Long non-coding RNA TUG1 recruits miR‑29c‑3p from its target gene RGS1 to promote proliferation and metastasis of melanoma cells.

Melanoma is an aggressive type of skin cancer, characterized by high mortality rates worldwide. Therefore, the identification of new diagnostic markers and therapeutic targets for melanoma is imperative. Accumulating evidence has demonstrated that long non-coding RNAs (lncRNAs) play important roles in tumor initiation and progression. It was recently reported that the expression of lncRNA taurine upregulated 1 (TUG1) was relatively higher in cancer compared with that in normal cells, and that TUG1 promoted the progression of various cancers. However, the pattern of expression and mechanism of action of TUG1 in melanoma remain unclear. The aim of the present study was to investigate whether TUG1 expression is relatively higher in melanoma tissues and whether this expression is correlated with poor overall survival. Knockdown of TUG1 was found to suppress melanoma cell growth and metastasis and induce cell apoptosis. By contrast, the overexpression of TUG1 promoted the growth and metastasis of melanoma cells, and inhibited their apoptosis. In addition, the results of the present study indicated that TUG1 sequestered endogenous miR‑29c‑3p and that it was able to suppress its expression. Furthermore, it was observed that miR‑29c‑3p could reverse the promoting effect of TUG1 on melanoma progression, which may be associated with the positive regulation of regulator of G-protein signaling 1 (RGS1), a target gene of miR‑29c‑3p. Taken together, the data of the present study demonstrated that TUG1 promoted proliferation and invasion and suppressed apoptosis in melanoma cells by regulating miR‑29c‑3p and its target gene, RGS1. Therefore, lncRNA TUG1 appears to be a promising diagnostic marker for melanoma patients.

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