Involvement of Blnk and Foxo1 in tumor suppression in BCR‑ABL1‑transformed pro‑B cells.

ABSTRACT: Oncogenic Bcr‑Abl kinase mimics pre‑B cell receptor (pre‑BCR) survival signals in BCR‑ABL1‑positive B‑cell acute lymphoblastic leukemia (BCR‑ABL1+ B‑ALL), driving B‑cell progenitor malignant transformation; thus, defining a particularly unfavorable prognosis for patients. During B‑cell development, pre‑BCR differentiation signaling components terminate proliferative expansion and promote B‑cell maturation. To study whether pre‑BCR differentiation signaling components regulate the initiation and development of BCR‑ABL1+ B‑ALL, the tumor suppression mechanism of differentiation‑related signaling molecules in BCR‑ABL1‑transformed pro‑B cells were analyzed. The results demonstrated that Bcr‑Abl kinase activated the PI3K/Akt pathway, promoting cell growth, and upregulated Aid expression, increa

SUBMITTER: Zhang P 

PROVIDER: S-EPMC7757083 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature