STAT3-induced upregulation of lncRNA SNHG17 predicts a poor prognosis of melanoma and promotes cell proliferation and metastasis through regulating PI3K-AKT pathway.

OBJECTIVE

Long noncoding RNAs (lncRNAs) have drawn increasing attention due to their critical roles in various diseases, including melanoma. In this study, we aimed to explore the potential roles and underlying mechanisms of Small nucleolar RNA host gene 17 (SNHG17) in the modulation of melanoma progression.

PATIENTS AND

METHODS

The levels of SNHG17 in melanoma tissues and cells were determined using RT-PCR. The clinical significance of SNHG17 in melanoma patients was analyzed using Chi-square tests, Kaplan-Meier methods, and multivariate assays. MTT assays, transwell assay, and flow cytometry were carried out to explore the biological functions of SNHG17. The biological mechanism underlying up-regulation of SNHG17 was explored using ChIP analysis and luciferase reporter assays. The related proteins of the PI3K-AKT pathway were determined by Western blot.

RESULTS

High expressions of SNHG17 were observed in both melanoma tissues and cells. Up-regulation of SNHG17 in melanoma patients was associated with lymph node metastasis and tumor stage. Survival assays revealed that those patients with high SNHG17 expression had significantly shorter survival time. SNHG17 was also confirmed to be independently associated with overall survival of melanoma patients. Functional studies confirmed that the proliferation, migration, and invasion of melanoma cells were noticeably reduced by the down-regulation of SNHG17. Mechanistically, the up-regulation of SNHG17 was induced by STAT3. We also found that knockdown of SNHG17 resulted in the remarkable diminution in the phosphorylation levels of PI3K and AKT, suggesting that the activity of the PI3K-AKT pathway was suppressed.

CONCLUSIONS

STAT3-induced upregulation of SNHG17 contributed to the progression of melanoma by promoting the PI3K-AKT signaling.