Oncotarget

Research Papers:

Biphasic regulation of autophagy by miR-96 in prostate cancer cells under hypoxia

Yi Ma, Hao-Zheng Yang, Bai-Jun Dong, Han-Bing Zou, Yan Zhou, Xian-Ming Kong and Yi-Ran Huang _

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Oncotarget. 2014; 5:9169-9182. https://doi.org/10.18632/oncotarget.2396

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Abstract

Yi Ma1,2, Hao-Zheng Yang3, Bai-Jun Dong1, Han-Bing Zou3, Yan Zhou3, Xian-Ming Kong2 and Yi-Ran Huang1

1 Department of urology, Renji Hospital, School of Medicine, Shanghai JiaoTong University, Shanghai, China

2 Department of biobank, Renji Hospital, School of Medicine, Shanghai JiaoTong University, Shanghai, China

3 Department of central laboratory, Renji Hospital, School of Medicine, Shanghai JiaoTong University, Shanghai, China

Correspondence:

Yi-Ran Huang, email:

Keywords: Autophagy, Hypoxia, microRNAs, Oncogene, Prostate Cancer

Received: July 04, 2014 Accepted: August 26, 2014 Published: August 27, 2014

Abstract

Autophagy favors cell survival under hypoxia, and increasing evidence revealed that microRNAs regulate autophagy. We report here hypoxia increased the expression of miR-96 in prostate cancer cells, and miR-96 stimulated autophagy by suppressing MTOR. We found that inhibition of miR-96 abolished hypoxia-induced autophagy. Paradoxically, ectopic over-expression of miR-96 to a certain threshold, also abolished the hypoxia-induced autophagy. Further studies have shown that high levels of miR-96 inhibited autophagy through suppressing ATG7, a key autophagy-associated gene. Importantly, the miR-96 expression level threshold was determined, and the effects of miR-96 on autophagy on either side of the threshold were opposite. These data demonstrate hypoxia-induced autophagy is at least partially regulated by miR-96; miR-96 can promote or inhibit autophagy by principally inhibiting MTOR or ATG7 depending on the expression levels of miR-96. Our observation might reveal a novel regulatory mode of autophagy by microRNAs under hypoxia.


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