Follow us on Google News (click on ☆)
As cells age, they change the way they function. The team at the Memorial Sloan Kettering Cancer Center (MSK) discovered that, in older mice, lung cells accumulate iron but act as if they are iron-deficient. This dysfunction reduces their capacity for regeneration, a key factor in slowing down the emergence of tumors.
Researchers have highlighted the role of a protein called NUPR1. With age, its production increases, disrupting iron metabolism within cells. This reaction limits uncontrolled cell proliferation, a central process in cancer development.
By studying genetically modified mice predisposed to developing lung cancer, they observed a significant reduction in tumors among older rodents. Conversely, treatments administering iron or inhibiting NUPR1 restored cellular regeneration... and the tumor risk.
These findings raise questions about current therapeutic approaches. Treatments targeting ferroptosis, a form of cell death induced by iron, appear to be less effective in elderly patients. Aging cells, resistant to this mechanism, require tailored strategies to maximize benefits and reduce risks.
This study also raises questions about prevention. Researchers emphasize that cancerogenic exposures during youth, such as smoking or excessive tanning, have potentially more severe effects than previously thought. Focusing on preventive measures at these critical stages could limit cancer incidence in the long term.
Beyond cancer, these discoveries open pathways for treating disorders linked to poor cellular regeneration, such as certain chronic lung diseases. However, researchers caution: stimulating regeneration could inadvertently promote tumors in at-risk patients.
Age thus transforms cells and their response to therapies, underscoring the importance of personalized medicine. Understanding these biological changes is a crucial step toward developing treatments tailored to each stage of life.