phosphotransferases</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>raf Kinases - genetics</subject><subject>Raf protein</subject><subject>RNA-mediated interference</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>Up-Regulation - genetics</subject><subject>Wound healing</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkkuLFDEUhYMozjDOzrUUuBG0nbwr2QhN44zC-MDRdUilbnVnSCc1SZUy_9403baPldncwP04OfeeIPSU4NeECHFBMcUXjDLRKvkAnVJG-EISTh4e74ydoPNSbnE9ikis5WN0wqimjLf6FH288QGi83HdLL8sL5ubeRwzlAKlmTbQfLDBr6ONU_N5AzFN92NtpKG5siF0wfY95GZlo9sVCKE8QY8GGwqcH-oZ-nb59uvq3eL609X71fJ64bjW06IFaxmQ6rDvmaauo1wKJXTHnNDEgRTa9QMMTlkMihIutOyksrQjQye4ZWfozV53nLst9A7ilG0wY_Zbm-9Nst783Yl-Y9bpu2m5YLTFVeDFQSCnuxnKZLa-uDqCjZDmYijnVGKiOKvo83_Q2zTnWMerFKuuma7bPFJrG8D4OKT6rtuJmqXkhAmpJK_Uqz3lciolw3C0TLDZJWp2iZpDohV_9ueYR_hXfhV4uQc2Pvb2h_9POagMDPY3Xb8JVoL9BM4PsG8</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Lu, Baochun</creator><creator>Yu, Jianhua</creator><creator>Li, Jiandong</creator><creator>Wang, Yali</creator><creator>Cen, Wenda</creator><creator>Zhang, Weiguang</creator><creator>Tong, Chenhao</creator><creator>Lin, Weiguo</creator><creator>Zhu, Zhiyang</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</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>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6661-6647</orcidid><orcidid>https://orcid.org/0000-0001-8350-0227</orcidid></search><sort><creationdate>2020</creationdate><title>Silencing ARAF Suppresses the Malignant Phenotypes of Gallbladder Cancer Cells</title><author>Lu, Baochun ; Yu, Jianhua ; Li, Jiandong ; Wang, Yali ; Cen, Wenda ; Zhang, Weiguang ; Tong, Chenhao ; Lin, Weiguo ; Zhu, Zhiyang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-7eaa3e1314dd392cb2465859b3c591ce659cdfefc8a0e8214596b68a2b1fb54a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Biliary tract</topic><topic>Biotechnology</topic><topic>Bladder cancer</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Cancer cells</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Baochun</au><au>Yu, Jianhua</au><au>Li, Jiandong</au><au>Wang, Yali</au><au>Cen, Wenda</au><au>Zhang, Weiguang</au><au>Tong, Chenhao</au><au>Lin, Weiguo</au><au>Zhu, Zhiyang</au><au>Li, Kui</au><au>Kui Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Silencing ARAF Suppresses the Malignant Phenotypes of Gallbladder Cancer Cells</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2020</date><risdate>2020</risdate><volume>2020</volume><issue>2020</issue><spage>1</spage><epage>8</epage><pages>1-8</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>ARAF is a member of the RAF kinase family that is necessary for mitogen-activated protein kinase (MAPK) activation in various malignancies, including lung, colorectal, pancreatic, and breast cancers. As the most common biliary tract tumor, gallbladder cancer (GBC) seriously harms human health while the function of ARAF in GBC remains elusive. Here, we found that ARAF expression was upregulated in gallbladder cancer tissues. In vitro, ARAF silencing mediated by RNA interference effectively inhibited cell proliferation, colony formation, migration, and invasion of GBC cells. Moreover, knocking down ARAF suppressed tumor growth in vivo. Our results indicated that ARAF functions as an oncogene in GBC and, thus, could be a potential therapeutic target for GBC.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>32923479</pmid><doi>10.1155/2020/3235786</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-6661-6647</orcidid><orcidid>https://orcid.org/0000-0001-8350-0227</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antibodies Biliary tract Biotechnology Bladder cancer Breast cancer Cancer Cancer cells Cell growth Cell Line, Tumor Cell migration Cell Movement - genetics Cell proliferation Cell Proliferation - genetics Female Fluorides Gallbladder Gallbladder - pathology Gallbladder cancer Gallbladder Neoplasms - genetics Gallbladder Neoplasms - pathology Gene Expression Regulation, Neoplastic - genetics Genetic aspects Health aspects Hospitals Humans Kinases Laboratory animals Lung cancer Male MAP kinase MAP Kinase Signaling System - genetics Medical prognosis Metastasis Mice Mice, Nude Mutation Pancreas Phenotype Phenotypes Phosphotransferases Protein kinase Proteins raf Kinases - genetics Raf protein RNA-mediated interference Tumorigenesis Tumors Up-Regulation - genetics Wound healing |
| title | Silencing ARAF Suppresses the Malignant Phenotypes of Gallbladder Cancer Cells |
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