Upregulated lncRNA SNHG1 contributes to progression of non-small cell lung cancer through inhibition of miR-101-3p and activation of Wnt/β-catenin signaling pathway.

Lung cancer is the most common and aggressive tumor in the world. Long non-coding RNA small nucleolar RNA host gene 1 (lncRNA SNHG1) play critical roles in the progression of cancers. However, the function and underlying mechanism remain unclear in lung cancer. In the current study, we found that expression of SNHG1 was up-regulated in non-small cell lung cancer (NSCLC) tissues and cell lines. NSCLC patients with high SNHG1 expression were significantly correlated with larger tumor size, advanced TNM stage, lymph node metastasis and poor overall survival than patients with low SNHG1 expression. Furthermore, function assays showed that SNHG1 inhibition suppressed NSCLC cell proliferation both in vitro and in vivo. We also found that miR-101-3p could act as a target of SNHG1 in NSCLC and the inhibition of NSCLC progression induced by SNHG1 knockdown required the activity of miR-101-3p. In addition, we identified that SOX9 acted as a target of miR-101-3p, and SOX9 played the oncogenic role in NSCLC by activating Wnt/β-catenin signaling pathway. Taken together, our study suggested that lncRNA SNHG1 could promote NSCLC progression via miR-101-3p and SOX9. The SNHG1/miR-101-3p/SOX9/Wnt/β-catenin axis regulatory network might provide a potential new therapeutic strategy for lung cancer treatment.