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Treatment of epigallocatechin-3-gallate inhibits matrix metalloproteinases-2 and -9 via inhibition of activation of mitogen-activated protein kinases, c-jun and NF-kappaB in human prostate carcinoma DU-145 cells.
Prostate. 2004 Apr 01; 59(1):33-42.P

Abstract

BACKGROUND

Matrix metalloproteinases (MMPs) are involved in tumor progression including the carcinoma of the prostate (CaP). Therefore, the effect of (-)-epigallocatechin-3-gallate (EGCG) was determined on the synthesis and activation of tumor invasion-specific MMP-2 and MMP-9 in human prostate carcinoma DU-145 cells.

METHODS

MMP-2 and MMP-9 were determined by zymography and Western blot analysis. Since fibroblast conditioned medium (FCM) partially mimics in vivo tumor-host microenvironment, DU145 cells were co-cultured in FCM.

RESULTS

Treatment of EGCG to DU-145 cells resulted in dose-dependent inhibition of FCM-induced pro and active both forms of MMP-2 and MMP-9 concomitant with marked inhibition of phosphorylation of ERK1/2 and p38. In identical conditions, treatment of EGCG or inhibitors of MEK or p38 to DU-145 cells inhibited FCM-induced phosphorylation of ERK1/2 and/or p38 concomitant reduction in MMP-2 and -9. EGCG also inhibited androgen-induced pro-MMP-2 expression in LNCaP cells. Further, treatment of EGCG also resulted in inhibition of activation of c-jun and NF-kappaB in in vitro DU-145 cells.

CONCLUSIONS

The inhibition of MMP-2 and MMP-9 in DU145 cells by EGCG is mediated via inhibition of phosphorylation of ERK1/2 and p38 pathways, and inhibition of activation of transcription factors c-jun and NF-kappaB. EGCG may play a role in prevention of invasive metastatic processes of both androgen-dependent and -independent prostate carcinoma.

Authors+Show Affiliations

Department of Dermatology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.No affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

14991864

Citation

Vayalil, Praveen K., and Santosh K. Katiyar. "Treatment of Epigallocatechin-3-gallate Inhibits Matrix Metalloproteinases-2 and -9 Via Inhibition of Activation of Mitogen-activated Protein Kinases, C-jun and NF-kappaB in Human Prostate Carcinoma DU-145 Cells." The Prostate, vol. 59, no. 1, 2004, pp. 33-42.
Vayalil PK, Katiyar SK. Treatment of epigallocatechin-3-gallate inhibits matrix metalloproteinases-2 and -9 via inhibition of activation of mitogen-activated protein kinases, c-jun and NF-kappaB in human prostate carcinoma DU-145 cells. Prostate. 2004;59(1):33-42.
Vayalil, P. K., & Katiyar, S. K. (2004). Treatment of epigallocatechin-3-gallate inhibits matrix metalloproteinases-2 and -9 via inhibition of activation of mitogen-activated protein kinases, c-jun and NF-kappaB in human prostate carcinoma DU-145 cells. The Prostate, 59(1), 33-42.
Vayalil PK, Katiyar SK. Treatment of Epigallocatechin-3-gallate Inhibits Matrix Metalloproteinases-2 and -9 Via Inhibition of Activation of Mitogen-activated Protein Kinases, C-jun and NF-kappaB in Human Prostate Carcinoma DU-145 Cells. Prostate. 2004 Apr 1;59(1):33-42. PubMed PMID: 14991864.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Treatment of epigallocatechin-3-gallate inhibits matrix metalloproteinases-2 and -9 via inhibition of activation of mitogen-activated protein kinases, c-jun and NF-kappaB in human prostate carcinoma DU-145 cells. AU - Vayalil,Praveen K, AU - Katiyar,Santosh K, PY - 2004/3/3/pubmed PY - 2004/4/15/medline PY - 2004/3/3/entrez SP - 33 EP - 42 JF - The Prostate JO - Prostate VL - 59 IS - 1 N2 - BACKGROUND: Matrix metalloproteinases (MMPs) are involved in tumor progression including the carcinoma of the prostate (CaP). Therefore, the effect of (-)-epigallocatechin-3-gallate (EGCG) was determined on the synthesis and activation of tumor invasion-specific MMP-2 and MMP-9 in human prostate carcinoma DU-145 cells. METHODS: MMP-2 and MMP-9 were determined by zymography and Western blot analysis. Since fibroblast conditioned medium (FCM) partially mimics in vivo tumor-host microenvironment, DU145 cells were co-cultured in FCM. RESULTS: Treatment of EGCG to DU-145 cells resulted in dose-dependent inhibition of FCM-induced pro and active both forms of MMP-2 and MMP-9 concomitant with marked inhibition of phosphorylation of ERK1/2 and p38. In identical conditions, treatment of EGCG or inhibitors of MEK or p38 to DU-145 cells inhibited FCM-induced phosphorylation of ERK1/2 and/or p38 concomitant reduction in MMP-2 and -9. EGCG also inhibited androgen-induced pro-MMP-2 expression in LNCaP cells. Further, treatment of EGCG also resulted in inhibition of activation of c-jun and NF-kappaB in in vitro DU-145 cells. CONCLUSIONS: The inhibition of MMP-2 and MMP-9 in DU145 cells by EGCG is mediated via inhibition of phosphorylation of ERK1/2 and p38 pathways, and inhibition of activation of transcription factors c-jun and NF-kappaB. EGCG may play a role in prevention of invasive metastatic processes of both androgen-dependent and -independent prostate carcinoma. SN - 0270-4137 UR - https://www.unboundmedicine.com/medline/citation/14991864/Treatment_of_epigallocatechin_3_gallate_inhibits_matrix_metalloproteinases_2_and__9_via_inhibition_of_activation_of_mitogen_activated_protein_kinases_c_jun_and_NF_kappaB_in_human_prostate_carcinoma_DU_145_cells_ L2 - https://doi.org/10.1002/pros.10352 DB - PRIME DP - Unbound Medicine ER -