CXCR4/RhoA signaling pathway is involved in miR-128-regulated proliferation and apoptosis of human thyroid cancer cells.

microRNA-128 (miR-128), a kind of short, noncoding RNAs, functioned as a tumor marker. However, the underlying function and mechanism of miR-128 in human thyroid cancer were uncertain. Therefore, in the present study, the effects of miR-128 on the proliferation and apoptosis of cultured human thyroid cancer cells were investigated. After slicing miR-128 in human thyroid cancer cells, the proliferation was measured by methyl thiazolyl tetrazolium (MTT) method, the expression of miR-128, CCAAT/enhancer binding protein-α (C/EBPα), peroxisome proliferator-activated receptor-γ (PPARγ), Caspase-3 and Caspase-9 was determined by RT-PCR, and protein expression of chemokine receptor 4 (CXCR4) and Ras homolog gene family, member A (RhoA) was analyzed by Western blot. It was found that knockdown of miR-128 promoted the optical density (OD) value of cells, enhanced mRNA expression of PPARγ and C/EBPα, while inhibited cell apoptotic rate, and Caspase-3, Caspase-9 expression. Furthermore, higher protein expression of CXCR4 and RhoA was found in the absence of miR-128. Notably, miRNA-128 over-expression-inhibited proliferation and induced-apoptosis of human thyroid cancer cells were partially changed following the block of CXCR4/RhoA signaling pathway by the CXCR4 inhibitor (AMD3100). It was indicated that miR-128 down-regulated proliferation while promoted apoptosis of human thyroid cancer cells through suppression of CXCR4/RhoA signaling pathway.