Background: Colorectal cancer (CRC) is the most common cause of cancer-related mortality in the world. Long non-coding RNAs (lncRNAs) are 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 are still few.
Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the expression levels of SNHG16, microRNA-132-3p (miR-132-3p) and ubiquitin specific peptidase 22 (USP22). The proliferation, apoptosis, migration and invasion of CRC cells were evaluated by the 3-(4,5-dimethyl-2 thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, flow cytometry and transwell assay, respectively. Dual-luciferase reporter assay was used to verify the interactions among SNHG16, miR-132-3p and USP22. Also, Western blot analysis was used to assess the protein levels of USP22 and metastasis-related markers. Moreover, mice xenograft models were used to determine the effect of SNHG16 on CRC tumor growth in vivo.
Results: 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 effect of silenced SNHG16 on CRC cell progression. Besides, USP22 was a target of miR-132-3p, and its overexpression restored the inhibition effect of miR-132-3p mimic on CRC cell progression. In addition, interference of SNHG16 reduced CRC tumor growth in vivo.
Conclusion: LncRNA SNHG16 might act as an oncogene in CRC. The discovery of the SNHG16/miR-132-3p/USP22 pathway provided new thinking for the treatment of CRC.
Keywords: colorectal cancer, progression, SNHG16, miR-132-3p, USP22