| Literature DB >> 27748826 |
Shun-Quan Wu1, Wen-Yan Niu2, Ya-Ping Li1, Hao-Bo Huang1, Rong Zhan1.
Abstract
The oncogene B-cell-specific Moloney murine leukemia virus insertion site‑1 (Bmi‑1) is overexpressed in multiple myeloma (MM). Our previous study demonstrated that Bmi‑1 silencing sensitized MM cells to bortezomib. Translational regulation has emerged as a prominent underlying mechanism of Bmi‑1 regulation, particularly via microRNA targeting. The present study determined that Bmi‑1 may be directly targeted by miR‑203 using a luciferase assay. In addition, enforced expression of miR-203 led to significant downregulation of Bmi‑1 protein and mRNA expression levels. Furthermore, restoration of miR-203 significantly inhibited cell growth and G1/S transition in MM cells. miR‑203 was downregulated in MM patients, and a negative correlation between the expression of miR‑203 and Bmi‑1 was observed. The results of the present study indicated that miR‑203 exerts growth‑inhibiting effects in MM through the suppression of Bmi‑1 expression. In conclusion, the present study demonstrated that Bmi‑1 is a direct functional target of miR-203 in MM.Entities:
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Year: 2016 PMID: 27748826 DOI: 10.3892/mmr.2016.5832
Source DB: PubMed Journal: Mol Med Rep ISSN: 1791-2997 Impact factor: 2.952