UVB-induced Epidermal Growth Factor Receptor Phosphorylation is Critical for Downstream Signaling and Keratinocyte Survival ¶

Péus, Dominik; Vasa, R; Meves, Alexander; Beyerle, Astrid; Pittelkow, Mark R.

doi:10.1562/0031-8655(2000)0720135uiegfr2.0.co2

Cited by 30 publications

(29 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Peus et al (1999bPeus et al ( , 2000 have demonstrated that ERK, JNK, and p38 are activated in human epidermal keratinocytes following exposure to UVB irradiation. Several lines of evidence have supported that the activation of these kinases correlates with skin cell death in response to UVB (Assefa et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

(+)-Catechin prevents ultraviolet B-induced human keratinocyte death via inhibition of JNK phosphorylation

Chiang

Fang

et al. 2006

Life Sciences

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

(+)-Catechin prevents ultraviolet B-induced human keratinocyte death via inhibition of JNK phosphorylation

Chiang

Fang

et al. 2006

Life Sciences

View full text Add to dashboard Cite

“…The activation of an EGFR-PI3K-AKT pathway is essential for the anti-apoptotic response of keratinocytes in response to ultraviolet B (UVB) radiation (FIGURE 5) (430). UV light inhibits the phosphatase activity, leading to activation of RTKs like EGFR (268).…”

Section: A Egfr Activation and Skin Homeostasismentioning

confidence: 99%

Expression and Function of the Epidermal Growth Factor Receptor in Physiology and Disease

Chen

Zeng

Forrester

et al. 2016

Physiological Reviews

220

156

View full text Add to dashboard Cite

The epidermal growth factor receptor (EGFR) is the prototypical member of a family of membrane-associated intrinsic tyrosine kinase receptors, the ErbB family. EGFR is activated by multiple ligands, including EGF, transforming growth factor (TGF)-α, HB-EGF, betacellulin, amphiregulin, epiregulin, and epigen. EGFR is expressed in multiple organs and plays important roles in proliferation, survival, and differentiation in both development and normal physiology, as well as in pathophysiological conditions. In addition, EGFR transactivation underlies some important biologic consequences in response to many G protein-coupled receptor (GPCR) agonists. Aberrant EGFR activation is a significant factor in development and progression of multiple cancers, which has led to development of mechanism-based therapies with specific receptor antibodies and tyrosine kinase inhibitors. This review highlights the current knowledge about mechanisms and roles of EGFR in physiology and disease.

show abstract

“…Epidermal growth factor (EGF) receptor, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), and tumor necrosis factor-a have been used to study UVB-mediated promotional events in JB6 cells (7,18). Inhibition of EGF pathway affords resistance to UVB-mediated cell transformation (7).…”

Section: Introductionmentioning

confidence: 99%

Silibinin inhibits UVB- and epidermal growth factor–induced mitogenic and cell survival signaling involving activator protein-1 and nuclear factor-κB in mouse epidermal JB6 cells

Singh

Dhanalakshmi²,

Mohan³

et al. 2006

Molecular Cancer Therapeutics

View full text Add to dashboard Cite

UVB radiation is the major etiologic factor in the development of nonmelanoma skin cancer. In addition to tumor-initiating effect, UVB also causes tumor promotion via mitogenic and survival signaling. Studies have shown strong preventive effects of silibinin against both UVB-induced and chemically induced tumor promotion in mouse skin models; however, mechanisms are not understood completely. Here, we used tumor promoter -sensitive JB6 mouse epithelial cell model and studied the effect of silibinin on two different mitogens [UVB and epidermal growth factor (EGF)] that induce mitogenic and cell survival signaling pathways. UVB (50 -800 mJ/cm 2 ) dose-dependently induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun-NH 2 -kinase 1/2 (JNK1/2), and p38 kinase (p38K) as well as Akt, with an optimum response at 400 mJ/cm 2 UVB dose. UVB caused a biphasic phosphorylation of ERK1/2 in a time kinetics study. Silibinin treatment before or immediately after UVB exposure, or both, resulted in a strong decrease in UVB-caused phosphorylation of ERK1/2 and Akt in both dose-and time-dependent manner, without any substantial response on JNK1/2 and p38K. Silibinin also suppressed UVB-induced activator protein-1 (AP-1) and nuclear factor-KB (NF-KB) activation, which are activated by ERK1/2 and Akt. Silibinin treatment under similar conditions also strongly inhibited EGF-induced ERK1/2, JNK1/2, and p38K as well as Akt phosphorylation, and also suppressed EGF-induced AP-1 and NF-KB activation. Because AP-1 and NF-KB are important nuclear transcription factors for tumor promotion, these results suggest that silibinin possibly prevents skin tumor promotion by inhibiting UVB-and EGF-induced mitogenic and cell survival signaling involving both AP-1 and NF-KB.

show abstract

UVB-induced Epidermal Growth Factor Receptor Phosphorylation is Critical for Downstream Signaling and Keratinocyte Survival ¶

Cited by 30 publications

References 44 publications

(+)-Catechin prevents ultraviolet B-induced human keratinocyte death via inhibition of JNK phosphorylation

(+)-Catechin prevents ultraviolet B-induced human keratinocyte death via inhibition of JNK phosphorylation

Expression and Function of the Epidermal Growth Factor Receptor in Physiology and Disease

Silibinin inhibits UVB- and epidermal growth factor–induced mitogenic and cell survival signaling involving activator protein-1 and nuclear factor-κB in mouse epidermal JB6 cells

Contact Info

Product

Resources

About