LncRNA NEAT1 regulates cervical carcinoma proliferation and invasion by targeting AKT/PI3K.

OBJECTIVE

Cervical cancer is a common tumor in gynecological malignancies. Recent studies showed that long non-coding RNAs (lncRNAs) play a key role in tumorigenesis and development. LncRNA nuclear-rich transcripts 1 (NEAT1) has been found to play a role in gynecological tumors, such as endometrial cancer. However, expression of lncRNA NEAT1 and mechanism in cervical cancer has not been elucidated.

MATERIALS AND METHODS

The tumor tissue and adjacent tissue of cervical cancer patients were collected. HeLa cells were cultured in vitro and lncRNA NEAT1 expression was interfered with small interfere RNA (siRNA). Cell proliferation was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Cell invasion ability was assessed by transwell assay. LncRNA NEAT1, Cyclin D1, and cyclin-dependent kinase 4 (CDK4) expressions were detected by Real-time PCR. Caspase 3 expression was detected by caspase 3 activity kit. Phosphorylated protein kinase B (p-AKT), phosphatidylinositol 3-kinase (p-PI3K), and matrix metalloproteinase-2 (MMP2) levels were evaluated by Western blot.

RESULTS

Compared with the adjacent tissue, lncRNA NEAT1 expression was significantly increased in cervical cancer (p<0.05). LncRNA NEAT1 level was decreased in HeLa cells transfected by siRNA, which inhibited the proliferation and invasion of tumor cells, reduced cyclin D1 and CDK4 expressions, enhanced caspase 3 activity, and declined the expressions of p-AKT, p-PI3K, and MMP2 (p<0.05).

CONCLUSIONS

LncRNA NEAT1 siRNA transfection can inhibit the proliferation of cervical cancer by regulating the AKT/PI3K signaling pathway, promote cell apoptosis, and restrain cell invasion. Therefore, the lncRNA NEAT1 may be used as a molecular potential for the diagnosis and treatment of cervical cancer through regulating AKT/PI3K signaling pathway, which would be confirmed in the following study.