The Long Non-Coding RNA PCAT-1 Promotes Prostate Cancer Cell Proliferation through cMyc

John R. Prensner(Michigan Center for Translational Pathology), Wei Chen(University of Michigan–Ann Arbor), Sumin Han(University of Michigan–Ann Arbor), Matthew K. Iyer(Michigan Center for Translational Pathology), Qi Cao(Michigan Center for Translational Pathology), Vishal Kothari(University of Michigan–Ann Arbor), Joseph R. Evans(University of Michigan–Ann Arbor), Karen E. Knudsen(Thomas Jefferson University), Michelle T. Paulsen(Michigan Center for Translational Pathology), Mats Ljungman(University of Michigan–Ann Arbor), Theodore S. Lawrence(University of Michigan–Ann Arbor), Arul M. Chinnaiyan(Michigan Center for Translational Pathology), Felix Y. Feng(University of Michigan–Ann Arbor)
Neoplasia
November 1, 2014
Cited by 254Open Access
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Abstract

Long non-coding RNAs (lncRNAs) represent an emerging layer of cancer biology, contributing to tumor proliferation, invasion, and metastasis. Here, we describe a role for the oncogenic lncRNA PCAT-1 in prostate cancer proliferation through cMyc. We find that PCAT-1-mediated proliferation is dependent on cMyc protein stabilization, and using expression profiling, we observed that cMyc is required for a subset of PCAT-1-induced expression changes. The PCAT-1-cMyc relationship is mediated through the post-transcriptional activity of the MYC 3' untranslated region, and we characterize a role for PCAT-1 in the disruption of MYC-targeting microRNAs. To further elucidate a role for post-transcriptional regulation, we demonstrate that targeting PCAT-1 with miR-3667-3p, which does not target MYC, is able to reverse the stabilization of cMyc by PCAT-1. This work establishes a basis for the oncogenic role of PCAT-1 in cancer cell proliferation and is the first study to implicate lncRNAs in the regulation of cMyc in prostate cancer.


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