Abstract

ROLE OF COX-2 AND ROS IN UV-B INDUCED SKIN CARCINOGENESIS

Archana G.*, Kusu Suasan Cyriac and Aliya Kouser N.

ABSTRACT

Non-melanoma skin tumors are among those 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 elevates with the moving inflammatory cells, are firmly related with cancer or malignant advancement and has been demonstrated to be related with beginning, advancement or movement measures during multistage carcinogenesis. UV generation of COX-2 illustration and 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-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 within cells act as secondary messengers in intracellular signalling cascades which induce and maintain the oncogenic phenotype of cancer cells, however, ROS can also induce cellular senescence and apoptosis and can therefore function as anti-tumorigenic species.

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