These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: MiR-501-3p promotes osteosarcoma cell proliferation, migration and invasion by targeting BCL7A. Author: Dai J, Lu L, Kang L, Zhang J. Journal: Hum Cell; 2021 Mar; 34(2):624-633. PubMed ID: 33415690. Abstract: Increasing numbers of evidences have demonstrated that microRNAs (miRNAs) play an important role in osteosarcoma (OS) cell functions. MiR-501-3p has been reported to play an important role in several types of tumors, including prostate cancer and hepatocellular carcinoma. However, the biological function and potential mechanism of miR-501-3p in OS have not been well investigated until now. Here, we analyzed the expression of miR-501-3p in OS tissues and cell lines and its clinical significance in OS patients. Quantitative reverse transcription PCR showed miR-501-3p was significantly up-regulated in OS tissues and cell lines. Up-regulated miR-501-3p expression was associated with TNM stage, distal metastasis and worse prognosis in OS patients. MiR-501-3p knockdown and overexpression were achieved by miR-501-3p inhibitor and mimics transfection, respectively. CCK-8, colony formation and transwell assays showed that miR-501-3p knockdown in U2OS and Saos-2 cells suppressed, while miR-501-3p overexpression in Saos-2 cells promoted cell proliferation, migration and invasion. Moreover, luciferase reporter assay supporting BCL7A was a target of miR-501-3p and its expression was increased by miR-501-3p inhibitor, but inhibited by miR-501-3p mimics. By performing rescue experiments, we further demonstrated that BCL7A was a downstream functional regulator involved in miR-501-3p promoting OS cell functions. In summary, our findings suggest that miR-501-3p targets BCL7A may provide novel therapeutic targets for the treatment of OS.[Abstract] [Full Text] [Related] [New Search]