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dc.contributor.author남진우-
dc.date.accessioned2017-06-02T07:48:41Z-
dc.date.available2017-06-02T07:48:41Z-
dc.date.issued2015-09-
dc.identifier.citationCELL DEATH AND DIFFERENTIATION, Page. 1-12en_US
dc.identifier.issn1350-9047-
dc.identifier.issn1476-5403-
dc.identifier.urihttps://www.nature.com/cdd/journal/v23/n3/full/cdd2015116a.html-
dc.identifier.urihttp://hdl.handle.net/20.500.11754/27590-
dc.description.abstractp130Cas regulates cancer progression by driving tyrosine receptor kinase signaling. Tight regulation of p130Cas expression is necessary for survival, apoptosis, and maintenance of cell motility in various cell types. Several studies revealed that transcriptional and post-translational control of p130Cas are important for maintenance of its expression and activity. To explore novel regulatory mechanisms of p130Cas expression, we studied the effect of microRNAs (miRs) on p130Cas expression in human breast cancer MCF7 cells. Here, we provide experimental evidence that miR-362-3p and miR-329 perform a tumor-suppressive function and their expression is downregulated in human breast cancer. miR-362-3p and miR-329 in hibited cellular proliferation, migration, and invasion, thereby suppressing tumor growth, by downregulating p130Cas. Ectopic expression of p130Cas attenuated the inhibitory effects of the two miRs on tumor progression. Relative expression levels of miR-362-3p/329 and p130Cas between normal and breast cancer correlated inversely; miR-362-3p/329 expression was decreased, whereas that of p130Cas increased in breast cancers. Furthermore, we showed that downregulation of miR-362-3p and miR-329 was caused by differential DNA methylation of miR genes. Enhanced DNA methylation (according to methylation-specific PCR) was responsible for downregulation of miR-362-3p and miR-329 in breast cancer. Taken together, these findings point to a novel role for miR-362-3p and miR-329 as tumor suppressors; the miR-362-3p/miR-329-p130Cas axis seemingly has a crucial role in breast cancer progression. Thus, modulation of miR-362-3p/miR-329 may be a novel therapeutic strategy against breast cancer.en_US
dc.description.sponsorshipWe appreciated to Hyosun Tak for technical assistance. This work is supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (2012M3A9D1054517, 2012R1A5A2047939 to EKL and 2009-0093826 to WK).en_US
dc.language.isoenen_US
dc.publisherNATURE PUBLISHING GROUPen_US
dc.subjectCELL-PROLIFERATIONen_US
dc.subjectGENE-EXPRESSIONen_US
dc.subjectRETT-SYNDROMEen_US
dc.subjectMOUSE MODELen_US
dc.subjectP130CASen_US
dc.subjectMECP2en_US
dc.subjectSUPPRESSESen_US
dc.subjectMETHYLATIONen_US
dc.subjectPROTEINen_US
dc.subjectBIOGENESISen_US
dc.titleDownregulation of microRNA-362-3p and microRNA-329 promotes tumor progression in human breast canceren_US
dc.typeArticleen_US
dc.identifier.doi10.1038/cdd.2015.116-
dc.relation.page1-12-
dc.relation.journalCELL DEATH AND DIFFERENTIATION-
dc.contributor.googleauthorKang, H.-
dc.contributor.googleauthorKim, C.-
dc.contributor.googleauthorLee, H.-
dc.contributor.googleauthorRho, J. G-
dc.contributor.googleauthorSeo, J-W-
dc.contributor.googleauthorNam, J-W-
dc.contributor.googleauthorSong, W. K.-
dc.contributor.googleauthorNam, S. W.-
dc.contributor.googleauthorKim, W.-
dc.contributor.googleauthorLee, E. K.-
dc.relation.code2015001311-
dc.sector.campusS-
dc.sector.daehakCOLLEGE OF NATURAL SCIENCES[S]-
dc.sector.departmentDEPARTMENT OF LIFE SCIENCE-
dc.identifier.pidjwnam-
Appears in Collections:
COLLEGE OF NATURAL SCIENCES[S](자연과학대학) > LIFE SCIENCE(생명과학과) > Articles
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