Harnessing the nuclear receptor PPARγ to inhibit the growth of lung adenocarcinoma by rewiring metabolic circuitries.
Altered metabolism and nuclear receptor activity have been reported in various cancer types. Here, we discuss our recent finding that the metabolic state of lung adenocarcinoma cells expressing the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) can be modulated by thiazolidinediones, culminating in accumulation of reactive oxygen species and decreased proliferation.
Eugene McDermott Center for Human Growth and Development; The University of Texas Southwestern Medical Center; Dallas, TX USA; Hamon Center for Therapeutic Oncology Research; The University of Texas Southwestern Medical Center; Dallas, TX USA.
Paul
P
Yenerall
Eugene McDermott Center for Human Growth and Development; The University of Texas Southwestern Medical Center; Dallas, TX USA; Simmons Comprehensive Cancer Center; The University of Texas Southwestern Medical Center; Dallas, TX USA; Department of Pharmacology; The University of Texas Southwestern Medical Center; Dallas, TX USA; Green Center for Reproductive Biology Sciences; The University of Texas Southwestern Medical Center; Dallas, TX USA.
Ralf
R
Kittler
PPARγ; lung cancer; metabolism; nuclear receptor; targeted therapy