MicroRNA–139–5p inhibits cell viability, migration and invasion and suppresses tumor growth by targeting HDGF in non–small cell lung cancer

22Citations
Citations of this article
11Readers
Mendeley users who have this article in their library.

Abstract

MicroRNA (miRNAs) serve key roles in the progress of various types of cancer. The expression of miRNA (miR)-139-5p is downregulated in several types of tumor and has been recognized as a tumor suppressor. However, the role of miR-139-5p in non-small cell lung cancer (NSCLC) has not been investigated in detail. In the present study, it was demonstrated that miR–139–5p was significantly downregulated in NSCLC cells and tissues, and the overexpression of miR-139-5p in vitro induced apoptosis and significantly inhibited the viability and proliferation of A549 and H1299 cells. In addition, upregulation of miR–139–5p significantly inhibited the migration and invasion of A549 and H1299 cells. Hepatoma-derived growth factor (HDGF) was identified as a direct target of miR-139-5p. Rescue experiments demonstrated that the inhibitory function of miR-139-5p on cell viability, migration and invasion was partially mediated by suppressing HDGF expression. Furthermore, miR-139-5p exhibited efficient inhibition of tumor growth in a xenograft tumor mouse model of A549 cells. In summary, the results from the present study suggested that miR-139-5p may serve an important role in NSCLC by targeting HDGF and causing inhibition of cell viability and metastasis, as well as induction of apoptosis. miR-139-5p may also have the potential to serve as a therapeutic target for the treatment of NSCLC.

Cite

CITATION STYLE

APA

Zhang, Z., Li, W., Jiang, D., Liu, C., & Lai, Z. (2020). MicroRNA–139–5p inhibits cell viability, migration and invasion and suppresses tumor growth by targeting HDGF in non–small cell lung cancer. Oncology Letters. Spandidos Publications. https://doi.org/10.3892/ol.2020.11296

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free