The Role And Mechanism Of LncRNA SNHG17 On Colorectal Cancer Cell Proliferation

Background: Mounting evidence has showed that long non-coding RNAs(lnc RNAs)exert crucial functions in many biological processes,such as cell proliferation,apoptosis,differentiation,invasion and metastasis.The dysregulation of lnc RNAs has close correlations with cancer development and progression.Lnc RNA SNHG17(Small nucleolar RNA host gene 17)is located on human chromosome 20,with a length of 1186 bp,and its role and clinical values in cancer development and progression still need to be clarified.Methods: The quantitative reverse transcriptase PCR(q RT-PCR)assays were performed to test SNHG17 levels in 56 pairs colorectal cancer(CRC)tissues,4 CRC cell lines and.human colonic epithelial cells(HCo Epi C).Cell proliferation assays,colony-formation assays and flow cytometry assays were used to explore the effects of SNHG17 dysregulation on CRC proliferation,cell cycle and cell apoptosis.The nude mouse transplantation tumor experiments were conducted to study the effects of SNHG17 knockdown on tumor growth in vivo.The regulatory mechanism between SNHG17 and P57 was clarified through subcellular fractionation location,RNA immunoprecipitation(RIP)and Chromatin immunoprecipitation(Ch IP)assays.Results: SNHG17 overexpression exhibits significant association with tumor size,TNM stage,and lymph node metastasis in CRC patients.SNHG17 knockdown inhibits cell proliferation,causes G1/G0 phase arrest and activates cell apoptosis in CRC.SNHG17 knockdown can significantly suppress tumor growth in vivo.P57 is a potential target of SNHG17.SNHG17 can interact with enhancer of zeste homolog 2(EZH2)to silence P57 expression.Conclusions: SNHG17 was selected as a potential gene correlated with CRC progression.SNHG17 can regulate CRC cell cycle and apoptosis both in vitro and in vivo.SNHG17 can downregulate P57 expression levels at transcriptional levels,thus contributing to CRC cell proliferation.