English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Prostate cancer (PCa) is the most common malignancy among males worldwide, and is one of the leading causes of cancer‑related mortality. MicroRNAs (miRs) are a type of endogenous, noncoding RNA that serve a key role in pathological processes, and have been demonstrated to be involved in the formation and progression of PCa. Previous studies have reported that miR‑106b acts as an oncogene; however, the specific effects of miR‑106b on PCa have not been fully elucidated. The present study aimed to investigate the role and underlying molecular mechanisms of miR‑106b in the initiation and progression of PCa. In this study, miR‑106b was reported to be overexpressed and la‑related protein 4B (LARP4B) was downregulated in PCa tissues compared with paracancerous tissues. In addition, LARP4B was identified as a target gene of miR‑106b by bioinformatics prediction analysis and a dual luciferase reporter gene assay. Furthermore, MTT, wound healing and Transwell assays were performed to evaluate PCa cell viability, and migration and invasive abilities. The data revealed that inhibition of miR‑106b significantly suppressed the viability, migration and invasion of PCa cells. In addition, inhibition of miR‑106b significantly suppressed the mRNA and protein expression of cancer‑related genes, including matrix metalloproteinase‑2, cluster of differentiation 44 and Ki‑67, and increased that of the tumor suppressor, mothers against decapentaplegic homolog 2. Collectively, the findings of the present study indicated that miR‑106b may target LAR4B to inhibit cancer cell viability, migration and invasion, and may be considered as a novel therapeutic target in PCa.

MicroRNA‑106b functions as an oncogene and regulates tumor viability and metastasis by targeting LARP4B in prostate cancer