TKT regulates the pentose phosphate pathway via RBKS to promote epithelial-mesenchymal transition during AML progression.

Abstract

Acute myeloid leukemia is a life-threaten disease. Researches have indicated that increased expression of TKT was closely related to the progression of malignant tumors. However, the mechanism of TKT in the pathogenesis of AML need to be further elucidated. Here, we showed that the expression levels of TKT was increased in AML patients and AML cells. TKT overexpression in AML cells significantly promoted the proliferation, migration and invasion of cells while TKT knockdown had opposite effects. Mechanistically. We proved that TKT was located on up-stream of RBKS and TKT promoted the growth of AML cells through RBKS. In addition, our data indicated that TKT regulates the pentose phosphate pathway via RBKS. Notably, we demonstrated that the pentose phosphate pathway is crucial for EMT program in AML cells. Taken together, this study identified the molecular mechanism by which TKT promotes AML progression, namely, TKT promotes EMT by regulating the pentose phosphate pathway through RBKS. Our results suggest that TKT maybe a novel therapeutic target for AML treatment.