Please use this identifier to cite or link to this item: https://doi.org/10.18632/oncotarget.21080
Title: MiR-23a modulates X-linked inhibitor of apoptosis-mediated autophagy in human luminal breast cancer cell lines
Authors: Chen, 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
Keywords: balanced salt solution
microRNA
microRNA 23a
unclassified drug
X linked inhibitor of apoptosis
3' untranslated region
animal experiment
animal model
Article
autophagy
breast cancer
cancer growth
cell invasion
cell migration
colony formation
controlled study
down regulation
enzyme inhibition
enzyme regulation
female
human
human cell
in vitro study
limit of quantitation
luciferase assay
mouse
nonhuman
protein expression
protein RNA binding
protein targeting
Issue Date: 2017
Citation: Chen, 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
Rights: Attribution 4.0 International
Abstract: Autophagy 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.
Source Title: Oncotarget
URI: https://scholarbank.nus.edu.sg/handle/10635/179545
ISSN: 19492553
DOI: 10.18632/oncotarget.21080
Rights: Attribution 4.0 International
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