RANBP9 suppresses tumor proliferation in colorectal cancer
RAN binding protein 9 (RANBP9) is widely expressed in mammalian tissues, including osteosarcoma, lung, gastric and breast cancer tissues. However, currently, not much is known about the role of RANBP9 in colorectal cancer (CRC). In the present study, RANBP9 expression in CRC tissues and cell lines w...
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| Veröffentlicht in: | Oncology letters 2019-05, Vol.17 (5), p.4409-4416 |
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| creator | Qin, Chunzhi Zhang, Qin Wu, Guangbin |
| description | RAN binding protein 9 (RANBP9) is widely expressed in mammalian tissues, including osteosarcoma, lung, gastric and breast cancer tissues. However, currently, not much is known about the role of RANBP9 in colorectal cancer (CRC). In the present study, RANBP9 expression in CRC tissues and cell lines was measured by immunohistochemistry and western blotting, respectively. Subsequently,
-short hairpin RNA (shRNA) and
plasmids were constructed and transfected into HCT116 and HT29 cells. The effects of RANBP9 knockdown were assessed by Cell Counting kit-8 and colony formation assays, and its effects on tumorigenicity in a nude mouse animal model were investigated. The effect of
-shRNA on cell cycle progression was analyzed by flow cytometry, while cell cycle-associated protein expression levels were examined by western blotting. Compared with in paired normal mucosa, RANBP9 was overexpressed in CRC tissues. Inhibition of RANBP9 in HCT116 and HT29 cells significantly promoted cell growth, colony formation and S phase transition, and increased tumorigenesis
. Accordingly, RANBP9 overexpression inhibited cell growth and colony formation. Knockdown of
was associated with upregulated cyclin A2 in the two cell lines. In conclusion, RANBP9 served an inhibitory role in CRC
and
. Therefore, RANBP9 may be considered a potential target for treatment of CRC. |
| doi_str_mv | 10.3892/ol.2019.10134 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6447939</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A583999508</galeid><sourcerecordid>A583999508</sourcerecordid><originalsourceid>FETCH-LOGICAL-c513t-c3615ceaf1c5759147c6198c9292972836a122779a968cf82cf885d76382730f3</originalsourceid><addsrcrecordid>eNptkttrFDEUxoNU2lL72FcZKJS-zJrL5NYHYVu8QVERfQ4xe6abkknGZKbgf2_WrWtXzCGckPzOF3LyIXRG8IIpTV-lsKCY6AXBhHXP0DGRmrYEK3qwW8vuCJ2Wco_r4IIoJQ7REcNaKUXIMbr6svx4_Vk3ZR7HDKVAaaZ5SLkZcwq-h2wnn2LjY-NSSBncZEPjbHSQX6DnvQ0FTh_zCfr29s3Xm_ft7ad3H26Wt63jhE2tY4JwB7YnjkuuSSedIFo5TWtIqpiwhFIptdVCuV7ROhVfScEUlQz37AS93uqO8_cBVg7ilG0wY_aDzT9Nst7sn0S_NnfpwYiuk5rpKnD5KJDTjxnKZAZfHIRgI6S5GEoJppxrKSt6_g96n-Yc6_O2lBRU8L_UnQ1gfOxTvddtRM2SK6a15lhVavEfqsYKBu9ShN7X_b2CiycFa7BhWpcU5s0PlH2w3YIup1Iy9LtmEGw2xjApmI0xzG9jVP7l0w7u6D82YL8AoMWvSw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2210276265</pqid></control><display><type>article</type><title>RANBP9 suppresses tumor proliferation in colorectal cancer</title><source>Spandidos Publications Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Qin, Chunzhi ; Zhang, Qin ; Wu, Guangbin</creator><creatorcontrib>Qin, Chunzhi ; Zhang, Qin ; Wu, Guangbin</creatorcontrib><description>RAN binding protein 9 (RANBP9) is widely expressed in mammalian tissues, including osteosarcoma, lung, gastric and breast cancer tissues. However, currently, not much is known about the role of RANBP9 in colorectal cancer (CRC). In the present study, RANBP9 expression in CRC tissues and cell lines was measured by immunohistochemistry and western blotting, respectively. Subsequently,
-short hairpin RNA (shRNA) and
plasmids were constructed and transfected into HCT116 and HT29 cells. The effects of RANBP9 knockdown were assessed by Cell Counting kit-8 and colony formation assays, and its effects on tumorigenicity in a nude mouse animal model were investigated. The effect of
-shRNA on cell cycle progression was analyzed by flow cytometry, while cell cycle-associated protein expression levels were examined by western blotting. Compared with in paired normal mucosa, RANBP9 was overexpressed in CRC tissues. Inhibition of RANBP9 in HCT116 and HT29 cells significantly promoted cell growth, colony formation and S phase transition, and increased tumorigenesis
. Accordingly, RANBP9 overexpression inhibited cell growth and colony formation. Knockdown of
was associated with upregulated cyclin A2 in the two cell lines. In conclusion, RANBP9 served an inhibitory role in CRC
and
. Therefore, RANBP9 may be considered a potential target for treatment of CRC.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2019.10134</identifier><identifier>PMID: 30988811</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Alzheimer's disease ; Breast cancer ; Cancer research ; Cell cycle ; Cell division ; Cell growth ; Colorectal cancer ; EDTA ; Growth factors ; Immunohistochemistry ; Kinases ; Medical prognosis ; Oncology ; Osteosarcoma ; Phase transitions ; Plasmids ; Protein binding ; Proteins ; RNA ; Signal transduction ; Tumors</subject><ispartof>Oncology letters, 2019-05, Vol.17 (5), p.4409-4416</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><rights>Copyright: © Qin et al. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c513t-c3615ceaf1c5759147c6198c9292972836a122779a968cf82cf885d76382730f3</citedby><cites>FETCH-LOGICAL-c513t-c3615ceaf1c5759147c6198c9292972836a122779a968cf82cf885d76382730f3</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/PMC6447939/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6447939/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30988811$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qin, Chunzhi</creatorcontrib><creatorcontrib>Zhang, Qin</creatorcontrib><creatorcontrib>Wu, Guangbin</creatorcontrib><title>RANBP9 suppresses tumor proliferation in colorectal cancer</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>RAN binding protein 9 (RANBP9) is widely expressed in mammalian tissues, including osteosarcoma, lung, gastric and breast cancer tissues. However, currently, not much is known about the role of RANBP9 in colorectal cancer (CRC). In the present study, RANBP9 expression in CRC tissues and cell lines was measured by immunohistochemistry and western blotting, respectively. Subsequently,
-short hairpin RNA (shRNA) and
plasmids were constructed and transfected into HCT116 and HT29 cells. The effects of RANBP9 knockdown were assessed by Cell Counting kit-8 and colony formation assays, and its effects on tumorigenicity in a nude mouse animal model were investigated. The effect of
-shRNA on cell cycle progression was analyzed by flow cytometry, while cell cycle-associated protein expression levels were examined by western blotting. Compared with in paired normal mucosa, RANBP9 was overexpressed in CRC tissues. Inhibition of RANBP9 in HCT116 and HT29 cells significantly promoted cell growth, colony formation and S phase transition, and increased tumorigenesis
. Accordingly, RANBP9 overexpression inhibited cell growth and colony formation. Knockdown of
was associated with upregulated cyclin A2 in the two cell lines. In conclusion, RANBP9 served an inhibitory role in CRC
and
. Therefore, RANBP9 may be considered a potential target for treatment of CRC.</description><subject>Alzheimer's disease</subject><subject>Breast cancer</subject><subject>Cancer research</subject><subject>Cell cycle</subject><subject>Cell division</subject><subject>Cell growth</subject><subject>Colorectal cancer</subject><subject>EDTA</subject><subject>Growth factors</subject><subject>Immunohistochemistry</subject><subject>Kinases</subject><subject>Medical prognosis</subject><subject>Oncology</subject><subject>Osteosarcoma</subject><subject>Phase transitions</subject><subject>Plasmids</subject><subject>Protein binding</subject><subject>Proteins</subject><subject>RNA</subject><subject>Signal transduction</subject><subject>Tumors</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkttrFDEUxoNU2lL72FcZKJS-zJrL5NYHYVu8QVERfQ4xe6abkknGZKbgf2_WrWtXzCGckPzOF3LyIXRG8IIpTV-lsKCY6AXBhHXP0DGRmrYEK3qwW8vuCJ2Wco_r4IIoJQ7REcNaKUXIMbr6svx4_Vk3ZR7HDKVAaaZ5SLkZcwq-h2wnn2LjY-NSSBncZEPjbHSQX6DnvQ0FTh_zCfr29s3Xm_ft7ad3H26Wt63jhE2tY4JwB7YnjkuuSSedIFo5TWtIqpiwhFIptdVCuV7ROhVfScEUlQz37AS93uqO8_cBVg7ilG0wY_aDzT9Nst7sn0S_NnfpwYiuk5rpKnD5KJDTjxnKZAZfHIRgI6S5GEoJppxrKSt6_g96n-Yc6_O2lBRU8L_UnQ1gfOxTvddtRM2SK6a15lhVavEfqsYKBu9ShN7X_b2CiycFa7BhWpcU5s0PlH2w3YIup1Iy9LtmEGw2xjApmI0xzG9jVP7l0w7u6D82YL8AoMWvSw</recordid><startdate>20190501</startdate><enddate>20190501</enddate><creator>Qin, Chunzhi</creator><creator>Zhang, Qin</creator><creator>Wu, Guangbin</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190501</creationdate><title>RANBP9 suppresses tumor proliferation in colorectal cancer</title><author>Qin, Chunzhi ; Zhang, Qin ; Wu, Guangbin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c513t-c3615ceaf1c5759147c6198c9292972836a122779a968cf82cf885d76382730f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Alzheimer's disease</topic><topic>Breast cancer</topic><topic>Cancer research</topic><topic>Cell cycle</topic><topic>Cell division</topic><topic>Cell growth</topic><topic>Colorectal cancer</topic><topic>EDTA</topic><topic>Growth factors</topic><topic>Immunohistochemistry</topic><topic>Kinases</topic><topic>Medical prognosis</topic><topic>Oncology</topic><topic>Osteosarcoma</topic><topic>Phase transitions</topic><topic>Plasmids</topic><topic>Protein binding</topic><topic>Proteins</topic><topic>RNA</topic><topic>Signal transduction</topic><topic>Tumors</topic><toplevel>online_resources</toplevel><creatorcontrib>Qin, Chunzhi</creatorcontrib><creatorcontrib>Zhang, Qin</creatorcontrib><creatorcontrib>Wu, Guangbin</creatorcontrib><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>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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>PubMed Central (Full Participant titles)</collection><jtitle>Oncology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qin, Chunzhi</au><au>Zhang, Qin</au><au>Wu, Guangbin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RANBP9 suppresses tumor proliferation in colorectal cancer</atitle><jtitle>Oncology letters</jtitle><addtitle>Oncol Lett</addtitle><date>2019-05-01</date><risdate>2019</risdate><volume>17</volume><issue>5</issue><spage>4409</spage><epage>4416</epage><pages>4409-4416</pages><issn>1792-1074</issn><eissn>1792-1082</eissn><abstract>RAN binding protein 9 (RANBP9) is widely expressed in mammalian tissues, including osteosarcoma, lung, gastric and breast cancer tissues. However, currently, not much is known about the role of RANBP9 in colorectal cancer (CRC). In the present study, RANBP9 expression in CRC tissues and cell lines was measured by immunohistochemistry and western blotting, respectively. Subsequently,
-short hairpin RNA (shRNA) and
plasmids were constructed and transfected into HCT116 and HT29 cells. The effects of RANBP9 knockdown were assessed by Cell Counting kit-8 and colony formation assays, and its effects on tumorigenicity in a nude mouse animal model were investigated. The effect of
-shRNA on cell cycle progression was analyzed by flow cytometry, while cell cycle-associated protein expression levels were examined by western blotting. Compared with in paired normal mucosa, RANBP9 was overexpressed in CRC tissues. Inhibition of RANBP9 in HCT116 and HT29 cells significantly promoted cell growth, colony formation and S phase transition, and increased tumorigenesis
. Accordingly, RANBP9 overexpression inhibited cell growth and colony formation. Knockdown of
was associated with upregulated cyclin A2 in the two cell lines. In conclusion, RANBP9 served an inhibitory role in CRC
and
. Therefore, RANBP9 may be considered a potential target for treatment of CRC.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30988811</pmid><doi>10.3892/ol.2019.10134</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Alzheimer's disease Breast cancer Cancer research Cell cycle Cell division Cell growth Colorectal cancer EDTA Growth factors Immunohistochemistry Kinases Medical prognosis Oncology Osteosarcoma Phase transitions Plasmids Protein binding Proteins RNA Signal transduction Tumors |
| title | RANBP9 suppresses tumor proliferation in colorectal cancer |
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