期刊
ONCOGENE
卷 38, 期 48, 页码 7357-7365出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41388-019-0921-4
关键词
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资金
- Association Laurette Fugain
- Conference de Coordination Interregionale du Grand Est - Bourgogne Franche-Comte (CCIRGE-BFC) de la Ligue contre le Cancer
- National Research Agency under the program Investissements d'Avenir [ANR-11-LABX-0021]
- (LipSTIC Labex)
- Conseil Regional de Bourgogne through the plan d'action regional pour l'innovation (PARI)
- European Union through the PO FEDER-FSE Bourgogne
- French Ministere de la Recherche et de l'Enseignement Superieur (MRES)
- Ligue contre le Cancer
- INSERM
- Universite Paris Diderot
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy characterized by an accumulation of immature T cells. Although patient outcomes have improved, novel targeted therapies are needed to reduce the intensity of chemotherapy and improve the prognosis of high-risk patients. Interleukin-7 (IL-7) modulates the survival and proliferation of normal and malignant T cells. Targeting the IL-7 signaling pathway is thus a potentially effective therapeutic strategy. To achieve such aim, it is essential to first understand how the IL-7 signaling pathway is activated. Although IL-7 production has been observed from multiple stromal tissues, T-ALL autocrine IL-7 secretion has not yet been described. Interestingly, using T-ALL cell lines, primary and patient-derived xenotransplanted (PDX) T-ALL cells, we demonstrate that T-ALL cells produce IL-7 whereas normal T cells do not. Finally, using knock down of IL7 gene in T-ALL cells, we describe to what extent IL-7 autocrine secretion is involved in the T-ALL cells propagation in bone marrow and how it affects the number of leukemia-initiating cells in PDX mice. Together, these results demonstrate how the autocrine production of the IL-7 cytokine mediated by T-ALL cells can be involved in the oncogenic development of T-ALL and offer novel insights into T-ALL spreading.
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