Metabolic rewiring promotes metastatic potential upon glutamine deprivation in STK11 null KRAS-driven lung adenocarcinoma
Conference Year
2024
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.
Primary Faculty Mentor Name
Paula Deming
Graduate Student Mentors
Shannon Prior
Status
Undergraduate
Student College
College of Arts and Sciences
Program/Major
Biological Science
Primary Research Category
Life Sciences
Metabolic rewiring promotes metastatic potential upon glutamine deprivation in STK11 null KRAS-driven lung adenocarcinoma
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.