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Abstract
T-cell protein tyrosine phosphatase (TC-PTP, also known as PTPN2) is a negative regulator
of the JAK/STAT pathway. STAT5 is activated by BCR-ABL kinase and STAT1 is an important
transcription factor for interferon (IFN)-α-induced signaling in chronic myeloid leukemia
(CML). We used siRNA to delete TC-PTP in the CML cell line, KT-1, and examined changes
in the sensitivity to imatinib and IFN-α. Suppression of TC-PTP induced activation
of STAT5, leading to imatinib resistance, while prolonged phosphorylation of STAT1
was induced by IFN-α, triggering cell death in KT-1 cells. These findings suggest
that TC-PTP modulates sensitivity to imatinib and IFN-α in CML.