Please use this identifier to cite or link to this item: https://doi.org/10.18632/oncotarget.21080
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dc.titleMiR-23a modulates X-linked inhibitor of apoptosis-mediated autophagy in human luminal breast cancer cell lines
dc.contributor.authorChen, P
dc.contributor.authorHe, Y.-H
dc.contributor.authorHuang, X
dc.contributor.authorTao, S.-Q
dc.contributor.authorWang, X.-N
dc.contributor.authorYan, H
dc.contributor.authorDing, K.-S
dc.contributor.authorLobie, P.E
dc.contributor.authorWu, W.-Y
dc.contributor.authorWu, Z.-S
dc.date.accessioned2020-10-23T04:56:04Z
dc.date.available2020-10-23T04:56:04Z
dc.date.issued2017
dc.identifier.citationChen, P, He, Y.-H, Huang, X, Tao, S.-Q, Wang, X.-N, Yan, H, Ding, K.-S, Lobie, P.E, Wu, W.-Y, Wu, Z.-S (2017). MiR-23a modulates X-linked inhibitor of apoptosis-mediated autophagy in human luminal breast cancer cell lines. Oncotarget 8 (46) : 80709-80721. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.21080
dc.identifier.issn19492553
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/179545
dc.description.abstractAutophagy is a conserved multi-step lysosomal process that is induced by diverse stimuli including cellular nutrient deficiency. X-linked inhibitor of apoptosis (XIAP) promotes cell survival and recently has been demonstrated to suppress autophagy. Herein, we examined regulation of XIAP-mediated autophagy in breast cancer cells and determined the underlying molecular mechanism. To investigate this process, autophagy of breast cancer cells was induced by Earle's balanced salt solution (EBSS). We observed discordant expression of XIAP mRNA and protein in the autophagic process induced by EBSS, suggesting XIAP may be regulated at a post-transcriptional level. By scanning several miRNAs potentially targeting XIAP, we observed that forced expression of miR-23a significantly decreased the expression of XIAP and promoted autophagy, wherever down-regulation of miR-23a increased XIAP expression and suppressed autophagy in breast cancer cells. XIAP was confirmed as a direct target of miR-23a by reporter assay utilizing the 3'UTR of XIAP. In vitro, forced expression of miR-23a promoted autophagy, colony formation, migration and invasion of breast cancer cell by down-regulation of XIAP expression. However, miR-23a inhibited apoptosis of breast cancer cells independent of XIAP. Xenograft models confirmed the effect of miR-23a on expression of XIAP and LC3 and that miR-23a promoted breast cancer cell invasiveness. Therefore, our study demonstrates that miR-23a modulates XIAP-mediated autophagy and promotes survival and migration in breast cancer cells and hence provides important new insights into the understanding of the development and progression of breast cancer. Copyright: Chen et al.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectbalanced salt solution
dc.subjectmicroRNA
dc.subjectmicroRNA 23a
dc.subjectunclassified drug
dc.subjectX linked inhibitor of apoptosis
dc.subject3' untranslated region
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectArticle
dc.subjectautophagy
dc.subjectbreast cancer
dc.subjectcancer growth
dc.subjectcell invasion
dc.subjectcell migration
dc.subjectcolony formation
dc.subjectcontrolled study
dc.subjectdown regulation
dc.subjectenzyme inhibition
dc.subjectenzyme regulation
dc.subjectfemale
dc.subjecthuman
dc.subjecthuman cell
dc.subjectin vitro study
dc.subjectlimit of quantitation
dc.subjectluciferase assay
dc.subjectmouse
dc.subjectnonhuman
dc.subjectprotein expression
dc.subjectprotein RNA binding
dc.subjectprotein targeting
dc.typeArticle
dc.contributor.departmentDEPT OF PHARMACOLOGY
dc.description.doi10.18632/oncotarget.21080
dc.description.sourcetitleOncotarget
dc.description.volume8
dc.description.issue46
dc.description.page80709-80721
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