The Effect Of Long Noncoding RNA SNHG5 On The Biological Characteristics Of Esophageal Cancer Cells And The Mechanism Of SNHG5 Suppressing Epithelial-mesenchymal Transition Of Cancer Cells

Objective: To investigate the effects of small nucleolar RNA host gene 5(SNHG5) on proliferation, migration and invasion of esophageal cancer cells and to explore the possible molecular mechanism of SNHG5 suppressing epithelial-mesenchymal transition of esophageal cancer cells.Methods:1 The expression levels of SNHG5 and MTA2 in esophageal carcinoma tissues and cells were detected by q PCR, and the correlation between SNHG5 RNA expression and MTA2 m RNA expression or clinicopathological characteristics of patients were also analyzed.2 The proliferation, migration and invasion abilities of esophageal cancer cells with SNHG5 over-expression or low-expression were detected by MTS, transwell migration and matrigel invasion chamber assays, respectively.3 The expression levels of SNHG5 and MTA2 in esophageal cancer cells treated with different dose of radiation were detected by q PCR.4 The effects of SNHG5 over-exoression on expression of MTA2 in esophageal cancer cells treated with actidione were detected by q PCR.5 RNA-pulldown combining with western blotting assay detects SNHG5 binding MTA2 proteins.6 The morphological changes of esophageal cancer cells with SNHG5 over-expression were observed by immunofluorescence assay.7 The expression levels of MTA2 and EMT related genes of esophageal cancer cells with SNHG5 over-expression or low-expression were detected by q PCR.8 The expression levels of MTA2 and EMT related proteins of esophageal cancer cells with SNHG5 over-expression were detected by western blotting.9 The migration, invasion and expression levels of EMT related genes as well as proteins of esophageal cancer cells with SNHG5 combining MTA2 over-expression were detected by transwell migration, matrigel invasion chamber assays, q PCR and western blotting, respectively.Results:1 q PCR demonstrated that the expression levels of SNHG5 in esophageal carcinoma tissues were lower than those in the adjacent normal esophageal tissues(P<0.05), while MTA2 were higher(P<0.05). q PCR demonstrated that the expression levels of SNHG5 in esophageal cancer cells were lower than those in normal esophageal epithelial cells(P<0.05),while MTA2 were higher(P<0.05). The correlation between SNHG5 RNA expression and MTA2 m RNA expression in esophageal carcinoma tissues and cells were negative correlation(r=-0.47,P<0.001;r=-0.74,P<0.05).The correlation between SNHG-5 RNA expression and U50 m RNA expression in esophageal carcinoma tissues was positive correlation(r=0.62,P<0.001). The expression level of SNHG5 was associated with invasion into lymph and distant metastasis(P<0.05), not age/year, histological grade, clincail stage and tumor size(P>0.05).2 MTS assay demonstrated that no obvious effect of SNHG5 over-expression on proliferation in KYSE-30 and KYSE-510(P>0.05).3 Transwell migration assays demonstrated that over-expression of SNHG5 inhibited migration abilities of KYSE-30 and KYSE-510(P<0.05), while low-expression of SNHG5 promoted migration abilities of KYSE-30 and KYSE-510(P<0.05). Matrigel invasion chamber assays demonstrated that over-expression of SNHG5 inhibited invasion abilities of KYSE-30(P<0.05), while low-expression of SNHG5 promoted invasion abilities of KYSE-30(P<0.05).4 q PCR demonstrated that the expression levels of SNHG5 in KYSE-30 cells treated with 1Gy and 5Gy were higher than those in the adjacent untreated cells(P<0.05), while MTA2 were lower(P<0.05).5 RNA-pulldown combining with western blotting assay demonstrated that SNHG5 could binding MTA2 proteins.6 The over-expression of SNHG5 induced mesenchymal-epithelial transition of KYSE-30 cells were detected by immunofluorescence assay.7 q PCR and Western blotting demonstrated that the over-expression of SNHG5 inhibited the expression of MTA2, N-cad, Vimentin, CD24, MYLK and IGF2BP1,while promoted the expression of E-cad(P<0.05). The low-expression of SNHG5 promoted the expression of MTA2, N-cad, Vimentin, CD24, MYLK and IGF2BP1,while inhibited the expression of E-cad(P<0.05).8 q PCR demonstrated that no obvious expression level changes of MTA2 in esophageal cancer cells transfected with CD511 B or SNHG5 after treating with actidione(P>0.05).9 Comparing to SNHG5 over-expression, the expression level of E-cad in SNHG5 combining MTA2 over-expression was decreased, while N-cad and Vimentin were increased. The cell migration and invasion abilities were significantly increased(P<0.05).Conclusions:The expression level of SNHG5 in esophageal carcinoma tissues and cells were decreased, while MTA2 were increased. The correlation between SNHG5 RNA expression and MTA2 m RNA expression were negative correlation. SNHG5 has no effect on proliferation, while inhibited the migration, invasion abilities and epithelial-mesenchymal transition of esophageal cancer cells, which was responsible for MTA2 low-expression.