Role of COX-2 and ROS in UV-B Induced Skin Carcinogenesis
Non-melanoma skin tumors are among the cutaneous basal cell and squamous cell tumors (cSCCs), are the most predominant malignancies. While UV-stimulated p53 transformations give off an impression of being an early and essential occasion in the enhancement of skin tumors, another significant provider is the over-expression of cyclooxygenase-2 (COX-2). Oxidative pressures elevate with the moving inflammatory cells, are firmly related with cancer or malignant advancement, and have been demonstrated to be related with beginning, advancement, or movement measures during multistage carcinogenesis. UV generation of COX-2 illustration and Prostaglandin E2 (PGE2) creation is thought to advance skin carcinogenesis, as well as add up to even the most initial stages of UV-instigated skin damage. ROS (Reactive Oxygen Species) - intervened DNA injury assumes participation in the induction of carcinogenesis as well as in dangerous malignant alteration, and it might signify a significant donor in the pathogenesis of human carcinogenesis. The induction of COX-2 expression by acute UV exposure and constitutive up-regulation of COX-2 in UV-induced benign and malignant tumors leads to increased PGE2 production. ROS present inside the cells which are intracellular signaling cascades perform a function such as secondary messengers where they induce and maintain the oncogenic phenotype of cancer cells; however, cellular senescence and apoptosis can also be induced by ROS, and hence they also, therefore, function as anti-tumorigenic species.