Abstract
The skin acts as the primary defense organ that protects the body from the external environment. Skin cancer is one of the most common cancers in the world. Skin carcinogenesis is usually caused by cell degeneration due to exposure to ultraviolet (UV) radiation, which causes changes in various signaling networks, disrupting the homeostasis of single skin cells. In this review, we summarize the roles of nicotinamide adenine dinucleotide phosphate oxidase (NOX) and epidermal growth factor receptor (EGFR) in UV-induced skin carcinogenesis. Furthermore, we describe the crosstalk that exists between NOX, EGFR, and protein tyrosine phosphatase κ and its oncogenic downstream signaling pathways. Chemoprevention is the use of chemical compounds to recover the healthy status of the skin or delay cancer development. Current evidence from in vitro and in vivo studies on chemopreventive phytochemicals that target NOX, EGFR, or both, as major regulators of skin carcinogenesis will also be discussed.
Highlights
Based on recent cancer statistics, 10 million people died of skin cancer (9.9 million excluding nonmelanoma skin cancers [NMSCs]) in 2020 [1]
While NMSC is the most frequently detected skin malignancy, which accounts for 40% of all cancers diagnosed in the United States [3], malignant melanomas are detected in only 4% of all skin cancers [4]
We reported in various studies that phytochemicals can prevent cancer by acting as inhibitors of the oncogenic molecules, Fyn, Src, aryl hydrocarbon receptor (AhR), phosphoinositide 3-kinase (PI3K), Raf, and extracellular signal-regulated kinase (ERK)2 both in vitro and in vivo
Summary
Based on recent cancer statistics, 10 million people died of skin cancer (9.9 million excluding nonmelanoma skin cancers [NMSCs]) in 2020 [1]. Epidemiological studies have proven that solar UV irradiation is the most important environmental carcinogen contributing to skin cancer development [7]. Prolonged exposure to UV impairs skin homeostasis and stimulates responses to environmental changes, including the production of reactive oxygen species (ROS) These responses lead to the activation of multiple signaling cascades, which switch on the expression of oncogenic and tumor suppressor genes. We introduce nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and epidermal growth factor receptor (EGFR) as molecular targets that can complement antioxidant activity and effectively inhibit skin cancer via the regulation of various signaling networks. By summarizing the results of our research and that of other scientists, we aim to introduce materials that could prevent or control skin cancer and skin diseases through the regulation of NOX and EGFR
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