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The Senescence-Associated Secretory Phenotype: Critical Effector in Skin Cancer and Aging

Kanad Ghosh1, Brian C Capell2

  • 1Epigenetics Program, Department of Cell and Developmental Biology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.

The Journal of Investigative Dermatology
|August 22, 2016
PubMed

Insights

Cellular senescence halts damaged cell growth but its associated secretory phenotype (SASP) can paradoxically promote skin cancer. Targeting SASP may offer new prevention and therapy strategies.

Area of Science:

  • Oncology
  • Cell Biology
  • Dermatology

Background:

  • Cellular senescence is a key anti-cancer mechanism that arrests proliferation of damaged cells.
  • Senescent cells secrete factors (SASP) that can paradoxically promote cancer.
  • Removing senescent cells and reducing SASP may delay cancer onset and extend lifespan.

Purpose of the Study:

  • To review the evidence linking SASP and inflammation to skin carcinogenesis.
  • To highlight SASP mechanisms as potential targets for skin cancer prevention and therapy.

Main Methods:

  • Literature review of studies on cellular senescence, SASP, and skin cancer.
  • Analysis of the dual role of SASP in tumor suppression and promotion.
  • Examination of SASP-like inflammation in skin carcinogenesis.

Main Results:

  • Senescence is a double-edged sword in cancer, initially protective but potentially promoting it via SASP.
  • SASP and SASP-like inflammation are implicated in driving skin carcinogenesis.
  • Evidence suggests SASP reduction could be a therapeutic strategy.

Conclusions:

  • Understanding SASP's role in skin cancer is crucial for developing novel therapeutic strategies.
  • Targeting SASP and related inflammation presents a promising avenue for skin cancer prevention and treatment.

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