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.
Original language | English |
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Pages (from-to) | 1145-1148 |
Number of pages | 4 |
Journal | Experimental and Toxicologic Pathology |
Volume | 65 |
Issue number | 7-8 |
DOIs | |
State | Published - Nov 2013 |
Keywords
- JB6 cell
- MicroRNA-21
- PDCD4
- Reactive oxygen species
- Ultraviolet light
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Toxicology
- Cell Biology