Investigating how metabolic alterations in STK11-null lung adenocarcinoma promote metastatic spread
Prior, Shannon
Prior, Shannon
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Abstract
Non-small cell lung adenocarcinomas (LUAD) with concurrent oncogenic KRAS and SKT11 loss-of-function mutations represent an aggressive subtype that is characterized, in part, by increased metastasis and enhanced dependence on glutamine metabolism. We aim to elucidate the metabolic rewiring of STK11-null KRAS-driven lung adenocarcinoma cells and determine how such altered metabolism may promote metastasis. Our preliminary results demonstrate an upregulation of metastatic markers and anoikis resistance upon exogenous glutamine deprivation in STK11-null cells. Given that glutamine deprivation is being considered as a therapeutic option to “starve” certain cancers, future studies will investigate the molecular mechanism(s) driving this enhanced metastatic potential.
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Graduate
Date
2023-01-01