Mouse model of a UV sensitivity syndrome illustrates skin stem cell dysfunction is linked to cancer pathology.
Cell lifespan is limited by telomeres, DNA sequences that cap chromosomes and control the number of times a cell may be copied. A new study reported in Disease Models & Mechanisms (DMM) describes how telomere dysfunction in skin cells can lead to increased skin cancer risk and pigmentation.
Researchers from Spain investigated the molecular mechanisms underlying skin cell telomere dysfunction using a mouse model of Xeroderma Pigmentosum (XP), a disease in which patients have increased sensitivity to ultraviolet (UV) radiation. Their studies revealed that these mice have impaired skin cell regeneration, and that limiting the activity of a tumor suppressor signaling protein, p53, restores cell regeneration and reduces hyperpigmentation. Surprisingly, limiting p53 activity also advances the progression of skin cancers.
This study establishes a link between telomere dysfunction, cancer progression and the dysfunction of DNA repair mechanisms in XP patients. Understanding the pathways which control cell regeneration and cancer progression in these patients will not only aid in treatments for XP patients, but can likewise provide clues on how to target and better treat other cases of skin cancer.
The report was written Gerdine J. Stout and Maria A. Blasco at the Spanish National Cancer Research Center in Madrid, Spain. The report is published in the March/April issue of Disease Models & Mechanisms (DMM), a research journal published by The Company of Biologists, a non-profit based in Cambridge, UK.
Materials provided by The Company of Biologists. Note: Content may be edited for style and length.
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