Aging cells fight cancer, but may help it spread

Scientists have found a stunning paradox in how aging affects cancer: While senescent cells can slow tumor growth, they may simultaneously create diseases that help cancer spread to other organs.

Studies published in aging show that different types of senescent cells have a hugely different impact on cancer progression, some acting as tumor suppressors, while others inadvertently promote metastasis.

This finding challenges traditional perspectives on the relationship between aging and cancer, suggesting that therapeutic strategies for senescent cells need to be much more precise than previously thought. This study could reshape how doctors receive cancer treatment in older patients who make up the vast majority of cancer cases.

Double-edged sword cell aging sword

Researchers at the University of Texas Health Science Center used transgenic mice to systematically turn off telomerase (the enzyme that maintains the end of the chromosome) in three specific cell types: immune cells, connective tissue cells, and vascular cells. This forces these cells to enter senescence, in which they stop dividing and begin secreting inflammatory signals.

When the team implanted breast, prostate and pancreatic cancer cells into these mice, they found that the aging of immune and connective tissue cells always slowed tumor growth. However, this obvious benefit presents an unsettling cost: The tumor shows signs of increased tissue damage and becoming more aggressive.

The greatest effect occurs when blood vessel cells are imposed on aging. Not only did these tumors shrink, but they also starved to death by insufficient blood supply. However, this oxygen deprivation poses an unexpected danger – pancreatic cancer cells become more likely to spread to the liver.

When oxygen is hungry.

This study reveals why targeting vascular aging can be particularly risky. When endothelial cells that are ducted into blood vessels become aging, they form abnormal, leaky blood vessels that cannot properly nourish the tumor. While this seems to be beneficial at first, the hypoxic environment produced triggers survival responses in cancer cells.

The main findings of vascular research include:

• Vascular decomposition: The blood vessels become smaller, the function is smaller, and the leakage is
• Oxygen Crisis: Tumors show massive activation of hypoxia-induced factors, a protein that helps cells survive hypoxia conditions
• Metabolic transfer: Cancer cells dramatically increase glucose consumption to survive without enough oxygen
• Transfer Advantages: Only mice with aging blood vessel cells have liver metastasis

This pattern reflects what happens in aggressive human cancers, where insufficient blood supply is often associated with an increased likelihood of metastasis.

Inflammation connection

When immune cells are imposed on aging, tumors grow slowly, but fibrous tissue and inflammation increase. The study shows that this is because aging immune cells turn toward producing inflammatory signals that can paradoxically fight cancer and promote tissue remodeling that can help tumors adapt.

Similarly, aging connective tissue cells form extensive scar-like tissue around the tumor. Although this appears to limit tumor growth initially, it also leads to the loss of normal cellular tissue, a marker of cancer progression.

Notably, the researchers found that by RNA sequencing analysis, the expression of a gene called PLOD2 in elderly vascular cells increased. The gene is known to promote epithelial to mesenchymal transition, a process that helps cancer cells become more fluid and invasive, explaining the increased metastasis observed in these mice.

Impact on cancer treatment

These findings are directly related to emerging “nose-soluble” therapies designed to eliminate senescent cells in aging. Although this treatment may benefit age-related diseases, this study suggests that they may have complex effects on cancer development and progression.

The study shows that senescent cell elimination strategies require specific cell types rather than broad targeting targets for all senescent cells. Removing aging immune or connective tissue cells may have benefits, and retaining functional blood vessels is essential for preventing metastasis.

Lead investigator Mikhail G. kolonin highlighted the complexity revealed by the institute: “This study shows that senescence and metabolic dysfunction caused by telomerase in different cells in the tumor microenvironment have different effects on tumor growth and metastasis of cancer.”

A new framework for understanding cancer

This study provides a new lens to understand why cancer has become more common and is often more aggressive with age. Instead of simply weakening the body’s defense, it seems to create a complex ecosystem where different cellular changes can help or hinder cancer progression.

This complexity could explain why many cancer studies conducted in young laboratory animals cannot capture the full picture of tumor manifestations in older organisms. The vast majority of human cancer patients have patients over 65 years of age, but most preclinical studies have used young animals that may not reflect the actual development of most cancers.

The results also suggest that cancer prevention and treatment strategies should take into account specific cellular senescence types that occur in different patients. Understand which cells are becoming aging and in which patterns help predict cancer risk and guide more effective interventions.

As population age and nasal soluble therapies move towards clinical use, this study provides crucial guidance for the development of therapies to exploit the anti-cancer effects of certain types of cellular aging while avoiding the promotion effects of others. The goal is no longer just to fight aging, but to understand and to its complex role in cancer biology.

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