Persistently activated is important for tumorigenesis in a variety of cancers, including melanoma. Although many co-factors in the regulation of duanyu18133 activity have been identified, it remains unclear how duanyu18133 phosphorylation is negatively regulated. Here, we report that SIPAR Protein As a Repressor) inhibits duanyu18133 activity by accelerating its dephosphorylation. We observed that SIPAR directly interacted with duanyu18133 upon IL-6 stimulation. Moreover, over-expression of SIPAR reduced, whereas depletion enhanced, the level of phosphorylated We further demonstrated that SIPAR inhibited the growth of melanoma cells by decreasing the level of phosphorylated duanyu18133 and the expression of its target genes. These results suggest that SIPAR, functioning as a new negative regulator, inhibits duanyu18133 activity by enhancing its dephosphorylation and represses melanoma progression.
KEYWORDS: Dephosphorylation, Melanoma, SIPAR, STAT3