MiR-183 regulates biological behavior in papillary thyroid carcinoma by targeting the programmed cell death 4.

Abstract

Numerous studies have demonstrated that microRNAs (miRNAs) play vital roles in papillary thyroid carcinoma (PTC). The aim of the present study was to examine the expression levels of miR-183 in PTC and investigate whether its potential roles involved targeting the programmed cell death 4 (PDCD4). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to examine the expression levels of miR-183 in 38 PTC specimens and 4 PTC cell lines. MTT, colony formation, wound-healing and Transwell invasion assays, and flow cytometry were conducted to explore the potential functions of miR-183 in human TPC1 papillary thyroid carcinoma cells. The dual-luciferase reporter assay was performed to validate whether PDCD4 was a direct target of miR-183. The effects of modulating miR-183 on endogenous levels of PDCD4 were subsequently confirmed via RT-qPCR and western blotting. Functional assays were used to indicate the roles of endogenous PDCD4 in TPC1. The results showed the miR-183 expression levels were significantly upregulated in PTC specimens and cell lines (P<0.05). Overexpression of miR-183 in TPC1 promoted cell proliferation, migration, invasion and decreased apoptosis. The dual-luciferase reporter assay confirmed that PDCD4 was a direct target of miR-183. RT-qPCR and western blotting showed that miR-183 negatively regulated PDCD4 protein expression but had no impact on mRNA expression of PDCD4. Knockdown of PDCD4 expression in TPC1 cells significantly enhanced cell proliferation, migration, invasion and inhibited apoptosis. The results of the present study suggested that miR-183 acts as a papillary thyroid carcinoma oncogene through the negative regulation of PDCD4 protein expression at the post-transcriptional levels. Therefore, targeting miR-183 provides a novel strategy for the diagnosis and treatment of patients with PTC.