STIM1 and STIM2 Mediate Cancer-Induced Inflammation in T Cell Acute Lymphoblastic Leukemia

Shella Saint Fleur-Lominy(New York University), Máté Maus(New York University), Martin Vaeth(New York University), Ingo Lange(New York University), Isabelle Zee(New York University), David Suh(New York University), Liu C(New York University), Xiaojun Wu(New York University), Anastasia N. Tikhonova(New York University), Iannis Aifantis(New York University), Stefan Feske(New York University)
Cell Reports
September 1, 2018
10.1016/j.celrep.2018.08.030
Cited by 29Open Access
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Abstract

channel ORAI1 and its activators STIM1 and STIM2 in T-ALL. Deletion of STIM1 and STIM2 in leukemic cells abolishes SOCE and significantly prolongs the survival of mice in a NOTCH1-dependent model of T-ALL. The survival advantage is unrelated to the leukemic cell burden but is associated with the SOCE-dependent ability of malignant T lymphoblasts to cause inflammation in leukemia-infiltrated organs. Mice with STIM1/STIM2-deficient T-ALL show a markedly reduced necroinflammatory response in leukemia-infiltrated organs and downregulation of signaling pathways previously linked to cancer-induced inflammation. Our study shows that leukemic T lymphoblasts cause inflammation of leukemia-infiltrated organs that is dependent on SOCE.

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