miR-532-3p inhibits the progression of tongue squamous cell carcinoma by targeting podoplanin.
10.1097/CM9.0000000000001563
- Author:
Zhi-Yun LIU
1
;
Chun-Guang ZHAO
Author Information
1. Department of Stomatology, The Sixth Hospital of Wuhan, Affiliated Hospital of Jianghan University, Wuhan, Hubei 430015, China.
- Publication Type:Journal Article
- MeSH:
Carcinoma, Squamous Cell/genetics*;
Cell Line, Tumor;
Cell Proliferation/genetics*;
Gene Expression Regulation, Neoplastic;
Humans;
Membrane Glycoproteins;
MicroRNAs/genetics*;
Tongue Neoplasms/genetics*
- From:
Chinese Medical Journal
2021;134(24):2999-3008
- CountryChina
- Language:English
-
Abstract:
BACKGROUND:The association between miR-532-3p and tongue squamous cell carcinoma (TSCC) has been examined in the literature to improve the survival rate of patients with this tumor. However, further studies are needed to confirm the regulatory roles of this microRNA (miRNA) in TSCC. The objective of this study was to investigate the roles played by and the underlying mechanism used by the miR-532-3p/podoplanin (PDPN) axis in TSCC development.
METHODS:Western blotting and quantitative real-time reverse transcription-polymerase chain reaction (RT-qPCR) were performed to evaluate the PDPN expression level in TSCC tissues and cells. The proliferative, adhesive, and migratory capabilities of TSCC cells (CAL-27 and CTSC-3) were examined using cell counting kit-8 (CCK-8), cell adhesion, and wound-healing assays, respectively. The dual-luciferase reporter (DLR) assay was later conducted to confirm the relationship between miR-532-3p and PDPN.
RESULTS:The results indicated that PDPN expression was enriched in TSCC tissues and cells, and that the expression of PDPN was associated with some clinicopathological parameters of TSCC, including lymph node metastasis (P = 0.001), tumor-node-metastasis (TNM) staging (P = 0.010), and grading (P = 0.010). Further analysis also showed that PDPN knockdown inhibited the viability, adhesive ability, and migratory capacity of CAL-27 and CTSC-3 cells, effects that could be reversed by the application of a miR-532-3p inhibitor. Additionally, PDPN was found to be a direct target of miR-532-3p.
CONCLUSIONS:This research suggested that by targeting PDPN, miR-532-3p could inhibit cell proliferation viability, adhesion, and migration in TSCC. Findings also revealed that the miR-532-3p/PDPN axis might provide more insights into the prognosis and treatment of TSCC.
