Metabolic rewiring promotes metastatic potential upon glutamine deprivation in STK11 null KRAS-driven lung adenocarcinoma
Sands, Logan Prior, Shannon
Sands, Logan
Prior, Shannon
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Abstract
Lung adenocarcinoma (LUAD) with concurrent oncogenic KRAS and STK11 loss-of-function mutations define an aggressive cancer subtype. STK11 null cancers are “glutamine addicted” and we have shown glutamine deprivation results in a significant increase in live, detached ∆STK11 cells with the ability to re-adhere and proliferate in full media. Additionally, expression of pro-survival, anti-apoptotic and EMT markers in ∆STK11 cells were increased upon glutamine deprivation. Assessment of O-GlcNAcylation levels revealed that ∆STK11 cells had enhanced HBP flux upon decreasing glutamine availability. We hypothesize that conditions of glutamine stress promote metastatic potential in STK11 null KRAS-driven LUAD due to metabolic rewiring.
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Undergraduate
Date
2024-01-01