Abstract IA13: The LKB1-AMPK pathway reprograms cancer cell metabolism

The serine/threonine kinase LKB1 is a tumor suppressor gene mutated in the familial cancer condition Peutz-Jeghers syndrome, as well as in 30% of non-small cell lung cancer (NSCLC). One of the critical substrates of LKB1 is AMPK, a highly conserved sensor of cellular energy status that restores metabolic homeostasis following stress. Thus LKB1 is a unique energy-state sensitive regulator of growth and metabolic reprogramming via its effects on AMPK. Our laboratory has performed a three-pronged screen to identify novel substrates of AMPK and related kinases that may mediate LKB1 effects on tumor suppression, metabolism, and metastasis. These findings have also spurred examination of whether compounds that activate AMPK may exhibit anti-cancer activities. Notably, the most widely used type 2 diabetes therapeutic in the US and worldwide, metformin, is a mitochondrial OXPHOS inhibitor that activates AMPK. We have therefore examined the potential anti-cancer effects of metformin and compounds against other metabolic targets.Citation Format: Reuben J. Shaw. The LKB1-AMPK pathway reprograms cancer cell metabolism. [abstract]. In: Proceedings of the AACR Special Conference: Metabolism and Cancer; Jun 7-10, 2015; Bellevue, WA. Philadelphia (PA): AACR; Mol Cancer Res 2016;14(1_Suppl):Abstract nr IA13.
Source: Molecular Cancer Research - Category: Cancer & Oncology Authors: Tags: Alterations of Nutrient/Fuel Sensing in Cancer: Oral Presentations - Invited Abstracts Source Type: research