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Induction of miR-21-PDCD4 signaling by UVB in JB6 cells involves ROS-mediated MAPK pathways.
Hou-LC; Bowman-L; Meighan-TG; Pratheeshkuma-P; Shi-X; Ding-M
Exp Toxicol Pathol 2013 Nov; 65(7-8):1145-1148
Ultraviolet (UV) irradiation plays a major role in the development of human skin cancer. The present study examined the alterations of miR-21-PDCD4 signaling in a mouse epidermal cell line (JB6 P+) post exposure to UVB irradiation. The results showed that (1) UVB caused PDCD4 inhibition in JB6 cells; (2) exposure of cells to UVB caused a significant increase of miR-21, the upstream regulator of PDCD4, expression; (3) both inhibition of ERKs with U0126 and inhibition of p38 with SB203580 significantly reversed UVB-induced PDCD4 inhibition; (4) ROS scavenger, N-acetyl-L-cysteine reversed the inhibitory effect of UVB on PDCD4 expression. The above results suggested that UVB induced PDCD4 inhibition, which may be mediated through ROS, especially endogenous H2O2 and p38 and ERKs phosphorylation. Unraveling the complex mechanisms associated with these events may provide insights into the initiation and progression of UVB-induced carcinogenesis. Published by Elsevier GmbH.
Cancer; Skin; Skin-cancer; Animals; Laboratory-animals; Cell-function; Cellular-function; Exposure-levels; Carcinogens; Author Keywords: JB6 cell; PDCD4; microRNA-21; Reactive oxygen species; Ultraviolet light
Lichao Hou, Graduate Center for Toxicology, College of Medicine, The University of Kentucky, Lexington, KY 40503
Issue of Publication
Experimental and Toxicologic Pathology
Page last reviewed: July 22, 2019
Content source: National Institute for Occupational Safety and Health Education and Information Division