LncRNA PVT1 Acts as a Tumor Promoter in Thyroid Cancer and Promotes Tumor Progression by Mediating miR-423-5p-PAK3.

INTRODUCTION

Thyroid cancer (TC) is an endocrine tumor whose risk of onset has been rising, so the deep understanding of its molecular mechanism helps formulate new treatment strategies.

METHODS

This paper was aimed at exploring the regulatory mechanism of long non-coding RNA (LncRNA) plasmacytoma variant translocation 1 (PVT1) in TC. The expression of PVT1, miR-423-5p and p21-activated kinase 3 (PAK3) in TC tissues and cell lines was detected by real-time PCR. PAK3 levels were detected by Western blot. Regulatory relationships between target genes and the proliferation, invasion and apoptosis of cells and genes were analyzed.

RESULTS

PVT1 and PAK3 upregulated while miR-423-5p downregulated in the tissues and cell lines. PVT1 downregulation inhibited TC cells from malignantly proliferating and invading, and promoted their apoptosis. PVT1 specifically regulated miR-423-5p, and its overexpression could weaken the anti-tumor effect of this miR on TC cells. In addition, miR-423-5p directly targeted PAK3, and knocking down its expression could weaken the inhibitory effect of PAK3 downregulation on TC progression. Besides, PVT1 acted as a competitive endogenous RNA to sponge this miR and thus regulate PAK3 expression.

DISCUSSION

In conclusion, PVT1 can mediate the molecular mechanism of the miR-423-5p-PAK3 axis regulatory network on regulating TC, so it is a new direction of treating the disease.