Long non-coding RNA SNHG16 activates USP22 expression to regulate colorectal cancer progression by sponging miR-132-3p

Colorectal cancer (CRC) is the most common cause of cancer-related mortality in the world. Long non-coding RNAs (lncRNAs) were involved in the development of many cancers. However, studies on the effect of lncRNA small nucleolar RNA host gene 16 (SNHG16) on the proliferation, metastasis and apoptosis of CRC cells were still few. SNHG16 was highly expressed in CRC tissues and cells. Knockdown of SNHG16 reduced the proliferation, migration, invasion, and promoted the apoptosis of CRC cells. MiR-132-3p could interact with SNHG16, and its inhibitor recovered the suppression effects of silenced-SNHG16 on CRC cell progression. Besides, USP22 was a target of miR-132-3p, and its overexpression restored the inhibition effects of miR-132-3p mimic on CRC cell progression. Interference of SNHG16 reduced the tumor growth in vivo. LncRNA SNHG16 played an oncogene in CRC progression. The discovery of SNHG16/ miR-132-3p/ USP22 pathway provided new thinking for the treatment of CRC.