Long non‑coding RNA SNHG20 promotes colorectal cancer cell proliferation, migration and invasion via miR‑495/STAT3 axis.

Abstract

Colorectal cancer (CRC) is one of the primary causes of cancer-associated mortality worldwide. However, the potential molecular mechanism of CRC progression remains unknown. Long non-coding RNA small nucleolar RNA host gene 20 (SNHG20) has been demonstrated to be involved in the development and progression of a variety of tumors, including CRC. However, the involvement of SNHG20 in CRC progression remains unclear. The aim of the present study was to investigate the functional role and molecular mechanism of SNHG20 in CRC progression. In the present study, SNHG20 expression was found to be significantly upregulated in CRC tissues and cell lines. Association analysis indicated that high SNHG20 expression was significantly association with greater tumor size (P=0.014), tumor invasion depth (P=0.019), positive lymph node status (P=0.022), distant metastasis (P=0.017) and advanced tumor node metastasis stage (P=0.038). Loss-of-function experiments indicated that SNHG20 knockdown could significantly suppress proliferation, migration and invasion in vitro. Notably, SNHG20 knockdown significantly inhibited tumor growth and lung metastasis in vivo. Bioinformatics analysis and luciferase reporter assays confirmed that microRNA (miR)-495 was a direct target of SNHG20. Rescue assays indicated that miR-495 inhibitor reversed the suppressive effects of SNHG20 knockdown on CRC progression. Moreover, STAT3 was identified as a downstream target of miR-495 in CRC. STAT3 overexpression partially rescued the inhibitory effects of SNHG20 knockdown on CRC progression. Taken together, the results revealed that SNHG20 facilitated CRC progression by regulating STAT3 expression and by sponging miR-495.