Format

Send to

Choose Destination
J BUON. 2019 Nov-Dec;24(6):2287-2293.

MiR-532-3p inhibits metastasis and proliferation of non-small cell lung cancer by targeting FOXP3.

Author information

1
Department of Hematology and Oncology, Taizhou First People's Hospital, Taizhou 318020, China.

Abstract

PURPOSE:

To investigate the potential effect of microRNA-532-5p (miR-532-3p) on the development of non-small cell lung cancer (NSCLC) and the relevant mechanism.

METHODS:

Thirty-seven patients who underwent primary NSCLC resection were studied. To examine the role of miR-532-3p in NSCLC development, we detected the level of miR-532-3p expression in NSCLC tissues and the para-cancer tissues by qRT-PCR. In order to investigate the potential target of miR-532-3p, we checked it in three publicly available algorithms, TargetScan, miRDB and microRNA, to elucidate the putative and possible targets of miR-532-3p. To test the function of miR-532-3p on the proliferation of NSCLC cell, we performed MTT assay to detect the cell proliferation rates. Migration and invasion were also studied.

RESULTS:

The expression level of miR-532-3p were detected in NSCLC tissues and cells by qRT-PCR, which indicated that the expression of miR-532-3p was low in both tissue and cell levels. Online prediction websites and luciferase reporter assay indicated that FOXP3 is a direct target of miR-532-3p in NSCLC cells. Further results showed that this miR significantly decreased the expression level of FOXP3. MTT assay showed that miR-532-3D remarkably suppressed the proliferation of NSCLC cells. Furthermore, transwell and scratch healing experiments suggested that miR-532-3p inhibited the invasion and migration of NSCLC cells.

CONCLUSIONS:

Our research discovered the suppressive function of miR-532-3p in NSCLC by targeting FOXP3, revealing that miR-532-3p/FOXP3 axis might be a potential therapeutic target for the treatment of NSCLC.

PMID:
31983096
Free full text

Supplemental Content

Full text links

Icon for Zerbinis, Medical Publications
Loading ...
Support Center