Long non-coding RNA SNHG16 promotes cell growth and metastasis in ovarian cancer.

Abstract

To investigate the expression of long non-coding RNA SNHG16 in ovarian cancer and to further investigate its role in the development of ovarian cancer as well as its potential regulatory mechanism. Quantitative Real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of SNHG16 in 103 ovarian cancer tissues and normal tissues; the relationship between the expression of SNHG16 and the pathological parameters of ovarian cancer and the prognosis of patients was also analyzed. qRT-PCR was used to further verify the expression of SNHG16 in the ovarian cancer cells. After establishment of SNHG16 knockdown expression model in ovarian cancer cells SKOV-3 and HO8910 using small interfering RNA, the effect of SNHG16 on biological function of ovarian cancer cells was analyzed via cell counting kit-8 (CCK8), transwell invasion and migration assay. Finally, its potential mechanism was analyzed by Western Blot. qRT-PCR results showed that the expression of SNHG16 in ovarian cancer was significantly higher than that in normal tissues, and the difference was statistically significant. Compared with patients with lower expression of SNHG16, patients with higher expression of SNHG16 had higher tumor stage, high rate of distant metastasis and low overall survival rate. Compared with the negative control si-NC group, the cell proliferation, invasion and migration ability in SNHG16 knockdown group (si-SNHG16) significantly decreased. Western Blot showed that after knockdown of SNHG16, expressions of P-AKT and MMP9 decreased significantly, while there was no significant change in the total AKT level. SNHG16 was highly expressed in ovarian cancer, and was correlated with staging, distant metastasis and poor prognosis of ovarian cancer. SNHG16 may activate phosphorylation of AKT and upregulate the expression of MMP9 to promote cell proliferation, invasion and migration of ovarian cancer.