Long noncoding RNA SNHG14 facilitates hepatocellular carcinoma progression through regulating miR-4673/SOCS1.

Long non-coding RNA (lncRNA) was recognized as crucial regulator for cancer progression. The functions of small nucleolar RNA host gene 14 (SNHG14) in cancers have been appreciated in recent years. However, its role in hepatocellular carcinoma (HCC) remains to be elucidated. SNHG14 expression level in HCC cells and tissues was analyzed at first. Effects of SNHG14 on HCC cell proliferation, colony formation, and apoptosis were analyzed by Cell Counting Kit-8 (CCK-8), colony formation assay and flow cytometry, respectively. The binding relationship of microRNA-4673 (miR-4673) with SNHG14 or suppressor of cytokine signaling 1 (SOCS1) was examined by bioinformatic analysis tools and luciferase reporter gene assays. Recue experiments were performed to analyze whether SHHG14 affect HCC cell proliferation, colony formation, and apoptosis via regulating miR-4673/SOCS1 axis. SNHG14 was found highly expressed in HCC cells and tissues. In addition, we found SNHG14 overexpression could accelerate HCC cell proliferation and colony formation bur inhibit cell apoptosis. On the contrary, knockdown of SNHG14 could cause the exactly opposite effects on HCC cells. Dual-Luciferase reporter assays confirmed miR-4673 could bind with SNHG14 and SOCS1. In addition, we showed overexpression of miR-4673 or knockdown of SOCS1 could partially reverse the effects of SNHG14 overexpression on HCC cells. SNHG14 was revealed could promote HCC cell proliferation, colony formation but inhibit cell apoptosis by sponging miR-4673 to regulate SOCS1 expression. AJTR