Cellular senescence in skin aging and cancer
Cellular senescence in skin aging and cancer
Aging is a natural process, but the reasons why aged tissues lose their ability to function properly are still not fully understood. One important factor is the accumulation of senescent cells: cells that stop dividing after stress or damage but remain alive and can influence surrounding tissues.
In this thesis, Chen Ge investigated how senescent cells contribute to skin aging and cancer development, and how their effects can be controlled. Ge found that senescent skin cells can escape immune surveillance and create a tissue environment that supports melanoma progression after UV-induced damage. I also showed that adapalene, a commonly used retinoid in dermatology, influences the fate of UV-damaged skin cells by promoting apoptosis before stable senescence is established, providing new insight into its potential role in photoaging.
Furthermore, we identified why senescent melanocytes are resistant to certain senolytic treatments and demonstrated that targeting their survival pathways can improve their elimination.
Together, this work shows that senescent cells are not merely inactive “aged cells”, but active regulators of tissue aging and cancer development. Understanding how these cells persist, communicate with the immune system, and respond to treatments may open new strategies for improving healthy aging and preventing age-related diseases.