Mir-629 Repressed LATS2 Expression and Promoted the Proliferation of Prostate Cancer Cells

Author:

Li Yuqiao1,Zeng Sha1,Cao Longbin1

Affiliation:

1. Department of Urology, Liaocheng People’s Hospital, Liaocheng City, China

Abstract

AbstractMicroRNAs (miRNAs) have been discovered to play critical role in regulating prostate cancer (PC) progression. The function role of miR-629 in tumor progression of PC has not been studied. Here, we found that miR-629 was markedly upregulated in PC as determined using the cancer genome atlas (TCGA) dataset, clinical tissues, and cell lines. Functional analysis (MTT assays, colony formation assays, soft agar growth assay and BrdU incorporation assay) indicated that overexpression of miR-629 was drastically promoted, while miR-629-in significantly suppressed cell proliferation. LATS2 was predicted as a direct target of miR-629 and was confirmed by western blot and dual luciferase assay. Through downregulation of large tumor suppressor 2 (LATS2) by overexpression of miR-629, the p21 mRNA and protein were decreased while the Cyclin D3 mRNA and protein were enhanced, suggesting promoting of cell proliferation process. Additionally, knockdown of LATS2 reversed the inhibitory effect by miR-629-in in PC. Our study indicated that miR-629 might serve as a new promising target for PC treatment.

Publisher

Georg Thieme Verlag KG

Subject

Biochemistry (medical),Clinical Biochemistry,Endocrinology,Biochemistry,General Medicine,Endocrinology, Diabetes and Metabolism

Reference35 articles.

1. Cancer statistics, 2019;R L Siegel;Cancer J Clin,2019

2. CCAR1 5’ UTR as a natural miRancer of miR-1254 overrides tamoxifen resistance;G Li;Cell Res,2016

3. miR-634 exhibits anti-tumor activities toward hepatocellular carcinoma via Rab1A and DHX33;C Z Zhang;Mol Oncol,2016

4. Targeting of TLE3 by miR-3677 in human breast cancer promotes cell proliferation, migration and invasion;L-N Peng;Oncology Lett,2020

5. A ZEB1-miR-375-YAP1 pathway regulates epithelial plasticity in prostate cancer;L A Selth;Oncogene,2017

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