A new study has determined that cancer development is promoted by switching to a high calorie diet after cancer has been detected. The generally accepted idea has always been that unhealthy diets promote cancer development. For the first time researchers have examined the specific gene and metabolic changes involved.
The change in diet was linked to stressing the endoplasmic reticulum contained in cells. The endoplasmic reticulum functions as a transport mechanism for the cell and is involved in protein regulation. A rise in stress in this area increases expression of chaperones, which are molecules that aid protein function.
The predominant effect of stressing the ER results in cell death. The team says changing to a high-calorie diet after tumor growth started, however, may fuel further growth because the tumor cells have already adapted to an increase in endoplasmic reticulum stress; more stress encourages further tumor cell proliferation.
“Our study does not show that, by eating junk food, people would be protected from lung cancer. But the high-calorie diet helped us discover a very specific molecular mechanism required for lung tumor cells to proliferate that could pave the way for new therapeutic approaches,” said Professor Giorgio Ramadori of the University of Geneva.
The team found that blocking a protein called FKBP10 impairs cells growth while avoiding healthy cells. RNA Molecules of long tumors from both low and high calorie diets were analyzed and it was determined that switching to a high-calorie diet significantly reduced expression of a chaperone protein called FKBP10, which was only found in lung cancer cells.
“In this study we show that knockdown of FKBP10 leads to reduced cancer growth. Human lung cancer cells express FKBP10 while the nearby healthy lung tissue does not; this is very interesting and appealing to eventually translate these findings to the clinical arena, said Professor Ramadori. “Hence, if we manage to identify the right inhibitor, we may open the door to new therapeutic strategies that will be able to hinder cancer cells’ proliferation without damaging the healthy cells. The inhibition of this protein is predicted to have minimal side effects as it is not expressed in healthy tissues, at least in adulthood.”
Diet-induced unresolved ER stress hinders KRAS-driven lung tumorigenesis, Roberto Coppari, et al., Cell Metabolism, published online 18 December 2014.