Inhibition of oncogenic Src induces FABP4-mediated lipolysis via PPARγ activation exerting cancer growth suppression.

ABSTRACT:

Background

c-Src is a driver oncogene well-known for tumorigenic signaling, but little for metabolic function. Previous reports about c-Src regulation of glucose metabolism prompted us to investigate its function in other nutrient modulation, particularly in lipid metabolism.

Methods

Oil-red O staining, cell growth assay, and tumor volume measurement were performed to determine lipid amount and growth inhibitory effect of treatments in lung cancer cells and xenograft model. Gene expression was evaluated by immunoblotting and relative RT-PCR. Transcriptional activity of peroxisome proliferator-activated receptor gamma (PPARγ) was assessed by luciferase assay. Reactive oxygen species (ROS) was measured using ROS sensing dye. Oxygen consumption rate was evaluated by Seahorse XF

SUBMITTER: Hua TNM 

PROVIDER: S-EPMC6442332 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature