Cellular Aging Isn’t Just About Wrinkles—It Can Drive Tumor Growth Too

We often think of wrinkles as signs of aging, but at the cellular level, aging can drive tumor growth. Cellular senescence refers to the condition in which damaged cells cease to divide but instead remain active without entering programmed cell death. Developed as a protective measure, cellular senescence ensures that damaged cells do not develop cancer. Once there are several such cells, they stop being defensive and start promoting tumour growth rather silently.

The real villain: SASP

With age and in response to various stressors, such as DNA damage and chemotherapy, senescent cells accumulate naturally. The real problem is the senescence-associated secretory phenotype (SASP), a mix of molecules that can push cancer forward. SASP is a range of bioactive chemicals, like cytokines, chemokines, growth factors, and proteases, which can affect the tumor microenvironment (TME). Senescent cells stay active and keep releasing SASP factors into nearby tissues, reshaping the environment around them.

How aging cells help tumors thrive

Through SASP, these aging cells create conditions that help tumors grow and spread. A constant release of these molecules can promote a tumoral environment known as the tumor microenvironment (TME). This cascade creates chronic inflammation that pushes cells to multiply uncontrollably. Moreover, it can lead to tissue remodeling, suppression of anti-tumor immunity by immunosuppressive cells, and triggering epithelial-to-mesenchymal transition (EMT) in neighboring pre-malignant cells, which makes these cells invasive.

Why do they make treatments struggle?

Chemotherapy and radiation work by causing heavy DNA damage in cancer cells. The remaining cells become harder to kill and more resistant to stress. These residual tumor cells are highly pro-survival. When SASP is released, it protects nearby cancer cells from the drug, accelerates tumor recurrence, and promotes cancer stemness. This sets the stage for the tumor to return faster and more aggressively after treatment.

Cutting off tumor support at the source

Senescent cells don’t stay harmless. They drive inflammation, weaken immune defenses, and create conditions that help tumors grow. Clearing them is emerging as a strong therapeutic strategy. Senolytic drugs lead this approach by targeting these aging cells and removing them without harming healthy tissue. Early preclinical findings show a clear pattern: reduced inflammation, improved immune activity, better treatment response, and a lower risk of recurrence or spread.