Targeting NLRP3 inhibits AML progression by inducing PERK/eIF2-mediated apoptosis.

ABSTRACT:

Background

Acute myeloid leukemia (AML) is characterized by the abnormal proliferation of myeloid precursor cells and presents significant challenges in treatment due to its heterogeneity. Recently, the NLRP3 inflammasome has emerged as a potential contributor to AML pathogenesis, although its precise mechanisms remain poorly understood.

Methods

Public genome datasets were utilized to evaluate the expression of NLRP3 inflammasome-related genes (IL-1β, IL-18, ASC, and NLRP3) in AML patients compared to healthy individuals. CRISPR/Cas9 technology was employed to generate NLRP3-deficient MOLM-13 AML cells, followed by comprehensive characterization using real-time PCR, western blotting, FACS analysis, and transmission electron and immunofluorescence microscopy. Proteomic analys

SUBMITTER: Luciano M 

PROVIDER: S-EPMC11367831 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature