Abstract
Melanoma is a common malignancy with a low survival rate worldwide. Long non-coding RNA Sprouty4-Intron 1 (SPRY4-IT1) is correlated with various cancers, including melanoma. Herein, the underlying molecular mechanisms of SPRY4-IT1 in melanoma were characterized. We found that SPRY4-IT1 level was upregulated in melanoma cells lines compared to the normal skin cells, while miR-22-3p was downregulated. According to of bioinformatics analysis, SPRY4-IT1 was a hypothetic target of miR-22-3p, and knockdown SPRY4-IT1 by sh-RNA (sh-SPRY4-IT1) markedly elevated the miR-22-3p level. Also, the target relationship was further confirmed by dual luciferase reporter assay. In addition, low-expression of SPRY4-IT1 impeded cell proliferation, invasion, migration, and epithelial-mesenchymal transition. Furthermore, western blot assay indicated that the enhanced miR-22-3p further decelerated the phosphorylation of p38MAPK, MAPKAPK and Hsp27, which indicates that miR-22-3p could inactivate the p38MAPK/MAPKAPK/Hsp27 signaling pathway. Overall, our results show that sh-SPRY4-IT1 inhibits cell proliferation and motility through inactivating MAPK signaling by up-regulating miR-22-3p. Therefore, designing targeted drugs against SPRY4-IT1 provides a new direction for the treatment of melanoma.