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Large intergenic non-coding RNA-ROR reverses gemcitabine-induced autophagy and apoptosis in breast cancer cells

Yao-Min Chen, Yu Liu, Hai-Yan Wei, Ke-Zhen Lv and Pei-Fen Fu _

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Oncotarget. 2016; 7:59604-59617. https://doi.org/10.18632/oncotarget.10730

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Yao-Min Chen1, Yu Liu1, Hai-Yan Wei1, Ke-Zhen Lv1, Pei-Fen Fu1

1Department of Breast Surgery, The First Affiliated Hospital of Zhejiang University, Hangzhou 310000, P.R. China

Correspondence to:

Pei-Fen Fu, email: [email protected]

Keywords: breast cancer, linc-ROR, gemcitabine, large intergenic non-coding

Received: April 08, 2016    Accepted: June 30, 2016    Published: July 20, 2016


The purpose of this study was to elucidate the potential role of long intergenic non-protein coding RNA, regulator of reprogramming (linc-ROR) in gemcitabine (Gem)-induced autophagy and apoptosis in breast cancer cells. MDA-MB-231 cells were treated with short hairpin RNA (shRNA) to knockdown Linc-ROR expression in the presence of Gem. Gem treatment alone decreased cell survival and increased both apoptosis and autophagy. Gem treatment also increased the expression of LC3-II, Beclin 1, NOTCH1 and Bcl-2, but decreased expression of p62 and p53. Untreated MDA-MB-231 cell lines strongly expressed linc-ROR, but linc-ROR knockdown decreased cell viability and expression of p62 and p53 while increasing apoptosis. Linc-ROR knockdown also increased LC3-II/β-actin, Beclin 1, NOTCH1, and Bcl-2 expression, as well as the number of autophagic vesicles in MDA-MB-231 cells. Linc-ROR negatively regulated miR-34a expression by inhibiting histone H3 acetylation in the miR-34a promoter. We conclude that linc-ROR suppresses Gem-induced autophagy and apoptosis in breast cancer cells by silencing miR-34a expression.

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