A new research has identified an "Achilles heel" in a metabolic pathway that is important in stopping the growth of lung cancer cells.
Research at University of Texas Southwestern Medical Center demonstrated that by activating peroxisome proliferation-activated receptor gamma (PPAR?), a protein that regulates glucose and lipid metabolism in normal cells, with antidiabetic drugs in lung cancer cells, they could stop these tumor cells from dividing.
Researcher Ralf Kittler said that activation of PPAR? causes a major metabolic change in cancer cells that impairs their ability to handle oxidative stress.
Kittler added that the increased oxidative stress ultimately inhibits the growth of the tumor, and on activation of PPAR?, it killed both cancer cells grown in a dish and tumors in mice, in which they observed near complete tumor growth inhibition.
The findings suggest that targeting PPAR? could be a promising new therapeutic approach for lung cancer and potentially other cancers and the researchers saw that activating PPAR? caused similar molecular changes in breast cancer cells.
Kittler continued that this is an important finding because the drugs that activate PPAR? include FDA-approved antidiabetic drugs that are relatively well tolerated compared to chemotherapy and knowing their mechanism of action provides them with clues for selecting tumors that may be responsive to this treatment, for combining these drugs with anti-cancer drugs to make therapy more effective, and for developing markers to measure the response of tumors to these drugs in patients.
The study is published in the journal Cell Metabolism.
