Down-regulation of circPVRL3 promotes the proliferation and migration of gastric cancer cells
Circular RNA (circRNA) is a key regulator in the development and progression of various types of carcinomas. However, its role in gastric cancer (GC) tumorigenesis is not well understood. The present study aimed to investigate the expression profile and potential modulation of circRNAs on GC carcino...
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description | Circular RNA (circRNA) is a key regulator in the development and progression of various types of carcinomas. However, its role in gastric cancer (GC) tumorigenesis is not well understood. The present study aimed to investigate the expression profile and potential modulation of circRNAs on GC carcinogenesis. Human circRNA microarray was performed to screen for abnormally expressed circRNA in GC tissue. Results showed that a decrease in the circPVRL3 expression level was associated with the presence of GC, and also with higher TNM stage and lower overall survival rates compared with that in adjacent noncancerous tissues.
In vitro
assays of the GC cell lines MKN-45 and MGC-803 demonstrated that knockdown of circPVRL3 promoted cell proliferation significantly. Prediction and annotation revealed circPVRL3 was able to sponge to 9 miRNAs and may be also able to have a binding with AGO2, FUS, LIN28A, PTB, and EIF4A3. In addition, based on the structure of internal ribosomal entry sites, open reading frame, and m
6
A modification, circPVRL3 may have the potential ability to encode proteins. Taken together, our study indicated that down-regulation of circPVRL3 could promote the proliferation in gastric carcinoma and have potential to encode protein. |
doi_str_mv | 10.1038/s41598-018-27837-9 |
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In vitro
assays of the GC cell lines MKN-45 and MGC-803 demonstrated that knockdown of circPVRL3 promoted cell proliferation significantly. Prediction and annotation revealed circPVRL3 was able to sponge to 9 miRNAs and may be also able to have a binding with AGO2, FUS, LIN28A, PTB, and EIF4A3. In addition, based on the structure of internal ribosomal entry sites, open reading frame, and m
6
A modification, circPVRL3 may have the potential ability to encode proteins. Taken together, our study indicated that down-regulation of circPVRL3 could promote the proliferation in gastric carcinoma and have potential to encode protein.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-018-27837-9</identifier><identifier>PMID: 29973643</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 14/105 ; 631/61/51/1844 ; 631/67/68 ; Argonaute 2 protein ; Carcinogenesis ; Carcinoma ; Cell migration ; Cell proliferation ; Circular RNA ; Gastric cancer ; Humanities and Social Sciences ; multidisciplinary ; N6-methyladenosine ; Ribonucleic acid ; RNA ; Science ; Science (multidisciplinary) ; Survival ; Tumorigenesis</subject><ispartof>Scientific reports, 2018-07, Vol.8 (1), p.10111-13, Article 10111</ispartof><rights>The Author(s) 2018</rights><rights>2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-db1d50f9bd583391d9c091020d450c8154966696f5447d14c602f7970e652fb63</citedby><cites>FETCH-LOGICAL-c474t-db1d50f9bd583391d9c091020d450c8154966696f5447d14c602f7970e652fb63</cites><orcidid>0000-0003-0297-3052</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/PMC6031698/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6031698/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29973643$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Han-Dong</creatorcontrib><creatorcontrib>Xu, Zhi-Peng</creatorcontrib><creatorcontrib>Sun, Zhi-Qiang</creatorcontrib><creatorcontrib>Zhu, Bin</creatorcontrib><creatorcontrib>Wang, Qian</creatorcontrib><creatorcontrib>Zhou, Jian</creatorcontrib><creatorcontrib>Jin, Hui</creatorcontrib><creatorcontrib>Zhao, Andi</creatorcontrib><creatorcontrib>Tang, Wei-Wei</creatorcontrib><creatorcontrib>Cao, Xiu-Feng</creatorcontrib><title>Down-regulation of circPVRL3 promotes the proliferation and migration of gastric cancer cells</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Circular RNA (circRNA) is a key regulator in the development and progression of various types of carcinomas. However, its role in gastric cancer (GC) tumorigenesis is not well understood. The present study aimed to investigate the expression profile and potential modulation of circRNAs on GC carcinogenesis. Human circRNA microarray was performed to screen for abnormally expressed circRNA in GC tissue. Results showed that a decrease in the circPVRL3 expression level was associated with the presence of GC, and also with higher TNM stage and lower overall survival rates compared with that in adjacent noncancerous tissues.
In vitro
assays of the GC cell lines MKN-45 and MGC-803 demonstrated that knockdown of circPVRL3 promoted cell proliferation significantly. Prediction and annotation revealed circPVRL3 was able to sponge to 9 miRNAs and may be also able to have a binding with AGO2, FUS, LIN28A, PTB, and EIF4A3. In addition, based on the structure of internal ribosomal entry sites, open reading frame, and m
6
A modification, circPVRL3 may have the potential ability to encode proteins. Taken together, our study indicated that down-regulation of circPVRL3 could promote the proliferation in gastric carcinoma and have potential to encode protein.</description><subject>13</subject><subject>14/105</subject><subject>631/61/51/1844</subject><subject>631/67/68</subject><subject>Argonaute 2 protein</subject><subject>Carcinogenesis</subject><subject>Carcinoma</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Circular RNA</subject><subject>Gastric cancer</subject><subject>Humanities and Social Sciences</subject><subject>multidisciplinary</subject><subject>N6-methyladenosine</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Survival</subject><subject>Tumorigenesis</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kU9P3DAQxS0EKgj4Aj2gSFy4pB3_jy9ICAqttBKoanurLK_jBKPEXuyEim9PltAtcKgvtjW_eTNPD6GPGD5hoNXnzDBXVQm4KomsqCzVFtojwHhJKCHbr9676DDnO5gOJ4ph9QHtEqUkFYzuod8X8U8ok2vHzgw-hiI2hfXJ3vz6vqDFKsU-Di4Xw61bfzrfuDRzJtRF79u06WpNHpK3hTXBulRY13X5AO00psvu8OXeRz8vv_w4_1ourq--nZ8tSsskG8p6iWsOjVrWvKJU4VpZUBgI1IyDrTBnSgihRMMZkzVmVgBppJLgBCfNUtB9dDrrrsZl72rrwpBMp1fJ9yY96mi8flsJ_la38UELoFioahI4eRFI8X50edC9z2sLJrg4Zk1AMCk5UDmhx-_QuzimMNl7pggFLtcbkZmyKeacXLNZBoNeB6jnAPUUoH4OUKup6ei1jU3L37gmgM5Ankqhdenf7P_IPgEI3KYB</recordid><startdate>20180704</startdate><enddate>20180704</enddate><creator>Sun, Han-Dong</creator><creator>Xu, Zhi-Peng</creator><creator>Sun, Zhi-Qiang</creator><creator>Zhu, Bin</creator><creator>Wang, Qian</creator><creator>Zhou, Jian</creator><creator>Jin, Hui</creator><creator>Zhao, Andi</creator><creator>Tang, Wei-Wei</creator><creator>Cao, Xiu-Feng</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</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>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-0297-3052</orcidid></search><sort><creationdate>20180704</creationdate><title>Down-regulation of circPVRL3 promotes the proliferation and migration of gastric cancer cells</title><author>Sun, Han-Dong ; Xu, Zhi-Peng ; Sun, Zhi-Qiang ; Zhu, Bin ; Wang, Qian ; Zhou, Jian ; Jin, Hui ; Zhao, Andi ; Tang, Wei-Wei ; Cao, Xiu-Feng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-db1d50f9bd583391d9c091020d450c8154966696f5447d14c602f7970e652fb63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>13</topic><topic>14/105</topic><topic>631/61/51/1844</topic><topic>631/67/68</topic><topic>Argonaute 2 protein</topic><topic>Carcinogenesis</topic><topic>Carcinoma</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Circular RNA</topic><topic>Gastric cancer</topic><topic>Humanities and Social Sciences</topic><topic>multidisciplinary</topic><topic>N6-methyladenosine</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Survival</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sun, Han-Dong</creatorcontrib><creatorcontrib>Xu, Zhi-Peng</creatorcontrib><creatorcontrib>Sun, Zhi-Qiang</creatorcontrib><creatorcontrib>Zhu, Bin</creatorcontrib><creatorcontrib>Wang, Qian</creatorcontrib><creatorcontrib>Zhou, Jian</creatorcontrib><creatorcontrib>Jin, Hui</creatorcontrib><creatorcontrib>Zhao, Andi</creatorcontrib><creatorcontrib>Tang, Wei-Wei</creatorcontrib><creatorcontrib>Cao, Xiu-Feng</creatorcontrib><collection>Springer Nature OA Free Journals</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>Medical 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 Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>Medical Database</collection><collection>Science Database</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, Han-Dong</au><au>Xu, Zhi-Peng</au><au>Sun, Zhi-Qiang</au><au>Zhu, Bin</au><au>Wang, Qian</au><au>Zhou, Jian</au><au>Jin, Hui</au><au>Zhao, Andi</au><au>Tang, Wei-Wei</au><au>Cao, Xiu-Feng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Down-regulation of circPVRL3 promotes the proliferation and migration of gastric cancer cells</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2018-07-04</date><risdate>2018</risdate><volume>8</volume><issue>1</issue><spage>10111</spage><epage>13</epage><pages>10111-13</pages><artnum>10111</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Circular RNA (circRNA) is a key regulator in the development and progression of various types of carcinomas. However, its role in gastric cancer (GC) tumorigenesis is not well understood. The present study aimed to investigate the expression profile and potential modulation of circRNAs on GC carcinogenesis. Human circRNA microarray was performed to screen for abnormally expressed circRNA in GC tissue. Results showed that a decrease in the circPVRL3 expression level was associated with the presence of GC, and also with higher TNM stage and lower overall survival rates compared with that in adjacent noncancerous tissues.
In vitro
assays of the GC cell lines MKN-45 and MGC-803 demonstrated that knockdown of circPVRL3 promoted cell proliferation significantly. Prediction and annotation revealed circPVRL3 was able to sponge to 9 miRNAs and may be also able to have a binding with AGO2, FUS, LIN28A, PTB, and EIF4A3. In addition, based on the structure of internal ribosomal entry sites, open reading frame, and m
6
A modification, circPVRL3 may have the potential ability to encode proteins. Taken together, our study indicated that down-regulation of circPVRL3 could promote the proliferation in gastric carcinoma and have potential to encode protein.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29973643</pmid><doi>10.1038/s41598-018-27837-9</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-0297-3052</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | 13 14/105 631/61/51/1844 631/67/68 Argonaute 2 protein Carcinogenesis Carcinoma Cell migration Cell proliferation Circular RNA Gastric cancer Humanities and Social Sciences multidisciplinary N6-methyladenosine Ribonucleic acid RNA Science Science (multidisciplinary) Survival Tumorigenesis |
title | Down-regulation of circPVRL3 promotes the proliferation and migration of gastric cancer cells |
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