Long Noncoding RNA LINC00520 Promotes The Process Of Malignant Melanoma By Inhibiting MiR-15a-3p

Background: Growing evidence has revealed an intimate relationship between non-coding RNAs and cancer progression.Altered expression of long noncoding RNAs(lnc RNAs)associated with human carcinogenesis,such as development,homeostatic maintenance and pathological responses.The functions of lnc RNAs in cancer have drawn wide attention recently.Until now,the expression patterns and roles of lnc RNAs in skin melanoma(CMM)have remained largely unknown.Methods: Microarray screening was used to screen differentially expressed novel lnc RNAs in CMM.QRT-PCR and in situ hybridization(ISH)were utilized to analyzed the expression of LINC00520 in CMM tissues and cell line.The effects of LINC00520 on CMM cell migration,invasion,proliferation and apoptosis,migration and invasion were measured by using Transwell assays,MTT and FACS.Dual ‐luciferase,RNA pulldown and q RT-PCR were applied to test the interaction between LINC00520 and mi R-15a-3p.Moreover,bioinformatics method and western blot were used for evaluate the proteins or signaling pathways regulated by LINC00520 expression.Results:We identified that LINC00520 was substantially upregulated in both CMM cell lines and human tumors,and LINC00520 levels were positively associated with distant metastasis stage and unfavorable prognosis of patients with CMM.Silencing of LINC00520 had significant anticancer effects as it suppressed the migration,invasion and proliferation of CMM cells while decreased CDDP chemoresistance,arrested cell‐cycle transition.Also,hsa‐mi R‐15a‐3p was confirmed to be the competing target of LINC00520 in CMM,and its knockdown in A375 and WM451 cells reversed the LINC00520 downregulation‐induced anticancer functions.Bioinformatics software analysis indicated that LINC00520 may participate in the regulating of apoptosis in CMM,Western blotting analysis of tumor cells expressing LINC00520 si RNA,and found that CHOP,EGLN2,AIF4 were significantly downregulated in CMM cell lines.Conclusions: LINC00520 is upregulated in CMM and can increase CMM CDDP chemoresistance through endogenously competing against hsa‐mi R‐15a‐3p,may regulating the apoptosis by promote the expression of CHOP /EGLN2 passway.Our research may provide a potential strategy to improve the treatment outcome of chemotherapy in CMM.