Exogenous dihomo-γ-linolenic acid triggers ferroptosis via ACSL4-mediated lipid metabolic reprogramming in acute myeloid leukemia cells.

Ferroptosis is a novel type of programmed cell death caused by excessive iron-dependent lipid peroxidation. According to various studies, there may be a link between ferroptosis and lipid metabolism. However, few studies have been reported on the lipid metabolism of ferroptosis in acute myeloid leukemia (AML).

[Effect of Sunitinib on Pyroptosis of Drug-Resistant Leukemia K562/ADR Cells and Its Pathway].

Objective: To investigate the inducing effect of sunitinib on the death of drug-resistant leukemia K562/ADR cells and the related signaling pathway.

Methods: K562/ADR cells were treated with different concentrations of sunitinib, and the cells were collected at 24, 48, 72, and 96 hours, respectively. MTS assay was used to detect the effect of sunitinib on the proliferation of K562/ADR cells, and the appropriate sunitinib intervention time and concentration were determined.

Comprehensive analysis of ferroptosis-related gene signatures as a potential therapeutic target for acute myeloid leukemia: A bioinformatics analysis and experimental verification.

Background: Ferroptosis plays an important role in the development of acute myeloid leukemia (AML); however, the exact role of ferroptosis-related genes in the prognosis of AML patients is unclear.

Methods: RNA sequencing data and the clinicopathological characteristics of AML patients were obtained from The Cancer Genome Atlas database, and ferroptosis-related genes were obtained from the FerrDb database. Cox regression analysis and least absolute shrinkage and selection operator analysis were performed to identify ferroptosis-related gene signatures.