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Inhibition of ultraviolet B--induced c-fos gene expression and p38 mitogen-activated protein kinase activation by (-)-epigallocatechin gallate in a human keratinocyte cell line.
Mol Carcinog 1999; 24(2):79-84MC

Abstract

(-)-Epigallocatechin gallate (EGCG), the major polyphenol isolated from green tea, is an active chemoprevention agent against cancer. However, the molecular mechanisms that underlie the inhibitory effects of EGCG are not well understood. In this study, we tested the effects of EGCG on ultraviolet (UV) B radiation-induced c-fos gene expression in a human keratinocyte cell line, HaCaT. EGCG inhibited UVB-induced steady-state message and transcriptional activation of the c-fos gene in a dose-dependent manner. Western analyses further indicated that EGCG had an inhibitory effect on UVB-induced accumulation of the c-fos protein within the same dose range. To further examine the mechanism by which EGCG inhibits UVB-induced c-fos expression, we tested the effect of EGCG on upstream activators of the c-fos gene. We found that EGCG significantly inhibited activation of p38 mitogen-activated protein kinase but not c-jun NH2-terminal kinase or extracellular signal-regulated protein kinase activation. Our previous studies have indicated that UVB-induced c-fos expression may play a key role in UVB-induced activation of the activator protein-1 transcription factor and EGCG-inhibited, UVB-induced activation of AP-1 in HaCaT cells. Because AP-1 is important for tumor promotion and c-fos is a major component of AP-1, the inhibitory effects of EGCG on c-fos expression may further explain the anti-tumor-promoting effects of EGCG.

Authors+Show Affiliations

Department of Radiation Oncology, Arizona Cancer Center, College of Medicine, The University of Arizona, Tucson 85721, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

10078934

Citation

Chen, W, et al. "Inhibition of Ultraviolet B--induced C-fos Gene Expression and P38 Mitogen-activated Protein Kinase Activation By (-)-epigallocatechin Gallate in a Human Keratinocyte Cell Line." Molecular Carcinogenesis, vol. 24, no. 2, 1999, pp. 79-84.
Chen W, Dong Z, Valcic S, et al. Inhibition of ultraviolet B--induced c-fos gene expression and p38 mitogen-activated protein kinase activation by (-)-epigallocatechin gallate in a human keratinocyte cell line. Mol Carcinog. 1999;24(2):79-84.
Chen, W., Dong, Z., Valcic, S., Timmermann, B. N., & Bowden, G. T. (1999). Inhibition of ultraviolet B--induced c-fos gene expression and p38 mitogen-activated protein kinase activation by (-)-epigallocatechin gallate in a human keratinocyte cell line. Molecular Carcinogenesis, 24(2), pp. 79-84.
Chen W, et al. Inhibition of Ultraviolet B--induced C-fos Gene Expression and P38 Mitogen-activated Protein Kinase Activation By (-)-epigallocatechin Gallate in a Human Keratinocyte Cell Line. Mol Carcinog. 1999;24(2):79-84. PubMed PMID: 10078934.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of ultraviolet B--induced c-fos gene expression and p38 mitogen-activated protein kinase activation by (-)-epigallocatechin gallate in a human keratinocyte cell line. AU - Chen,W, AU - Dong,Z, AU - Valcic,S, AU - Timmermann,B N, AU - Bowden,G T, PY - 1999/3/17/pubmed PY - 2000/6/20/medline PY - 1999/3/17/entrez SP - 79 EP - 84 JF - Molecular carcinogenesis JO - Mol. Carcinog. VL - 24 IS - 2 N2 - (-)-Epigallocatechin gallate (EGCG), the major polyphenol isolated from green tea, is an active chemoprevention agent against cancer. However, the molecular mechanisms that underlie the inhibitory effects of EGCG are not well understood. In this study, we tested the effects of EGCG on ultraviolet (UV) B radiation-induced c-fos gene expression in a human keratinocyte cell line, HaCaT. EGCG inhibited UVB-induced steady-state message and transcriptional activation of the c-fos gene in a dose-dependent manner. Western analyses further indicated that EGCG had an inhibitory effect on UVB-induced accumulation of the c-fos protein within the same dose range. To further examine the mechanism by which EGCG inhibits UVB-induced c-fos expression, we tested the effect of EGCG on upstream activators of the c-fos gene. We found that EGCG significantly inhibited activation of p38 mitogen-activated protein kinase but not c-jun NH2-terminal kinase or extracellular signal-regulated protein kinase activation. Our previous studies have indicated that UVB-induced c-fos expression may play a key role in UVB-induced activation of the activator protein-1 transcription factor and EGCG-inhibited, UVB-induced activation of AP-1 in HaCaT cells. Because AP-1 is important for tumor promotion and c-fos is a major component of AP-1, the inhibitory effects of EGCG on c-fos expression may further explain the anti-tumor-promoting effects of EGCG. SN - 0899-1987 UR - https://www.unboundmedicine.com/medline/citation/10078934/Inhibition_of_ultraviolet_B__induced_c_fos_gene_expression_and_p38_mitogen_activated_protein_kinase_activation_by_____epigallocatechin_gallate_in_a_human_keratinocyte_cell_line_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0899-1987&date=1999&volume=24&issue=2&spage=79 DB - PRIME DP - Unbound Medicine ER -