Role of FAM168A Protein in Proliferation of CML Cells
Posted: Monday, August 5, 2019
According to findings presented in BMC Cancer, the tongue cancer resistance–associated protein FAM168A may act as a linker protein that binds BCR-ABL1 and AKT proteins, “further mediating” the downstream signaling pathways for patients with chronic myeloid leukemia (CML). This discovery, by Xiaorong Liu, MD, of the Shenzhen Children’s Hospital, China, and colleagues, may shed light on the role FAM168A plays in the regulation of the AKT1/nuclear factor kappa beta (NFκB) signaling pathway and cell cycle in this hematologic malignancy.
“The discovery of our study provides a new target for the diagnosis and treatment of CML,” the authors noted.
In this study, the investigators performed FAM168A interference and measured the expression and phosphorylation of FAM168A downstream proteins in K562 CML cell lines. They investigated the potential roles of FAM168A by investigating in vitro cell cultures, in vivo animal models, and clinical specimens (three children diagnosed with CML).
Dr. Liu and colleagues found that the expression of FAM168A increased significantly in the peripheral blood mononuclear cells of patients with CML, compared with those in normal healthy controls. The interference of FAM168A did not seem to result in any changes to AKT1 protein expression, but it did significantly decrease AKT1 phosphorylation, as well as significantly increase IκB-α protein levels and significantly reduce nuclear NFκB protein levels.
According to the researchers, the results from the animal models confirmed that FAM168A interference prolonged survival and reduced tumor formation in the mice inoculated with K562 cells. In the three children with CML, FAM168A expression and AKT1 phosphorylation were significantly elevated. The authors noted that these results were consistent in the cell study.
Disclosure: The study authors reported no conflicts of interest.