Metabolic rewiring promotes metastatic potential in STK11 null KRAS-driven lung adenocarcinoma
Conference Year
2024
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 lung adenocarcinoma (LUAD), patients have a worsened prognosis and increased metastasis. Interestingly, this lung cancer subtype also exhibits increased dependence on glutamine metabolism to support energetic and redox homeostasis. Our results suggest that “starving” KS LUAD cells of glutamine results in exacerbation of their aggressive phenotype via enhanced flux of the hexosamine biosynthetic pathway. This study aims to specifically identify how the rewired metabolism and utilization of glutamine in KS LUAD cells promotes metastasis.
Primary Faculty Mentor Name
Paula Deming
Status
Graduate
Student College
College of Nursing and Health Sciences
Program/Major
Cellular, Molecular and Biomedical Sciences
Primary Research Category
Life Sciences
Metabolic rewiring promotes metastatic potential in STK11 null KRAS-driven lung adenocarcinoma
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 lung adenocarcinoma (LUAD), patients have a worsened prognosis and increased metastasis. Interestingly, this lung cancer subtype also exhibits increased dependence on glutamine metabolism to support energetic and redox homeostasis. Our results suggest that “starving” KS LUAD cells of glutamine results in exacerbation of their aggressive phenotype via enhanced flux of the hexosamine biosynthetic pathway. This study aims to specifically identify how the rewired metabolism and utilization of glutamine in KS LUAD cells promotes metastasis.