LncRNA SNHG17 promotes proliferation and invasion of ovarian cancer cells through up-regulating FOXA1.

OBJECTIVE

This study was designed to investigate the specific mechanism through which long non-coding RNA (lncRNA) SNHG17 promotes the proliferative capacity and invasiveness of ovarian tumor cells.

PATIENTS AND METHODS

Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) detected the expressions of SNHG17 and FOXA1 in 30 pairs of ovarian cancer tissue specimens and corresponding adjacent ones. Meanwhile, in ovarian cancer cell lines (A2780, OVCAR3, SKOV3, CAOV3) and normal ovarian epithelial cell line (IOSE80), SNHG17 and FOXA1 mRNA levels were also examined. In in vitro experiment, si-SNHG17, si-FOXA1, and their corresponding negative controls were transfected into ovarian cancer cell lines, respectively. After that, Cell Counting Kit-8 (CCK-8) and plate cloning experiments were carried out to examine cell proliferation ability, while transwell assay was performed for cell invasiveness detection. Lastly, the interplay between SNHG17 and FOXA1 was further assessed via qRT-PCR and Western blot.

RESULTS

qRT-PCR results indicated that SNHG17 expression was remarkably enhanced in ovarian cancer tissue samples compared with that in adjacent ones. In addition, ovarian cancer cells also contained higher expression of SNHG17 than the normal ovarian epithelial cells. However, down-regulating SNHG17 attenuated the cell proliferation and invasive ability. At the same time, compared with that in adjacent tissue samples, FOXA1 also showed a higher expression in ovarian cancer tissues, which was positively correlated with SNHG17. Silencing SNHG17 markedly downregulated FOXA1 expression at both mRNA and protein levels. Furthermore, downregulation of FOXA1 expression was found to be able to inhibit cell proliferation and invasion as well.

CONCLUSIONS

LncRNA SNHG17 can promote ovarian tumor cell proliferative ability and invasiveness by upregulating FOXA1, and serve as a potential therapeutic target for ovarian cancer.