Open Access

Suppression of α‑methylacyl‑coenzyme A racemase by miR200c inhibits prostate adenocarcinoma cell proliferation and migration

  • Authors:
    • Hanbing Xie
    • Ling Nie
    • Mengni Zhang
    • Zhengzheng Su
    • Xueqin Chen
    • Miao Xu
    • Jing Gong
    • Ni Chen
    • Qiao Zhou
  • View Affiliations

  • Published online on: December 31, 2019     https://doi.org/10.3892/etm.2019.8406
  • Pages: 1806-1816
  • Copyright: © Xie et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Overexpression of α‑methylacyl‑coenzyme A racemase (AMACR/P504S) is a major abnormality that has been observed in prostate cancer, whereas microRNA (miRNA/miR) 200c, is downregulated. The aim of the present study was to explore whether miR200c was able to exert any regulatory effects on AMACR. To meet this aim, bioinformatics analysis was performed to identify potential binding sites for miR200c in the 3'‑untranslated region (3'‑UTR) of AMACR. Recombinant adenoviral and dual reporter gene assays were designed to examine the binding of miR200c to the potential seed sequences in the AMACR 3'‑UTR. Conventional reverse transcription (RT)‑PCR, RT‑quantitative (q)PCR and western blotting were also used to examine the regulatory effects of miR200c on AMACR at the mRNA and protein levels. Furthermore, Cell Counting Kit‑8, wound healing and Transwell assays were performed to investigate the biological effects of miR200c‑AMACR deregulation on prostate cancer cell proliferation, migration and invasion. It was revealed that miR200c post‑transcriptionally suppressed AMACR expression by interacting with the 90‑97 nucleotide sequence of the AMACR mRNA 3'‑UTR. Artificial overexpression of miR200c significantly downregulated the mRNA and protein levels of AMACR in DU145 and PC‑3 prostate cancer cells. Knockdown of AMACR by RNA interference, or overexpression of miR200c by recombinant adenoviral Ad‑miR200c, inhibited prostate cancer cell proliferation, migration and invasiveness. Taken together, the results of the present study revealed that miR200c may suppress the AMACR expression level post‑transcriptionally. The results also indicate that perturbation of the miR200c‑AMACR regulatory mechanism may be involved in prostate carcinogenesis and that this may be exploited in future therapeutic approaches to prostate cancer.
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March 2020
Volume 19 Issue 3

Print ISSN: 1792-0981
Online ISSN:1792-1015

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APA
Xie, H., Nie, L., Zhang, M., Su, Z., Chen, X., Xu, M. ... Zhou, Q. (2020). Suppression of α‑methylacyl‑coenzyme A racemase by miR200c inhibits prostate adenocarcinoma cell proliferation and migration. Experimental and Therapeutic Medicine, 19, 1806-1816. https://doi.org/10.3892/etm.2019.8406
MLA
Xie, H., Nie, L., Zhang, M., Su, Z., Chen, X., Xu, M., Gong, J., Chen, N., Zhou, Q."Suppression of α‑methylacyl‑coenzyme A racemase by miR200c inhibits prostate adenocarcinoma cell proliferation and migration". Experimental and Therapeutic Medicine 19.3 (2020): 1806-1816.
Chicago
Xie, H., Nie, L., Zhang, M., Su, Z., Chen, X., Xu, M., Gong, J., Chen, N., Zhou, Q."Suppression of α‑methylacyl‑coenzyme A racemase by miR200c inhibits prostate adenocarcinoma cell proliferation and migration". Experimental and Therapeutic Medicine 19, no. 3 (2020): 1806-1816. https://doi.org/10.3892/etm.2019.8406