miR‐124 interacts with the Notch1 signalling pathway and has therapeutic potential against gastric cancer
Aberrant Notch signalling plays an important role in cancer progression. However, little is known about the interaction between miRNA and the Notch signalling pathway and its role in gastric cancer (GC). In this study, we found that miR‐124 was down‐regulated in GC compared with adjacent normal tiss...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2016-02, Vol.20 (2), p.313-322 |
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| creator | Jiang, Lei Lin, Tiesu Xu, Chaochao Hu, Sunkuan Pan, Yangyang Jin, Rong |
| description | Aberrant Notch signalling plays an important role in cancer progression. However, little is known about the interaction between miRNA and the Notch signalling pathway and its role in gastric cancer (GC). In this study, we found that miR‐124 was down‐regulated in GC compared with adjacent normal tissue. Forced expression of miR‐124 inhibited GC cell growth, migration and invasion, and induced cell cycle arrest. miR‐124 negatively regulated Notch1 signalling by targeting JAG1. miR‐124 levels were also shown to be inversely correlated with JAG1 expression in GC. Furthermore, we found that the overexpression of the intracellular domain of Notch1 repressed miR‐124 expression, promoted GC cell growth, migration and invasion. Conversely, blocking Notch1 using a γ‐secretase inhibitor up‐regulated miR‐124 expression, inhibited GC cell growth, migration and invasion. In conclusion, our data demonstrates a regulatory feedback loop between miR‐124 and Notch1 signalling in GC cells, suggesting that the miR‐124/Notch axis may be a potential therapeutic target against GC. |
| doi_str_mv | 10.1111/jcmm.12724 |
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However, little is known about the interaction between miRNA and the Notch signalling pathway and its role in gastric cancer (GC). In this study, we found that miR‐124 was down‐regulated in GC compared with adjacent normal tissue. Forced expression of miR‐124 inhibited GC cell growth, migration and invasion, and induced cell cycle arrest. miR‐124 negatively regulated Notch1 signalling by targeting JAG1. miR‐124 levels were also shown to be inversely correlated with JAG1 expression in GC. Furthermore, we found that the overexpression of the intracellular domain of Notch1 repressed miR‐124 expression, promoted GC cell growth, migration and invasion. Conversely, blocking Notch1 using a γ‐secretase inhibitor up‐regulated miR‐124 expression, inhibited GC cell growth, migration and invasion. In conclusion, our data demonstrates a regulatory feedback loop between miR‐124 and Notch1 signalling in GC cells, suggesting that the miR‐124/Notch axis may be a potential therapeutic target against GC.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.12724</identifier><identifier>PMID: 26612211</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Adult ; Aged ; Amyloid Precursor Protein Secretases - genetics ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation - genetics ; Down-Regulation - genetics ; Feedback ; Female ; Gastric cancer ; Gene Expression Regulation, Neoplastic - genetics ; Humans ; intracellular domain of Notch1 ; JAG1 ; Male ; MicroRNAs - genetics ; Middle Aged ; miRNA ; miR‐124 ; Notch1 ; Notch1 protein ; Original ; Receptor, Notch1 - genetics ; Secretase ; Signal transduction ; Signal Transduction - genetics ; Stomach Neoplasms - genetics ; Up-Regulation - genetics</subject><ispartof>Journal of cellular and molecular medicine, 2016-02, Vol.20 (2), p.313-322</ispartof><rights>2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2016. 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-c4484-6635c5ecf5ec1bcc0ba059ab9df0cfd18892514c3b29e40381f8f144064eaa183</citedby><cites>FETCH-LOGICAL-c4484-6635c5ecf5ec1bcc0ba059ab9df0cfd18892514c3b29e40381f8f144064eaa183</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/PMC4727557/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4727557/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26612211$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Lei</creatorcontrib><creatorcontrib>Lin, Tiesu</creatorcontrib><creatorcontrib>Xu, Chaochao</creatorcontrib><creatorcontrib>Hu, Sunkuan</creatorcontrib><creatorcontrib>Pan, Yangyang</creatorcontrib><creatorcontrib>Jin, Rong</creatorcontrib><title>miR‐124 interacts with the Notch1 signalling pathway and has therapeutic potential against gastric cancer</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Aberrant Notch signalling plays an important role in cancer progression. However, little is known about the interaction between miRNA and the Notch signalling pathway and its role in gastric cancer (GC). In this study, we found that miR‐124 was down‐regulated in GC compared with adjacent normal tissue. Forced expression of miR‐124 inhibited GC cell growth, migration and invasion, and induced cell cycle arrest. miR‐124 negatively regulated Notch1 signalling by targeting JAG1. miR‐124 levels were also shown to be inversely correlated with JAG1 expression in GC. Furthermore, we found that the overexpression of the intracellular domain of Notch1 repressed miR‐124 expression, promoted GC cell growth, migration and invasion. Conversely, blocking Notch1 using a γ‐secretase inhibitor up‐regulated miR‐124 expression, inhibited GC cell growth, migration and invasion. In conclusion, our data demonstrates a regulatory feedback loop between miR‐124 and Notch1 signalling in GC cells, suggesting that the miR‐124/Notch axis may be a potential therapeutic target against GC.</description><subject>Adult</subject><subject>Aged</subject><subject>Amyloid Precursor Protein Secretases - genetics</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Down-Regulation - genetics</subject><subject>Feedback</subject><subject>Female</subject><subject>Gastric cancer</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Humans</subject><subject>intracellular domain of Notch1</subject><subject>JAG1</subject><subject>Male</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>miRNA</subject><subject>miR‐124</subject><subject>Notch1</subject><subject>Notch1 protein</subject><subject>Original</subject><subject>Receptor, Notch1 - genetics</subject><subject>Secretase</subject><subject>Signal transduction</subject><subject>Signal Transduction - genetics</subject><subject>Stomach Neoplasms - genetics</subject><subject>Up-Regulation - genetics</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kd9qFDEUxoNYbK3e-AAS8EYKW3MymczkRpDFqqVVEL0OZ7KZmazzr0nGZe98BJ_RJzHb3Rb1wkBI4Pz4-M73EfIM2Dmk82pt-v4ceMHFA3ICeckXQmXi4eEPZVYek8chrBnLJGTqETnmUgLnACfkW-8-__rxE7igbojWo4mBblxsaWwt_ThG0wINrhmw69zQ0Alju8EtxWFFWww7yuNk5-gMncZoh-iwo9igG0KkDYbo08TgYKx_Qo5q7IJ9enhPydeLt1-W7xdXn959WL65WhghSrGQMstNbk2dLlTGsApZrrBSq5qZegVlqXgOwmQVV1awrIS6rEEIJoVFTOuektd73WmuersyyZTHTk_e9ei3ekSn_54MrtXN-F2Lghd5XiSBlwcBP97MNkTdu2Bs1-FgxzloKCSwMgUoEvriH3Q9zj6llSiVUs2UlCpRZ3vK-DEEb-t7M8D0rkO961Dfdpjg53_av0fvSksA7IGN6-z2P1L6cnl9vRf9DXNZqVE</recordid><startdate>201602</startdate><enddate>201602</enddate><creator>Jiang, Lei</creator><creator>Lin, Tiesu</creator><creator>Xu, Chaochao</creator><creator>Hu, Sunkuan</creator><creator>Pan, Yangyang</creator><creator>Jin, Rong</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201602</creationdate><title>miR‐124 interacts with the Notch1 signalling pathway and has therapeutic potential against gastric cancer</title><author>Jiang, Lei ; Lin, Tiesu ; Xu, Chaochao ; Hu, Sunkuan ; Pan, Yangyang ; Jin, Rong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4484-6635c5ecf5ec1bcc0ba059ab9df0cfd18892514c3b29e40381f8f144064eaa183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Amyloid Precursor Protein Secretases - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Lei</au><au>Lin, Tiesu</au><au>Xu, Chaochao</au><au>Hu, Sunkuan</au><au>Pan, Yangyang</au><au>Jin, Rong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR‐124 interacts with the Notch1 signalling pathway and has therapeutic potential against gastric cancer</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2016-02</date><risdate>2016</risdate><volume>20</volume><issue>2</issue><spage>313</spage><epage>322</epage><pages>313-322</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Aberrant Notch signalling plays an important role in cancer progression. However, little is known about the interaction between miRNA and the Notch signalling pathway and its role in gastric cancer (GC). In this study, we found that miR‐124 was down‐regulated in GC compared with adjacent normal tissue. Forced expression of miR‐124 inhibited GC cell growth, migration and invasion, and induced cell cycle arrest. miR‐124 negatively regulated Notch1 signalling by targeting JAG1. miR‐124 levels were also shown to be inversely correlated with JAG1 expression in GC. Furthermore, we found that the overexpression of the intracellular domain of Notch1 repressed miR‐124 expression, promoted GC cell growth, migration and invasion. Conversely, blocking Notch1 using a γ‐secretase inhibitor up‐regulated miR‐124 expression, inhibited GC cell growth, migration and invasion. In conclusion, our data demonstrates a regulatory feedback loop between miR‐124 and Notch1 signalling in GC cells, suggesting that the miR‐124/Notch axis may be a potential therapeutic target against GC.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>26612211</pmid><doi>10.1111/jcmm.12724</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Amyloid Precursor Protein Secretases - genetics Cell cycle Cell growth Cell Line, Tumor Cell Movement - genetics Cell Proliferation - genetics Down-Regulation - genetics Feedback Female Gastric cancer Gene Expression Regulation, Neoplastic - genetics Humans intracellular domain of Notch1 JAG1 Male MicroRNAs - genetics Middle Aged miRNA miR‐124 Notch1 Notch1 protein Original Receptor, Notch1 - genetics Secretase Signal transduction Signal Transduction - genetics Stomach Neoplasms - genetics Up-Regulation - genetics |
| title | miR‐124 interacts with the Notch1 signalling pathway and has therapeutic potential against gastric cancer |
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