Inhibition of LIN28B impairs leukemia cell growth and metabolism in acute myeloid leukemia.

ABSTRACT:

Background

Current conventional chemotherapy for acute myeloid leukemia (AML) can achieve remission in over 70% of patients, but a majority of them will relapse within 5 years despite continued treatment. The relapse is postulated to be due to leukemia stem cells (LSCs), which are different from normal hematopoietic stem cells (HSCs). LIN28B is microRNA regulator and stem cell reprogramming factor. Overexpression of LIN28B has been associated with advance human malignancies and cancer stem cells (CSCs), including AML. However, the molecular mechanism by which LIN28B contributes to the development of AML remains largely elusive.

Methods

We modulated LIN28B expression in AML and non-leukemic cells and investigated functional consequences in cell proliferation, cell cycle, and

SUBMITTER: Zhou J 

PROVIDER: S-EPMC5504806 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature