(−)-Epigallocatechin-3-gallate (EGCG) inhibits HGF-induced invasion and metastasis in hypopharyngeal carcinoma cells

Lim, Young Chang; Park, Hun Yi; Hwang, Hye Sook; Kang, Sung Un; Pyun, Jung Hee; Lee, Mi-Hye; Choi, Eun Chang; Kim, Chul‐Ho

doi:10.1016/j.canlet.2008.05.048

Cited by 74 publications

(49 citation statements)

References 37 publications

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“…We found that overexpression of HGF and c-Met was noted in more than half of oral cancer cases by immunohistochemical staining and that c-Met staining correlated significantly with lymph node metastasis, tumor stage and recurrence (data not shown). In a previous study, we demonstrated that HGF increased c-Met tyrosine phosphorylation and that HGF-induced phosphorylated c-Met expression was attenuated by EGCG in FaDu cells, a hypopharyngeal cancer cell line [28]. Based on these previous results, we tested whether HGF could induce oral cancer progression and if EGCG could inhibit HGF-induced invasion and metastasis in oral cavity cancer in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

Green tea (−)-epigallocatechin-3-gallate inhibits HGF-induced progression in oral cavity cancer through suppression of HGF/c-Met

Koh

Choi

Kang

et al. 2011

The Journal of Nutritional Biochemistry

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Section: Discussionmentioning

confidence: 99%

Green tea (−)-epigallocatechin-3-gallate inhibits HGF-induced progression in oral cavity cancer through suppression of HGF/c-Met

Koh

Choi

Kang

et al. 2011

The Journal of Nutritional Biochemistry

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“…Recent studies revealed that EGCG modulates the cell signaling pathways associated with angiogenesis, metastasis, and migration of prostate, liver and breast cancer cells [17] . Lim et al found that EGCG effectively inhibited HGF-induced invasion and metastasis of hypopharyngeal carcinoma cells via several intracellular signaling pathways [18] . In the current study, we investigated whether EGCG was able to interfere or factor VIIa (10 nmol/L) in the absence or presence of EGCG (100 μg/ mL) for 2 h or 24 h. Then the total RNAs (2 h) and cell lysates (24 h) were collected for caspase-7 mRNA (A) and its protein (B) determination using QT-PCR and Western blot analysis, respectively.…”

Section: Discussionmentioning

confidence: 99%

“…For example, Annabi et al demonstrated that EGCG directly and indirectly decreased MMP-9 secretion in macrophage-like HL-60 cells [23] . Lim et al showed that EGCG was able to inhibit the HGF-induced MMP-9 activity in hypopharyngeal carcinoma cells [18] . Taken together, these results suggest that EGCG is capable of blocking the expression of some key molecules in tumor cells and, therefore, it contributes to the suppression of cell proliferation, migration and metastasis.…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-gallate inhibits proliferation and migration of human colon cancer SW620 cells in vitro

Zhou

Wang

et al. 2011

Acta Pharmacol Sin

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Aim: Epigallocatechin-3-gallate (EGCG) is the major polyphenolic constituent in green tea. The aim of this study is to investigate the effects of EGCG on proliferation and migration of the human colon cancer SW620 cells. Methods: Proliferation and migration of SW620 cells were induced by the protease-activated receptor 2-agonist peptide (PAR2-AP, 100 μmol/L) or factor VIIa (10 nmol/L), and analyzed using MTT and Transwell assays, respectively. The cellular cytoskeleton was stained with rhodamine-conjugated phalloidin and examined with a laser scanning confocal fluorescence microscope. The expression of caspase-7, tissue factor (TF) and matrix metalloproteinase (MMP)-9 in the cells was examined using QT-PCR, ELISA and Western blot assays. The activation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and nuclear factor-kappa B (NF-κB) signaling pathways was analyzed with Western blot. Results: Both PAR2-AP and factor VIIa promoted SW620 cell proliferation and migration, and caused cytoskeleton reorganization (increased filopodia and pseudopodia). Pretreatment with EGCG (25, 50, 75, and 100 μg/mL) dose-dependently blocked the cell proliferation and migration induced by PAR2-AP or factor VIIa. EGCG (100 μg/mL) prevented the cytoskeleton changes induced by PAR2-AP or factor VIIa. EGCG (100 μg/mL) counteracted the down-regulation of caspase-7 expression and up-regulation of TF and MMP-9 expression in the cells treated with PAR2-AP or factor VIIa. Furthermore, it blocked the activation of ERK1/2 and NF-κB (p65/RelA) induced by PAR2-AP or factor VIIa. Conclusion: EGCG blocks the proliferation and migration of SW620 cells induced by PAR2-AP and factor VIIa via inhibition of the ERK1/2 and NF-κB pathways. The compound may serve as a preventive and therapeutic agent for colon cancers.

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“…These observations are in line with earlier studies showing that HGF stimulates the secretion of MMP-9 in other cell lines. 25,26 In the present study, NFD inhibited HGF-induced MMP-9 expression and activity in MDA-MB-231 cells. The MMP-9 inhibitor significantly suppressed HGFinduced migration and invasion.…”

Section: Discussionmentioning

confidence: 87%

Inhibitory action of naphtho[1,2‐b]furan‐4,5‐dione on hepatocyte growth factor‐induced migration and invasion of MDA‐MB‐231 cells: Mechanisms of action

Tsai

Chu

Tseng

et al. 2014

Clin Exp Pharma Physio

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SUMMARYNaphtho [1,2-b]furan-4,5-dione (NFD), a bioactive component of Avicennia marina, has been shown to exhibit anticancer activity. The aim of the present study was to explore the effect of NFD on hepatocyte growth factor (HGF)-induced cell migration and invasion of MDA-MB-231 human breast cancer cells, as well as the underlying mechanism of action. Cell viability was determined using the 3-(4,5-dimethyl-2 thiazoyl)-2,5-diphenyl-2H-tetrazolium bromide assay, western blot analysis was used to measure protein expression and cell migration and invasion were evaluated by the cell wound healing assay, Boyden chamber assay and gelatin zymography. When cells were treated with non-toxic concentrations of NFD (1-3 lmol/L, 24 h), NFD concentration-dependently inhibited HGF-promoted cell migration and invasion. Simultaneously, NFD efficiently suppressed c-Met phosphorylation and downstream activation of phosphatidylinositol 3-kinase (PI3K) and Akt. In addition, NFD inhibited the phosphorylation of IjB kinases and IjBa and nuclear translocation of nuclear factor (NF)-jB, as well as matrix metalloproteinase (MMP)-9 activity. Furthermore, the c-Met inhibitor PHA665752 (10 lmol/L) inhibited HGF-induced MMP-9 expression, cell migration and invasion, as well as the activation of PI3K/Akt, suggesting that PI3K/Akt activation occur downstream of c-Met activation. In conclusion, the results of the present study suggest that NFD inhibits HGF-induced invasion and migration of MDA-MB-231 cells via HGF-and/ or c-Met-mediated PI3K/Akt and NF-jB signalling pathways, leading to downregulation of MMP-9 expression and cell migration.

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(−)-Epigallocatechin-3-gallate (EGCG) inhibits HGF-induced invasion and metastasis in hypopharyngeal carcinoma cells

Cited by 74 publications

References 37 publications

Green tea (−)-epigallocatechin-3-gallate inhibits HGF-induced progression in oral cavity cancer through suppression of HGF/c-Met

Green tea (−)-epigallocatechin-3-gallate inhibits HGF-induced progression in oral cavity cancer through suppression of HGF/c-Met

Epigallocatechin-3-gallate inhibits proliferation and migration of human colon cancer SW620 cells in vitro

Inhibitory action of naphtho[1,2‐b]furan‐4,5‐dione on hepatocyte growth factor‐induced migration and invasion of MDA‐MB‐231 cells: Mechanisms of action

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