Resumen
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.
| Idioma original | English |
|---|---|
| Páginas (desde-hasta) | 1145-1148 |
| Número de páginas | 4 |
| Publicación | Experimental and Toxicologic Pathology |
| Volumen | 65 |
| N.º | 7-8 |
| DOI | |
| Estado | Published - nov 2013 |
ODS de las Naciones Unidas
Este resultado contribuye a los siguientes Objetivos de Desarrollo Sostenible
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Good health and well being
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Toxicology
- Cell Biology
Huella
Profundice en los temas de investigación de 'Induction of miR-21-PDCD4 signaling by UVB in JB6 cells involves ROS-mediated MAPK pathways'. En conjunto forman una huella única.Citar esto
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