Rewiring of glutamine metabolism in STK11-null lung cancer
Conference Year
January 2022
Abstract
STK11 is a tumor suppressor that down-regulates cell growth upon energetic depletion. When mutations leading to STK11 loss-of-function cooccur with KRAS driving mutations (KS) in non-small cell lung cancer (NSCLC), patients have a worsened prognosis and increased rate of metastasis. Interestingly, this lung cancer subtype also exhibits increased dependence on glutamine metabolism to support energetic and redox homeostasis. Our preliminary results suggest that “starving” KS NSCLC cells of glutamine results in rewired metabolism and exacerbation of their aggressive phenotype. This study aims to specifically identify how the rewired metabolism and utilization of glutamine in KS NSCLC cells promotes metastasis.
Primary Faculty Mentor Name
Paula Deming
Faculty/Staff Collaborators
David Seward, MD, PhD and Eyal Amiel, PhD
Student Collaborators
Sean Lenahan, Tyler Hogan and Hailey Sarausky
Status
Graduate
Student College
College of Nursing and Health Sciences
Program/Major
Cellular, Molecular and Biomedical Sciences
Primary Research Category
Health Sciences
Rewiring of glutamine metabolism in STK11-null lung cancer
STK11 is a tumor suppressor that down-regulates cell growth upon energetic depletion. When mutations leading to STK11 loss-of-function cooccur with KRAS driving mutations (KS) in non-small cell lung cancer (NSCLC), patients have a worsened prognosis and increased rate of metastasis. Interestingly, this lung cancer subtype also exhibits increased dependence on glutamine metabolism to support energetic and redox homeostasis. Our preliminary results suggest that “starving” KS NSCLC cells of glutamine results in rewired metabolism and exacerbation of their aggressive phenotype. This study aims to specifically identify how the rewired metabolism and utilization of glutamine in KS NSCLC cells promotes metastasis.