New study shows aging may act as a protective factor against cancer despite long-held beliefs.
Researchers are uncovering surprising insights about the relationship between aging and cancer, challenging some longstanding assumptions about how these two processes interact. While it is well-known that age increases the likelihood of developing cancer due to the accumulation of genetic mutations over time, oddly enough, a new study conducted at Memorial Sloan Kettering Cancer Center shows aging can also act as a protective factor against certain types of cancer due to decreasing cell growth.
Using a rodent model focused specifically on lung cancer, the team found that as cells age, their ability to regenerate diminishes, which helps with decreasing unchecked proliferation driving tumor formation. This phenomenon provides a potential explanation for decreasing cancer incidences among the oldest age groups, particularly beyond 80 years of age.
The researchers focused on a protein called NUPR1, which becomes more abundant in lung cells as mice age. Increased levels of NUPR1 caused these cells to behave as though they were deficient in iron, despite having sufficient iron stores. This altered iron metabolism seemed to reduce the regenerative capacity of the cells, curbing the formation of new tumors. However, when older mice were given additional iron or had NUPR1 levels reduced, their cells regained regenerative abilities, which also restored the potential for cancer development.
This discovery suggests that therapies targeting iron metabolism might need to be tailored based on a patient’s age. For younger individuals, where cells retain high regenerative potential, treatments that manipulate iron-related pathways might be more effective. Older patients, whose cells show resistance to these changes, could require alternative therapeutic strategies.
One area of interest among the research team is the role of ferroptosis—a form of cell death driven by iron—in cancer treatments. Drugs designed to induce ferroptosis have shown promise in targeting cancer cells, but the effectiveness of these treatments may vary depending on the age of the patient. Older cells, which behave as though they are iron deficient, appear less susceptible to ferroptosis than younger cells. This insight could help refine clinical approaches, ensuring treatments are more precisely matched to the biological characteristics of patients at different stages of life.
The findings also emphasize the importance of preventive measures during youth and middle age, when the biological conditions that lead to cancer initiation are most active. Lifestyle factors such as smoking, excessive sun exposure, and other carcinogenic behaviors during these years may set the stage for cancer later in life. The data suggest that efforts to reduce these risks early on could have a substantial impact on long-term health outcomes.
Beyond its implications for cancer prevention and treatment, this research opens new avenues for addressing age-related conditions involving diminished cellular regeneration. For instance, in individuals with impaired lung function due to infection or other damage, improving regeneration through iron supplementation could offer therapeutic benefits. However, this approach must be applied cautiously, as restoring cellular regeneration could inadvertently heighten cancer risk in certain populations.
The study also highlights the importance of tailoring medical treatments to reflect the unique biological changes that occur with age. By accounting for how aging impacts cellular processes such as iron metabolism and regeneration, clinicians can design therapies that are more effective and safer for patients across the lifespan.
Sources:
Aging reduces cancer risk by limiting cell regeneration
Ageing limits stemness and tumorigenesis by reprogramming iron homeostasis
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