MicroRNA-300 Inhibits the Proliferation and Metastasis of Cervical Cancer Cells via Posttranscriptional Suppression of G Protein-Coupled Receptor 34 (GPR34)

Abstract

Cervical cancer is one of the dominant gynecological disorders which has poor prognosis and often diagnosed at advanced stages where it becomes nearly impossible to effectively manage this disorder. MicroRNA-300 (miR-300) has dual role in human tumorogenesis. However, characterization of its regulatory action has not been made in cervical cancer. The molecular role of miR-300 in cervical cancer was thus explored in the present study with prime focus on elucidating its mechanism of action. The results showed significant (P < 0.05) downregulation of miR-300 in cervical cancer. Overexpression of miR-300 in cervical cancer cells inhibited their proliferation in vitro by inducing apoptosis. Cervical cancer cells overexpressing miR-300 also showed decreased rates of migration and invasion. G protein-coupled receptor 34 (GPR34) was found to be the functional regulatory target of miR-300 in cervical cancer. GPR34 was found to be significantly (P < 0.05) overexpressed in cervical cancer tissues and cell lines. Silencing of GPR34 inhibited the growth of the cervical cancer cells. However, overexpression of GPR34 could prevent the tumor-suppressive effects of miR-300 on cervical cancer cells. Collectively, the results of the current study are indicative of the tumor-suppressive regulatory role of miR-300 in cervical cancer and suggestive of the potential therapeutic value of miR-300/GPR34 molecular axis.