Background: Melanoma is aggressive and lethal melanocytic neoplasm, and its incidence has increased worldwide in recent decades. Accumulating evidence has showed that various long noncoding RNAs (lncRNAs) participated in occurrence of malignant tumors, including melanoma. The present study was designed to investigate function of lncRNA colon cancerassociated transcript-1 (CCAT1) in melanoma. Methods: The expression levels of CCAT1, miR-296-3p and Integrin alpha9 (ITGA9) in melanoma tissues or cells were measured using real-time quantitative polymerase chain reaction (RT-qPCR). The concentrations of glucose and lactate were measured for assessing glycolysis of melanoma cells. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT), flow cytometry, and transwell assays were conducted to assess proliferation, apoptosis, and migration of melanoma cells. Western blot assay was performed to measure the protein expression of ITGA9, hexokinase 2 (HK2), and epithelial-mesenchymal transition (EMT)-related proteins in melanoma tissues or cells. The relationship among CCAT1, miR-296-3p, and ITGA9 was predicted and confirmed by bioinformatics analysis, dualluciferase reporter, and RNA immunoprecipitation (RIP) assay, respectively. A xenograft experiment was established to assess the effect of CCAT1 knockdown in vivo. Results: CCAT1 was effectively increased in melanoma tissues and cells compared with matched controls, and deficiency of CCAT1 impeded cell glycolysis, proliferation, migration while induced apoptosis, which were abrogated by knockdown of miR-296-3p in melanoma cells. In addition, our findings revealed that ITGA9 overexpression abolished miR-296-3p overexpression-induced effects on melanoma cells. Importantly, CCAT1 regulated ITGA9 expression by sponging miR-296-3p. The results of xenograft experiment suggested that CCAT1 silencing inhibited melanoma cell growth in vivo. Conclusion: LncRNA CCAT1 promoted ITGA9 expression by sponging miR-296-3p in melanoma.

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Abstract. Although the T241M polymorphism in the X-ray cross-complementing group 3 (XRCC3) gene has been implicated in the pathogenesis of melanoma, the results have been inconsistent. In this study, a meta-analysis was performed to assess the association of XRCC3 T241M polymorphism with melanoma. Published literature from PubMed and Embase databases was retrieved. The pooled odds ratio (OR) with 95% confidence interval (CI) was calculated using fixed-or random-effects models. A total of six case-control studies containing 2,133 patients and 3,141 controls were enrolled into this meta-analysis. In a combined analysis, the results revealed no significant association between XRCC3 T241M polymorphism and melanoma risk in the overall population. In the subgroup analysis by ethnicity, no significant associations between the XRCC3 T241M polymorphism and melanoma risk were identified in Caucasians. However, when the analyses were restricted to three larger studies (n>500 cases), a significant association was noted with melanoma (TT vs. MT: OR=1.20, 95% CI=1.04-1.38; dominant model: OR=0.86, 95% CI=0.75-0.98). In conclusion, the meta-analysis results suggest that the XRCC3 T241M polymorphism was associated with risk of melanoma. Further large and well-designed studies are needed to confirm this conclusion.