Silencing of long non-coding RNA NCK1-AS1 inhibits cell proliferation and migration via inhibition of microRNA-134 in cervical cancer.

Abstract

Long non-coding RNA NCK1-antisense 1 (AS1) has recently been demonstrated to promote cell proliferation and induce cell cycle progression through the crosstalk NCK1-AS1/microRNA (miR)-6857/cyclin dependent kinase 1 pathway in cervical cancer. However, the regulatory mechanism of NCK1-AS1 in cervical cancer growth and metastasis remains largely unclear. In the present study, it was identified that NCK1-AS1 was significantly upregulated in cervical cancer tissues compared with the levels in adjacent non-tumour tissues. High expression levels of NCK1-AS1 were associated with tumour progression and poor prognosis in patients with cervical cancer. Silencing of NCK1-AS1 expression significantly decreased the levels of proliferation and migration of cervical cancer cells, and decreased the protein expression levels of matrix metalloproteinase (MMP)-2 and MMP-9. The results of the luciferase reporter gene assay indicated that there was an miR-134 binding site within the NCK1-AS1 gene in cervical cancer cells. miR-134 was significantly downregulated in cervical cancer tissues compared with the miR-134 levels in adjacent non-tumour tissues, and the expression level of miR-134 was inversely correlated with the NCK1-AS1 expression levels in cervical cancer tissues. Knockdown of miR-134 attenuated the inhibitory effects of NCK1-AS1 downregulation on the proliferation and migration of cervical cancer cells. Therefore, the data from the present study suggested that NCK1-AS1 serves a promotive role in cervical cancer cell proliferation and migration by functioning as a molecular sponge for miR-134. NCK1-AS1 may become a novel therapeutic target for cervical cancer.