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

Authors
Hou-LC; Bowman-L; Meighan-TG; Pratheeshkuma-P; Shi-X; Ding-M
Source
Exp Toxicol Pathol 2013 Nov; 65(7-8):1145-1148
NIOSHTIC No.
20043547
Abstract
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.
Keywords
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
Contact
Lichao Hou, Graduate Center for Toxicology, College of Medicine, The University of Kentucky, Lexington, KY 40503
CODEN
ETPAEK
Publication Date
20131101
Document Type
Journal Article
Email Address
lichao.hou@hotmail.com
Fiscal Year
2014
NTIS Accession No.
NTIS Price
Identifying No.
M122013
Issue of Publication
7-8
ISSN
0940-2993
NIOSH Division
HELD
Priority Area
Construction; Manufacturing
Source Name
Experimental and Toxicologic Pathology
State
KY; WV
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