Expression of STAT5A is abrogated in cells expressing NPM-ALK fusions by high levels of promoter methylation. Hypermethylation of the STAT5A enhancer provides binding sites for the methyl binding protein MeCP2 as assessed by chromatin immunoprecipitation, and precludes binding of the normal transcriptional activator Sp1. As a consequence of these events, STAT5A expression is repressed in NPM-ALK + T-cell lymphomas. siRNA-mediated depletion of the NPM-ALK effector STAT3 restores STAT5A expression in these cells, highlighting the role for STAT3 in NPM-ALK-mediated oncogenesis (Zhang et al, 2007; Zhang et al, 2002).
Liu, X, Wasik, MA, Zhang, Q, Wang, HY
Wasik, MA, Zhang, Q, Carpentieri, DF, Morris, S, Odum, N, Skorski, T, Raghunath, PN, Majewski, M, Xue, L
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