NF-κB suppresses ROS levels in BCR-ABL(+) cells to prevent activation of JNK and cell death.

ABSTRACT: Elevated levels of reactive oxygen species (ROS) are found in most oncogenically transformed cells and are proposed to promote cellular transformation through mechanisms such as inhibition of phosphatases. BCR-ABL, the oncoprotein associated with the majority of chronic myeloid leukemias (CMLs), induces accumulation of intracellular ROS, causing enhanced signaling downstream of PI3K. Previously we have shown that the transcription factor nuclear factor-kappa B (NF-κB) is activated by BCR-ABL expression and is required for BCR-ABL-mediated cellular transformation. Inhibition of IκB kinase (IKKβ) and NF-κB leads to cell death through an unknown mechanism. Here, we analyze the potential involvement of NF-κB in moderating BCR-ABL-induced ROS levels to protect from death. The data confirm that

SUBMITTER: Stein SJ 

PROVIDER: S-EPMC3165082 | biostudies-literature | 2011 Nov

REPOSITORIES: biostudies-literature