miR-326 Inhibits Gastric Cancer Cell Growth Through Downregulating NOB1
MicroRNAs (miRNAs) play a crucial role in the development and progression of human cancers, including gastric cancer (GC). The discovery of miRNAs may provide a new and powerful tool for studying the mechanism, diagnosis, and treatment of GC. In this study, we aimed to investigate the role of miR-32...
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| Veröffentlicht in: | Oncology research 2017-07, Vol.25 (6), p.853-861 |
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| creator | Ji, Sheqing Zhang, Bin Kong, Ye Ma, Fei Hua, Yawei |
| description | MicroRNAs (miRNAs) play a crucial role in the development and progression of human cancers, including gastric cancer (GC). The discovery of miRNAs may provide a new and powerful tool for studying the mechanism, diagnosis, and treatment of GC. In this study, we aimed to investigate the
role of miR-326 in the development and progression of GC. Quantitative PCR (qPCR) was used to measure the expression level of miR-326 in GC tissues and cell lines. We found that miR-326 was significantly downregulated during GC. In addition, overexpression of miR-326 inhibited GC cell proliferation.
Fluorescence-activated cell sorting (FACS) further showed that miR-326 significantly induced GC cell G2/M arrest. Subsequent dual-luciferase reporter assay identified one of the proto-oncogene NOB1 as a direct target of miR-326, and NOB1 can save growth inhibition caused by miR-326.
We also confirmed that the growth inhibition caused by miR-326 is associated with AKT pathway activation. Taken together, our results indicate that miR-326 could serve as a potential diagnostic biomarker and therapeutic option for GC in the near future. |
| doi_str_mv | 10.3727/096504016X14759582767486 |
| format | Article |
| fullrecord | <record><control><sourceid>pubtec_cross</sourceid><recordid>TN_cdi_crossref_primary_10_3727_096504016X14759582767486</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><ingid>cog/or/2017/00000025/00000006/art00001</ingid><sourcerecordid>cog/or/2017/00000025/00000006/art00001</sourcerecordid><originalsourceid>FETCH-LOGICAL-c545t-9d6c1b2a536b00fdea60f3c557a41068eda44f37ab881b304af91fda28e564c93</originalsourceid><addsrcrecordid>eNp1kU1v1DAQhi0EokvhL6AcuQQ8_s4FCbawVCpUQkXiZjmOk7jKxsV2WtFfXy-7LSCELx5p3nlm5h2EKsCvqSTyDW4ExwyD-A5M8oYrIoVkSjxCK-Cc17TB4jFa7WR10ckj9CylS4wJk6x5io6IlJQSYCu02fqvNSWiOp1H3_qcqo1JOXpbrc1sXazWbpqqTQw3eawuxhiWYaxOws0c3bBMJvt5qL6cv4fn6ElvpuReHP5j9O3jh4v1p_rsfHO6fndWW854rptOWGiJ4VS0GPedMwL31HIuDQMslOsMYz2VplUKWoqZ6RvoO0OU44LZhh6jt3vu1dJuXWfdnKOZ9FX0WxN_6mC8_jsz-1EP4VpLxQAwL4BXB0AMPxaXst76ZMuSZnZhSRoU5Qw3jEGRqr3UxpBSdP1DG8B6dwf9vzuU0pd_jvlQeG98EXzeC4qBZVKjL8MS5-Kc9lbbMNyjpb4mfBaaYAJYlb5lB6w715tlyjqbqIdbneC3L__wdrAQCwDKvL8e4YcAC21i3gVA7wBgjLAw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1835409441</pqid></control><display><type>article</type><title>miR-326 Inhibits Gastric Cancer Cell Growth Through Downregulating NOB1</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central Open Access</source><source>IngentaConnect Free/Open Access Journals</source><source>PubMed Central</source><creator>Ji, Sheqing ; Zhang, Bin ; Kong, Ye ; Ma, Fei ; Hua, Yawei</creator><creatorcontrib>Ji, Sheqing ; Zhang, Bin ; Kong, Ye ; Ma, Fei ; Hua, Yawei</creatorcontrib><description>MicroRNAs (miRNAs) play a crucial role in the development and progression of human cancers, including gastric cancer (GC). The discovery of miRNAs may provide a new and powerful tool for studying the mechanism, diagnosis, and treatment of GC. In this study, we aimed to investigate the
role of miR-326 in the development and progression of GC. Quantitative PCR (qPCR) was used to measure the expression level of miR-326 in GC tissues and cell lines. We found that miR-326 was significantly downregulated during GC. In addition, overexpression of miR-326 inhibited GC cell proliferation.
Fluorescence-activated cell sorting (FACS) further showed that miR-326 significantly induced GC cell G2/M arrest. Subsequent dual-luciferase reporter assay identified one of the proto-oncogene NOB1 as a direct target of miR-326, and NOB1 can save growth inhibition caused by miR-326.
We also confirmed that the growth inhibition caused by miR-326 is associated with AKT pathway activation. Taken together, our results indicate that miR-326 could serve as a potential diagnostic biomarker and therapeutic option for GC in the near future.</description><identifier>ISSN: 0965-0407</identifier><identifier>EISSN: 1555-3906</identifier><identifier>DOI: 10.3727/096504016X14759582767486</identifier><identifier>PMID: 27733214</identifier><language>eng</language><publisher>Elmsford, NY: Cognizant Communication Corporation</publisher><subject>Akt ; Cell Cycle ; Cell Cycle Checkpoints - genetics ; Cell Line, Tumor ; Cell Proliferation - genetics ; Down-Regulation - genetics ; Gastric Cancer (gc) ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs - genetics ; Mir-326 ; Nob1 ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Proliferation ; Proto-Oncogene Proteins c-akt - metabolism ; RNA-Binding Proteins - genetics ; RNA-Binding Proteins - metabolism ; Stomach Neoplasms - genetics ; Stomach Neoplasms - metabolism ; Stomach Neoplasms - pathology</subject><ispartof>Oncology research, 2017-07, Vol.25 (6), p.853-861</ispartof><rights>Copyright © 2017 Cognizant, LLC. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c545t-9d6c1b2a536b00fdea60f3c557a41068eda44f37ab881b304af91fda28e564c93</citedby><cites>FETCH-LOGICAL-c545t-9d6c1b2a536b00fdea60f3c557a41068eda44f37ab881b304af91fda28e564c93</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/PMC7841105/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7841105/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,288,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27733214$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ji, Sheqing</creatorcontrib><creatorcontrib>Zhang, Bin</creatorcontrib><creatorcontrib>Kong, Ye</creatorcontrib><creatorcontrib>Ma, Fei</creatorcontrib><creatorcontrib>Hua, Yawei</creatorcontrib><title>miR-326 Inhibits Gastric Cancer Cell Growth Through Downregulating NOB1</title><title>Oncology research</title><addtitle>Oncol Res</addtitle><description>MicroRNAs (miRNAs) play a crucial role in the development and progression of human cancers, including gastric cancer (GC). The discovery of miRNAs may provide a new and powerful tool for studying the mechanism, diagnosis, and treatment of GC. In this study, we aimed to investigate the
role of miR-326 in the development and progression of GC. Quantitative PCR (qPCR) was used to measure the expression level of miR-326 in GC tissues and cell lines. We found that miR-326 was significantly downregulated during GC. In addition, overexpression of miR-326 inhibited GC cell proliferation.
Fluorescence-activated cell sorting (FACS) further showed that miR-326 significantly induced GC cell G2/M arrest. Subsequent dual-luciferase reporter assay identified one of the proto-oncogene NOB1 as a direct target of miR-326, and NOB1 can save growth inhibition caused by miR-326.
We also confirmed that the growth inhibition caused by miR-326 is associated with AKT pathway activation. Taken together, our results indicate that miR-326 could serve as a potential diagnostic biomarker and therapeutic option for GC in the near future.</description><subject>Akt</subject><subject>Cell Cycle</subject><subject>Cell Cycle Checkpoints - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Down-Regulation - genetics</subject><subject>Gastric Cancer (gc)</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>MicroRNAs - genetics</subject><subject>Mir-326</subject><subject>Nob1</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Proliferation</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>RNA-Binding Proteins - genetics</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Stomach Neoplasms - pathology</subject><issn>0965-0407</issn><issn>1555-3906</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU1v1DAQhi0EokvhL6AcuQQ8_s4FCbawVCpUQkXiZjmOk7jKxsV2WtFfXy-7LSCELx5p3nlm5h2EKsCvqSTyDW4ExwyD-A5M8oYrIoVkSjxCK-Cc17TB4jFa7WR10ckj9CylS4wJk6x5io6IlJQSYCu02fqvNSWiOp1H3_qcqo1JOXpbrc1sXazWbpqqTQw3eawuxhiWYaxOws0c3bBMJvt5qL6cv4fn6ElvpuReHP5j9O3jh4v1p_rsfHO6fndWW854rptOWGiJ4VS0GPedMwL31HIuDQMslOsMYz2VplUKWoqZ6RvoO0OU44LZhh6jt3vu1dJuXWfdnKOZ9FX0WxN_6mC8_jsz-1EP4VpLxQAwL4BXB0AMPxaXst76ZMuSZnZhSRoU5Qw3jEGRqr3UxpBSdP1DG8B6dwf9vzuU0pd_jvlQeG98EXzeC4qBZVKjL8MS5-Kc9lbbMNyjpb4mfBaaYAJYlb5lB6w715tlyjqbqIdbneC3L__wdrAQCwDKvL8e4YcAC21i3gVA7wBgjLAw</recordid><startdate>20170705</startdate><enddate>20170705</enddate><creator>Ji, Sheqing</creator><creator>Zhang, Bin</creator><creator>Kong, Ye</creator><creator>Ma, Fei</creator><creator>Hua, Yawei</creator><general>Cognizant Communication Corporation</general><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170705</creationdate><title>miR-326 Inhibits Gastric Cancer Cell Growth Through Downregulating NOB1</title><author>Ji, Sheqing ; Zhang, Bin ; Kong, Ye ; Ma, Fei ; Hua, Yawei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c545t-9d6c1b2a536b00fdea60f3c557a41068eda44f37ab881b304af91fda28e564c93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Akt</topic><topic>Cell Cycle</topic><topic>Cell Cycle Checkpoints - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Down-Regulation - genetics</topic><topic>Gastric Cancer (gc)</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>MicroRNAs - genetics</topic><topic>Mir-326</topic><topic>Nob1</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Proliferation</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>RNA-Binding Proteins - genetics</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Stomach Neoplasms - pathology</topic><toplevel>online_resources</toplevel><creatorcontrib>Ji, Sheqing</creatorcontrib><creatorcontrib>Zhang, Bin</creatorcontrib><creatorcontrib>Kong, Ye</creatorcontrib><creatorcontrib>Ma, Fei</creatorcontrib><creatorcontrib>Hua, Yawei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ji, Sheqing</au><au>Zhang, Bin</au><au>Kong, Ye</au><au>Ma, Fei</au><au>Hua, Yawei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-326 Inhibits Gastric Cancer Cell Growth Through Downregulating NOB1</atitle><jtitle>Oncology research</jtitle><addtitle>Oncol Res</addtitle><date>2017-07-05</date><risdate>2017</risdate><volume>25</volume><issue>6</issue><spage>853</spage><epage>861</epage><pages>853-861</pages><issn>0965-0407</issn><eissn>1555-3906</eissn><abstract>MicroRNAs (miRNAs) play a crucial role in the development and progression of human cancers, including gastric cancer (GC). The discovery of miRNAs may provide a new and powerful tool for studying the mechanism, diagnosis, and treatment of GC. In this study, we aimed to investigate the
role of miR-326 in the development and progression of GC. Quantitative PCR (qPCR) was used to measure the expression level of miR-326 in GC tissues and cell lines. We found that miR-326 was significantly downregulated during GC. In addition, overexpression of miR-326 inhibited GC cell proliferation.
Fluorescence-activated cell sorting (FACS) further showed that miR-326 significantly induced GC cell G2/M arrest. Subsequent dual-luciferase reporter assay identified one of the proto-oncogene NOB1 as a direct target of miR-326, and NOB1 can save growth inhibition caused by miR-326.
We also confirmed that the growth inhibition caused by miR-326 is associated with AKT pathway activation. Taken together, our results indicate that miR-326 could serve as a potential diagnostic biomarker and therapeutic option for GC in the near future.</abstract><cop>Elmsford, NY</cop><pub>Cognizant Communication Corporation</pub><pmid>27733214</pmid><doi>10.3727/096504016X14759582767486</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; IngentaConnect Free/Open Access Journals; PubMed Central |
| subjects | Akt Cell Cycle Cell Cycle Checkpoints - genetics Cell Line, Tumor Cell Proliferation - genetics Down-Regulation - genetics Gastric Cancer (gc) Gene Expression Regulation, Neoplastic Humans MicroRNAs - genetics Mir-326 Nob1 Nuclear Proteins - genetics Nuclear Proteins - metabolism Proliferation Proto-Oncogene Proteins c-akt - metabolism RNA-Binding Proteins - genetics RNA-Binding Proteins - metabolism Stomach Neoplasms - genetics Stomach Neoplasms - metabolism Stomach Neoplasms - pathology |
| title | miR-326 Inhibits Gastric Cancer Cell Growth Through Downregulating NOB1 |
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