BCAT1 contributes to the development of TKI-resistant CML.

ABSTRACT:

Purpose

Although most of chronic myeloid leukemia (CML) patients can be effectively treated by the tyrosine kinase inhibitors (TKIs), such as Imatinib, TKI-resistance still occurs in approximately 15-17% of cases. Although many studies indicate that branched chain amino acid (BCAA) metabolism may contribute to the TKI resistance in CML, the detailed mechanisms remains largely unknown.

Method

The cell proliferation, colony formation and in vivo transplantation were used to determined the functions of BCAT1 in leukemogenesis. Quantitative real-time PCR (RT-PCR), western blotting, RNA sequencing, BCAA stimulation in vitro were applied to characterize the underlying molecular mechanism that control the leukemogenic activity of BCAT1-knockdown cells.

Results

In this report

SUBMITTER: Jiang Y 

PROVIDER: S-EPMC11996995 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature