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Int. J. Mol. Sci. 2017, 18(7), 1375; doi:10.3390/ijms18071375

Induction of miR-3648 Upon ER Stress and Its Regulatory Role in Cell Proliferation

Chinese Academy of Sciences (CAS) Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Molecular Cell Science, School of Life Sciences, University of Science and Technology of China, Hefei 230027, China
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Received: 3 May 2017 / Revised: 20 June 2017 / Accepted: 22 June 2017 / Published: 29 June 2017
(This article belongs to the Collection Regulation by Non-Coding RNAs)
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MicroRNAs (miRNAs) play important roles under multiple cellular conditions including endoplasmic reticulum (ER) stress. We found that miR-3648, a human specific microRNA, was induced under ER stress. Moreover, Adenomatous polyposis coli 2 (APC2), a tumor suppressor and a negative regulator of Wnt signaling, was found to be the direct target of miR-3648. Levels of APC2 were downregulated when cells were under ER stress or after overexpressing miR-3648. Inhibition of miR-3648 by antagomir increased APC2 levels and decreased cell proliferation. Conversely, when miR-3648 was overexpressed, APC2 levels were decreased and the cell growth increased. Our data demonstrated that ER stress mediated induction of miR-3648 in human cells, which then downregulated APC2 to increase cell proliferation. View Full-Text
Keywords: miR-3648; endoplasmic reticulum stress; Adenomatous polyposis coli 2; proliferation; Wnt miR-3648; endoplasmic reticulum stress; Adenomatous polyposis coli 2; proliferation; Wnt

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Rashid, F.; Awan, H.M.; Shah, A.; Chen, L.; Shan, G. Induction of miR-3648 Upon ER Stress and Its Regulatory Role in Cell Proliferation. Int. J. Mol. Sci. 2017, 18, 1375.

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