USP13 promotes acute myeloid leukemia cell proliferation and autophagy by promoting ATG5.

Objective: To elucidate the role of USP13 in acute myeloid leukemia (AML) by investigating its effects on cell growth, apoptosis and autophagy, and to explore the underlying mechanisms.
Methods: The expression of USP13 in AML cells was assessed using quantitative PCR (qPCR) and immunoblotting. Cell Counting Kit-8 (CCK-8) and Edu staining were employed to evaluate the impact of USP13 on AML cell growth. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and immunostaining assays were conducted to examine the effects of USP13 on apoptosis and autophagy in AML cells, and immunoblot assays were performed to determine the potential underlying mechanistic pathway.
Results: USP13 expression was significantly elevated in AML cells, correlating with enhanced cell proliferation and resistance to apoptosis. Moreover, USP13 promoted autophagy in AML cells. Mechanistically, USP13 was found to be associated with upregulating ATG5 expression, which promoted AML progression.
Conclusion: USP13 promotes AML cell growth and autophagy by upregulating ATG5.
Competing Interests: Declaration of Competing Interest The authors state that there are no conflicts of interest to disclose.
(Copyright © 2024. Published by Elsevier Ltd.)