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Exp Toxicol Pathol. 2013 Nov;65(7-8):1145-8. doi: 10.1016/j.etp.2013.05.006. Epub 2013 Jul 26.

Induction of miR-21-PDCD4 signaling by UVB in JB6 cells involves ROS-mediated MAPK pathways.

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Graduate Center for Toxicology, College of Medicine, The University of Kentucky, Lexington, KY 40503, USA; Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA; Department of Anesthesiology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi Province 710032, PR China.


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.


JB6 cell; PDCD4; Reactive oxygen species; Ultraviolet light; microRNA-21

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