Crizotinib-driven IL10RA gene expression in NPM1-ALK

Stable Identifier
R-HSA-9851068
Type
Reaction [omitted]
Species
Homo sapiens
Compartment
nucleoplasm, plasma membrane
ReviewStatus
5/5
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Crizotinib-driven IL10RA gene expression in NPM1-ALK
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Expression of IL10RA is upregulated in NPM1-ALK cells treated with crizotinib, contributing to an inhibition bypass mechanism. Upregulation of IL10RA stimulates STAT3 phosphorylation independent of NPM1-ALK and results in upregulation of STAT3-dependent targets such as MYC, IRF4 and CD30. In addition, phosphorylated STAT3 binds to the promoters of the IL10RA, IL10RB and IL10 genes in response to crizotinib treatment of NPM1-ALK cells, in this way setting up a positive feedback loop (Prokoph et al, 2020).
Literature References
PubMed ID Title Journal Year
32573700 IL10RA modulates crizotinib sensitivity in NPM1-ALK+ anaplastic large cell lymphoma

Prokoph, N, Probst, NA, Lee, LC, Monahan, JM, Matthews, JD, Liang, HC, Bahnsen, K, Montes-Mojarro, IA, Karaca-Atabay, E, Sharma, GG, Malik, V, Larose, H, Forde, SD, Ducray, SP, Lobello, C, Wang, Q, Luan, SL, Pospisilova, S, Gambacorti-Passerini, C, Burke, GAA, Pervez, S, Attarbaschi, A, Janíková, A, Pacquement, H, Landman-Parker, J, Lambilliotte, A, Schleiermacher, G, Klapper, W, Jauch, R, Woessmann, W, Vassal, G, Kenner, L, Merkel, O, Mologni, L, Chiarle, R, Brugières, L, Geoerger, B, Barbieri, I, Turner, SD

Blood 2020
Participants
Input
Output
Participates
as an event of
This event is regulated
Positively by
Regulator
crizotinib:NPM1-ALK fusion dimer [cytosol] (Homo sapiens)
Disease
Name Identifier Synonyms
anaplastic large cell lymphoma DOID:0050744
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
Cross References
Mondo
Authored
Rothfels, K  (2023-10-14)
Reviewed
Turner, S  (2023-11-08)
Created
Rothfels, K  (2023-10-12)
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