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dc.contributor.authorYuan, Y.
dc.contributor.authorAnbalagan, D.
dc.contributor.authorLee, L.
dc.contributor.authorSamy, R.
dc.contributor.authorShanmugam, M.
dc.contributor.authorKumar, Alan Prem
dc.contributor.authorSethi, G.
dc.contributor.authorLobie, P.
dc.contributor.authorLim, L.
dc.date.accessioned2018-02-06T06:14:36Z
dc.date.available2018-02-06T06:14:36Z
dc.date.created2018-02-06T05:49:56Z
dc.date.issued2016
dc.identifier.citationYuan, Y. and Anbalagan, D. and Lee, L. and Samy, R. and Shanmugam, M. and Kumar, A.P. and Sethi, G. et al. 2016. ANXA1 inhibits miRNA-196a in a negative feedback loop through NF-kB and C-Myc to reduce breast cancer proliferation. Oncotarget. 7 (19): pp. 27007-27020.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/62958
dc.identifier.doi10.18632/oncotarget.8875
dc.description.abstract

MiRNAs are endogenous ~22 nt RNAs which play critical regulatory roles in a wide range of biological and pathological processes, which can act as oncogenes or tumor suppressor genes depending on their target genes. We have recently shown that ANXA1 inhibits the expression of miRNAs including miR196a. Here, we show that miR196a was highly expressed in ER+ MCF-7 breast cancer cells when compared to normal mammary gland cells, with expression levels negatively correlating to ANXA1. ANXA1 inhibits the biogenesis of oncogenic miR-196a by suppressing primarymiR196a indirectly through the stimulation of c-myc and NFkB expression and activity in breast cancer cells. In a negative feedback loop, miR-196a directly inhibits ANXA1 and enhances breast cancer cell proliferation in vitro. Finally, miR196a promotes breast tumor growth in vivo. This study reports a novel regulatory circuit between ANXA1, NF-kB, c-myc and miR-196a which regulates breast cancer cell proliferation and tumor growth.

dc.publisherImpact Journals LLC
dc.titleANXA1 inhibits miRNA-196a in a negative feedback loop through NF-kB and C-Myc to reduce breast cancer proliferation
dc.typeJournal Article
dcterms.source.volume7
dcterms.source.number19
dcterms.source.startPage27007
dcterms.source.endPage27020
dcterms.source.issn1949-2553
dcterms.source.titleOncotarget
curtin.departmentSchool of Biomedical Sciences
curtin.accessStatusOpen access via publisher


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