FAM168A participates in the development of chronic myeloid leukemia via BCR-ABL1/AKT1/NFκB pathway.

ABSTRACT:

Background

Although the prognosis of chronic myeloid leukemia (CML) has dramatically improved, the pathogenesis of CML remains elusive. Studies have shown that sustained phosphorylation of AKT1 plays a crucial role in the proliferation of CML cells. Evidence indicates that in tongue cancer cells, FAM168A, also known as tongue cancer resistance-associated protein (TCRP1), can directly bind to AKT1 and regulate AKT1/NFκB signaling pathways. This study aimed to investigate the role of FAM168A in regulation of AKT1/NFκB signaling pathway and cell cycle in CML.

Methods

FAM168A interference was performed, and the expression and phosphorylation of FAM168A downstream proteins were measured in K562 CML cell line. The possible roles of FAM168A in the proliferation of CML cells were in

SUBMITTER: Liu X 

PROVIDER: S-EPMC6617578 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature