SNHG1 Promotes Development And Progression Of Colorectal Cancer Through Negatively Regulating MiR-137

Background & Aims: Long non-coding RNAs(lncRNAs)are RNAs with a length of over 200 nt and no protein coding.At present,the role of lncRNAs in tumor has become a research hotspot,such as CCAT1 and MALAT1.Among them,Long non-coding RNA small nucleolar RNA host gene 1(lncRNA SNHG1)as a member of the family of lncRNAs,research has confirmed that it can promote gastric cancer,liver cancer,small cell lung cancer tumor development.However,the function and underlying mechanism remain unclear in colorectal cancer(CRC).Recently,a novel regulatory mechanism has been proposed in which RNAs can cross-talk with each other via competing shared for micro RNAs(miRNAs).Based on the above background,the purpose of this study was to explore the role of SNHG1 in colorectal cancer and its relationship with miRNAs.Methods: 1、The SNHG1 expression levels of 80 patients with colorectal cancer tissues and corresponding normal tissues were detected by q RT-PCR.The expression of SNHG1 in 4 colorectal cancer cells and non-cancerous colorectal cells was detected by the same method.The expression differences of the above results were detected by the paired T test.2 、 Online software(http://starbase.sysu.edu.cn/mir Lnc RNA.php)was utilized to search potential miRNAs bind to the complementary site on the 3’?untranslated region(UTR)of SNHG1.The expression levels of miRNAs in the Lo Vo cells were measured after SNHG1 silencing by si RNA.The potential target miRNA of SNHG1 was determined according to the change of miRNA expression level.The target miRNA was further verified in the patients’ colorectal cancer tissues.3、To further determine the interaction between SNHG1 and miR-137,luciferase reporter gene was detected in the colon cancer cell Lo Vo,HT29.The expression level of SNHG1 and miR-137 was also detected by q RT-PCR after overexpressing SNHG1.4、In CRC Lo Vo cells,the carcinogenic activity of two molecular(SNHG1,miR-137)were detected by the Flow cytometry and transwell invasion assay.And the relationship between them was analyzed through the assay.5、Lo Vo cells with SNHG1-knockdown were grown as xenograft tumors in nude mice,miR-137 inhibitors were added to it.Observing tumor growth and statistical analysis was performed.6、To discuss the potential mechanism of SNHG1 negatively regulating expression of miR-137,the expression level of pre-miR-137 and mature miR-137 were measured after knockout of SNHG1.Results: 1、SNHG1 expression are up-regulated both in CRC tissue and CRC cell.2、SNHG1 can work on miR-137 and negatively regulate the expression of miR-137.3、The in vitro carcinogenic activity of SNHG1 was realized partly through negatively regulating miR-137.4、The in vivo carcinogenic activity of SNHG1 was realized partly through negatively regulating miR-137.5、SNHG1 does not regulate miR-137 through the pre-miR-137 pathway.Conclusions: SNHG1 is the driving factor of malignancy,and can promote the development of colorectal cancer through regulating miR-137.