Green tea (−)-epigallocatechin-3-gallate inhibits HGF-induced progression in oral cavity cancer through suppression of HGF/c-Met
Hepatocyte growth factor (HGF) and c-Met have recently attracted a great deal of attention as prognostic indicators of patient outcome, and they are important in the control of tumor growth and invasion. Epigallocatechin-3-gallate (EGCG) has been shown to modulate multiple signal pathways in a manne...
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Published in | The Journal of nutritional biochemistry Vol. 22; no. 11; pp. 1074 - 1083 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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Elsevier Inc
01.11.2011
Elsevier |
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Abstract | Hepatocyte growth factor (HGF) and c-Met have recently attracted a great deal of attention as prognostic indicators of patient outcome, and they are important in the control of tumor growth and invasion. Epigallocatechin-3-gallate (EGCG) has been shown to modulate multiple signal pathways in a manner that controls the unwanted proliferation and invasion of cells, thereby imparting cancer chemopreventive and therapeutic effects. In this study, we investigated the effects of EGCG in inhibiting HGF-induced tumor growth and invasion of oral cancer
in vitro and
in vivo. We examined the effects of EGCG on HGF-induced cell proliferation, migration, invasion, induction of apoptosis and modulation of HGF/c-Met signaling pathway in the KB oral cancer cell line. We investigated the antitumor effect and inhibition of c-Met expression by EGCG in a syngeneic mouse model (C3H/HeJ mice, SCC VII/SF cell line). HGF promoted cell proliferation, migration, invasion and induction of MMP (matrix metalloproteinase)-2 and MMP-9 in KB cells. EGCG significantly inhibited HGF-induced phosphorylation of Met and cell growth, invasion and expression of MMP-2 and MMP-9. EGCG blocked HGF-induced phosphorylation of c-Met and that of the downstream kinases AKT and ERK, and inhibition of p-AKT and p-ERK by EGCG was associated with marked increases in the phosphorylation of p38, JNK, cleaved caspase-3 and poly-ADP-ribose polymerase. In C3H/HeJ syngeneic mice, as an
in vivo model, tumor growth was suppressed and apoptosis was increased by EGCG. Our results suggest that EGCG may be a potential therapeutic agent to inhibit HGF-induced tumor growth and invasion in oral cancer. |
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AbstractList | Hepatocyte growth factor (HGF) and c-Met have recently attracted a great deal of attention as prognostic indicators of patient outcome, and they are important in the control of tumor growth and invasion. Epigallocatechin-3-gallate (EGCG) has been shown to modulate multiple signal pathways in a manner that controls the unwanted proliferation and invasion of cells, thereby imparting cancer chemopreventive and therapeutic effects. In this study, we investigated the effects of EGCG in inhibiting HGF-induced tumor growth and invasion of oral cancer in vitro and in vivo. We examined the effects of EGCG on HGF-induced cell proliferation, migration, invasion, induction of apoptosis and modulation of HGF/c-Met signaling pathway in the KB oral cancer cell line. We investigated the antitumor effect and inhibition of c-Met expression by EGCG in a syngeneic mouse model (C3H/HeJ mice, SCC VII/SF cell line). HGF promoted cell proliferation, migration, invasion and induction of MMP (matrix metalloproteinase)-2 and MMP-9 in KB cells. EGCG significantly inhibited HGF-induced phosphorylation of Met and cell growth, invasion and expression of MMP-2 and MMP-9. EGCG blocked HGF-induced phosphorylation of c-Met and that of the downstream kinases AKT and ERK, and inhibition of p-AKT and p-ERK by EGCG was associated with marked increases in the phosphorylation of p38, JNK, cleaved caspase-3 and poly-ADP-ribose polymerase. In C3H/HeJ syngeneic mice, as an in vivo model, tumor growth was suppressed and apoptosis was increased by EGCG. Our results suggest that EGCG may be a potential therapeutic agent to inhibit HGF-induced tumor growth and invasion in oral cancer. Hepatocyte growth factor (HGF) and c-Met have recently attracted a great deal of attention as prognostic indicators of patient outcome, and they are important in the control of tumor growth and invasion. Epigallocatechin-3-gallate (EGCG) has been shown to modulate multiple signal pathways in a manner that controls the unwanted proliferation and invasion of cells, thereby imparting cancer chemopreventive and therapeutic effects. In this study, we investigated the effects of EGCG in inhibiting HGF-induced tumor growth and invasion of oral cancer in vitro and in vivo. We examined the effects of EGCG on HGF-induced cell proliferation, migration, invasion, induction of apoptosis and modulation of HGF/c-Met signaling pathway in the KB oral cancer cell line. We investigated the antitumor effect and inhibition of c-Met expression by EGCG in a syngeneic mouse model (C3H/HeJ mice, SCC VII/SF cell line). HGF promoted cell proliferation, migration, invasion and induction of MMP (matrix metalloproteinase)-2 and MMP-9 in KB cells. EGCG significantly inhibited HGF-induced phosphorylation of Met and cell growth, invasion and expression of MMP-2 and MMP-9. EGCG blocked HGF-induced phosphorylation of c-Met and that of the downstream kinases AKT and ERK, and inhibition of p-AKT and p-ERK by EGCG was associated with marked increases in the phosphorylation of p38, JNK, cleaved caspase-3 and poly-ADP-ribose polymerase. In C3H/HeJ syngeneic mice, as an in vivo model, tumor growth was suppressed and apoptosis was increased by EGCG. Our results suggest that EGCG may be a potential therapeutic agent to inhibit HGF-induced tumor growth and invasion in oral cancer. |
Author | Choi, Eun Chang Lee, Mi Hye Pyun, JungHee Koh, Yoon Woo Hwang, Hye Sook Kim, Chul-Ho Park, RaeHee Kang, Sung Un Lee, YoungDon |
Author_xml | – sequence: 1 givenname: Yoon Woo surname: Koh fullname: Koh, Yoon Woo organization: Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, Republic of Korea – sequence: 2 givenname: Eun Chang surname: Choi fullname: Choi, Eun Chang organization: Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, Republic of Korea – sequence: 3 givenname: Sung Un surname: Kang fullname: Kang, Sung Un organization: Department of Otolaryngology, School of Medicine, Ajou University, Suwon, Republic of Korea – sequence: 4 givenname: Hye Sook surname: Hwang fullname: Hwang, Hye Sook organization: Department of Otolaryngology, School of Medicine, Ajou University, Suwon, Republic of Korea – sequence: 5 givenname: Mi Hye surname: Lee fullname: Lee, Mi Hye organization: Department of Otolaryngology, School of Medicine, Ajou University, Suwon, Republic of Korea – sequence: 6 givenname: JungHee surname: Pyun fullname: Pyun, JungHee organization: Department of Otolaryngology, School of Medicine, Ajou University, Suwon, Republic of Korea – sequence: 7 givenname: RaeHee surname: Park fullname: Park, RaeHee organization: Department of Anatomy, School of Medicine, Ajou University, Suwon, Republic of Korea – sequence: 8 givenname: YoungDon surname: Lee fullname: Lee, YoungDon organization: Department of Anatomy, School of Medicine, Ajou University, Suwon, Republic of Korea – sequence: 9 givenname: Chul-Ho surname: Kim fullname: Kim, Chul-Ho email: ostium@ajou.ac.kr organization: Department of Otolaryngology, School of Medicine, Ajou University, Suwon, Republic of Korea |
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Keywords | Head and neck cancer c-Met Oral cancer HGF EGCG Tumor invasion Stomatology Epigallocatechin-3-gallate Malignant tumor Oral cavity Vertebrata Mammalia ENT disease Oral cavity disease Green tea Cancer |
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SubjectTerms | animal models Animals apoptosis Biological and medical sciences c-Met caspase-3 Catechin - analogs & derivatives Catechin - pharmacology cell growth Cell Movement - drug effects cell proliferation Cell Proliferation - drug effects Chemoprevention Disease Progression EGCG Feeding. Feeding behavior Female Fundamental and applied biological sciences. Psychology gelatinase A green tea Head and neck cancer hepatocyte growth factor Hepatocyte Growth Factor - antagonists & inhibitors HGF Humans KB Cells Matrix Metalloproteinase 2 - biosynthesis Matrix Metalloproteinase 9 - biosynthesis Mice mitogen-activated protein kinase Mouth Neoplasms - pathology Neoplasm Invasiveness Oral cancer phosphorylation Proto-Oncogene Proteins c-met - antagonists & inhibitors Proto-Oncogene Proteins c-met - biosynthesis Signal Transduction - drug effects Tea therapeutics Tumor invasion Vertebrates: anatomy and physiology, studies on body, several organs or systems |
Title | Green tea (−)-epigallocatechin-3-gallate inhibits HGF-induced progression in oral cavity cancer through suppression of HGF/c-Met |
URI | https://dx.doi.org/10.1016/j.jnutbio.2010.09.005 https://www.ncbi.nlm.nih.gov/pubmed/21292466 https://search.proquest.com/docview/898841832 |
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