Understanding cellular and molecular events of skin aging and cancer: An integrative perspective

Abstract

Aging of the skin is a gradual process, which is associated with changes in the appearance, characteristics, and function of the skin. Skin aging occurs through genetic, lifestyle, dietary, and environmental factors. Within the skin the production of collagen and elastin slows down, dead skin cells do not shed quickly, and the turnover of new skin cells decreases between the age group of 20 and 50. In addition to natural aging premature aging can also result which is due to sunlight exposure, chemical exposure, or other environmental pollutions. Ultraviolet radiation in sunlight damages the elastin and collagen fibers in the skin, which ultimately results in wrinkling of the skin at early stages of life. UV light induces approximately 99% of non-melanoma and 95% of melanoma-type skin cancers in humans. Excessive UV exposure produces genetic mutation that can lead to skin cancer. Skin carcinogenesis by DNA damage is considered a predominant paradigm for UV toxicity. Exposure to UV radiation can activate many oncogenes, which leads to skin cancer. Initiation and progression of skin carcinogenesis mediated by UV radiation involve complex pathways including those of apoptosis, proliferation, autophagy, DNA repair, metabolism, and inflammation. PTEN (phosphatase tensin homolog) is well established as a tumor suppressor gene that induces apoptosis and reduces cell proliferation by inhibition of the P13K/AKT pathway. p53 gene present in humans is being positioned on chromosome number 17 and mutations analyzed in the tumor suppressor gene p53 are one of prior genetic events which lead to the development of cancer in the skin due to exposure to UV rays. In this chapter we have discussed the mechanism of aging and skin cancer as an integrative phenomenon. We have also discussed briefly regarding the molecular biology methods and computational approaches to study the skin cancer and aging in a greater depth.