Biologicol Function Of Long-chain Noncoding RNA SNHG5 In Hepg2 Cells

Hepatocellular carcinoma?HCC?is the second leading cause of cancer-related death worldwide^[1,2].The rising incidence,genetic heterogeneity,multiple etiologies,and concurrent chronic liver diseases make diagnosis,staging,and selection of treatment options challenging in patients with HCC^[3].Long non-coding RNAs?lncRNAs?are a class of RNA molecules with more than 200 nucleotides that function as RNAs with little or no protein-coding capacity^[4].In recent years,it has been found that many functional lncRNAs had a role in cancers.LncRNA nucleolar RNA host gene 5?SNHG5?was expressed abnormally in cancers such as gastric cancer,colorectal cancer,esophageal cancer,etc.There is no reports of SNHG5 in liver cancer.In order to explore the fuction of SNHG5 in liver cancer,firstly,we measured the expression level of SNHG5 in HCC cell lines?HepG2,MHCC97-L,MHCC97-H,QGY-7701 and SK-Hep1?and normal liver cell line?HL7702?by q RT-PCR.It showed that the expression of SNHG5in HCC cells was significantly up-regulated compared to normal hepatocytes.Secondly,after SNHG5 was silenced in HepG2,it showed that the proliferation,migration,cell cycle and clone formation of HepG2were all downregulated significantly,while the apoptosis was upregulated obviously.In addition,the related reports suggested that SPATS2 and PITRM1 might be the target genes of SNHG5.Thus,we deteced the expression of SPATS2 and PITRM1 in nomol HepG2 and HepG2silenced or over-expressed SNHG5 by qRT-PCR and Western blot.The results showed that the mRNA and protein expression of SPATS2 and PITRM1 were also significantly down-regulated or up-regulated especially when we inhibited or over-expressed SNHG5 in HepG2.Thirdly,the dual luciferase reporter gene assay indicated that there were complementary binding sites between SPATS2 and SNHG5.Finally,we silenced SPATS2 or PITRM1 in Hep G2 to verify their effects in HepG2.The results demonstrated that proliferation,migration,cell cycle and colony formation of Hep G2 were inhibited and apoptosis was significantly increased in HepG2 with silenced SPATS2 or PITRM1,which was similar to the effects of SNHG5 slience in HepG2.