Abstract
Chromatin remodeling factor lymphoid-specific helicase inhibits ferroptosis through lipid metabolic genes in lung cancer progression
Highlights
Using RNA sequencing and the gene ontology analysis, we first identified a significant enrichment in pathways that related to metabolic process and the Warburg effect [6]
The ferroptotic mode of programmed necrosis was recently discovered as an apoptosis-independent form of cell death in Ras-transformed cells; the K-ras mutant is common in lung cancer [8]
We found previously that oncometabolites activated LSH expression [4]; on the basis of this, our recent study found that EGLN1 up-regulated LSH expression by inhibiting hypoxia-inducible factor (HIF)‐1α, which highlights HIF‐1α as a key repressor of LSH expression [6]
Summary
Using RNA sequencing and the gene ontology analysis, we first identified a significant enrichment in pathways that related to metabolic process and the Warburg effect [6]. The ferroptotic mode of programmed necrosis was recently discovered as an apoptosis-independent form of cell death in Ras-transformed cells; the K-ras mutant is common in lung cancer [8]. The iron-dependent enzymes Egl nine homolog (EGLNs) catalyze hypoxia-inducible factor (HIF) prolyl hydroxylation, which leads to HIF-1α and HIF-2α degradation. HIF-1α regulates oxygen-dependent glucose and glutamine metabolism, playing a critical role in cancer progression [9].
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