MECP2 binds the STAT5A gene

Stable Identifier
R-HSA-9701810
Type
Reaction
Species
Homo sapiens
Compartment
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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).

Literature References
PubMed ID Title Journal Year
17922009 STAT5A is epigenetically silenced by the tyrosine kinase NPM1-ALK and acts as a tumor suppressor by reciprocally inhibiting NPM1-ALK expression

Liu, X, Wasik, MA, Zhang, Q, Wang, HY

Nat. Med. 2007
11751994 Multilevel dysregulation of STAT3 activation in anaplastic lymphoma kinase-positive T/null-cell lymphoma

Wasik, MA, Zhang, Q, Carpentieri, DF, Morris, S, Odum, N, Skorski, T, Raghunath, PN, Majewski, M, Xue, L

J. Immunol. 2002
Participants
Participates
This event is regulated
Disease
Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
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