Title : (-)-Epigallocatechin gallate downregulates EGF receptor via phosphorylation at Ser1046/1047 by p38 MAPK in colon cancer cells.

Pub. Date : 2009 Sep

PMID : 19578043






14 Functional Relationships(s)
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1 We previously reported that (-)-epigallocatechin gallate (EGCG) in green tea alters plasma membrane organization and causes internalization of epidermal growth factor receptor (EGFR), resulting in the suppression of colon cancer cell growth. epigallocatechin gallate epidermal growth factor receptor Homo sapiens
2 We previously reported that (-)-epigallocatechin gallate (EGCG) in green tea alters plasma membrane organization and causes internalization of epidermal growth factor receptor (EGFR), resulting in the suppression of colon cancer cell growth. epigallocatechin gallate epidermal growth factor receptor Homo sapiens
3 We previously reported that (-)-epigallocatechin gallate (EGCG) in green tea alters plasma membrane organization and causes internalization of epidermal growth factor receptor (EGFR), resulting in the suppression of colon cancer cell growth. epigallocatechin gallate epidermal growth factor receptor Homo sapiens
4 We previously reported that (-)-epigallocatechin gallate (EGCG) in green tea alters plasma membrane organization and causes internalization of epidermal growth factor receptor (EGFR), resulting in the suppression of colon cancer cell growth. epigallocatechin gallate epidermal growth factor receptor Homo sapiens
5 In the present study, we investigated the detailed mechanism underlying EGCG-induced downregulation of EGFR in SW480 colon cancer cells. epigallocatechin gallate epidermal growth factor receptor Homo sapiens
6 Prolonged exposure to EGCG caused EGFR degradation. epigallocatechin gallate epidermal growth factor receptor Homo sapiens
7 In addition, EGCG induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), a stress-inducible kinase believed to negatively regulate tumorigenesis, and the inhibition of p38 MAPK by SB203580, a specific p38 MAPK inhibitor, or the gene silencing using p38 MAPK-small interfering RNA (siRNA) suppressed the internalization and subsequent degradation of EGFR induced by EGCG. epigallocatechin gallate epidermal growth factor receptor Homo sapiens
8 EGFR underwent a gel mobility shift upon treatment with EGCG and this was canceled by SB203580, indicating that EGCG causes EGFR phosphorylation via p38 MAPK. epigallocatechin gallate epidermal growth factor receptor Homo sapiens
9 EGFR underwent a gel mobility shift upon treatment with EGCG and this was canceled by SB203580, indicating that EGCG causes EGFR phosphorylation via p38 MAPK. epigallocatechin gallate epidermal growth factor receptor Homo sapiens
10 EGFR underwent a gel mobility shift upon treatment with EGCG and this was canceled by SB203580, indicating that EGCG causes EGFR phosphorylation via p38 MAPK. epigallocatechin gallate epidermal growth factor receptor Homo sapiens
11 EGFR underwent a gel mobility shift upon treatment with EGCG and this was canceled by SB203580, indicating that EGCG causes EGFR phosphorylation via p38 MAPK. epigallocatechin gallate epidermal growth factor receptor Homo sapiens
12 Moreover, EGCG caused phosphorylation of EGFR at Ser1046/1047, a site that is critical for its downregulation and this was also suppressed by SB203580 or siRNA of p38 MAPK. epigallocatechin gallate epidermal growth factor receptor Homo sapiens
13 Taken together, our results strongly suggest that phosphorylation of EGFR at serine 1046/1047 via activation of p38 MAPK plays a pivotal role in EGCG-induced downregulation of EGFR in colon cancer cells. epigallocatechin gallate epidermal growth factor receptor Homo sapiens
14 Taken together, our results strongly suggest that phosphorylation of EGFR at serine 1046/1047 via activation of p38 MAPK plays a pivotal role in EGCG-induced downregulation of EGFR in colon cancer cells. epigallocatechin gallate epidermal growth factor receptor Homo sapiens