Investigating how metabolic alterations in STK11-null lung adenocarcinoma promote metastatic spread
Conference Year
2023
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.
Primary Faculty Mentor Name
Paula Deming
Status
Graduate
Student College
College of Nursing and Health Sciences
Program/Major
Medical Laboratory Science
Primary Research Category
Life Sciences
Investigating how metabolic alterations in STK11-null lung adenocarcinoma promote metastatic spread
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.