Inhibitory Effect of (-)-Epigallocatechin and (-)-Epigallocatechin Gallate against Heregulin .BETA.1-Induced Migration/Invasion of the MCF-7 Breast Carcinoma Cell Line

Kushima, Yukihiro; Iida, Kei; Nagaoka, Yasuo; Kawaratani, Yasuyuki; Shirahama, Tatsuya; Sakaguchi, Minoru; K, Baba; Hara, Yukihiko; Uesato, Shinichi

doi:10.1248/bpb.32.899

Cited by 37 publications

(24 citation statements)

References 26 publications

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“…These effects resulted from the inhibition of MMP-2; MT1-MMP; NF-kB; VEGF; integrin receptor-α5, integrin receptor-β1, integrin receptor-αv, integrin receptor-β3; VASP; FAK; and Rac1 by EGCG [91,92]. When MCF-7 cells were first stimulated with heregulin-β1, EGCG and EGC treatment inhibited the induced migration and invasion via suppression of the activation of the epidermal growth factor receptor-related protein B2 (ErbB2)/ErbB3 pathway [93]. Treatment with 50 μg/ml EGCG blocked the invasion in vitro in MCF-7Tam cells, a breast carcinoma cell line resistant to tamoxifen (a drug for breast carcinoma therapy), by downregulating EGFR, MMP-2/MMP-9, and EMM-PRIN and by increasing TIMP-1/TIMP-2 [94].…”

Section: Egcg Egc Ecg and Ecmentioning

confidence: 99%

Flavonoids, a ubiquitous dietary phenolic subclass, exert extensive in vitro anti-invasive and in vivo anti-metastatic activities

Weng

Yen

2012

Cancer Metastasis Rev

191

128

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Cancer metastasis refers to the spread of cancer cells from the primary neoplasm to distant sites, where secondary tumors are formed, and is the major cause of death from cancer. Natural phytochemicals containing phenolic compounds have been widely demonstrated to have the capability to prevent cancer metastasis. Among phenolic compounds, flavonoids are a very large subclass, and they are abundant in food and nutraceuticals. The number of reports demonstrating that flavonoids are an effective natural inhibitor of cancer invasion and metastasis is increasing in the scientific literature. Catechin derivatives, (−)-epigallocatechin-3-gallate, (−)-epigallocatechin, (−)-epicatechin-3-gallate,and (−)-epicatechin, are the most studied compounds in this topic so far; genistein/genistin, silibinin, quercetin, and anthocyanin have also been widely investigated for their inhibitory activities on invasion/metastasis. Other flavonoids in dietary vegetable foods that are responsible for anti-invasive and anti-metastatic activities of tumors include luteolin,apigenin, myricetin, tangeretin, kaempferol, glycitein, licoricidin,daidzein, and naringenin. To effectively overcome the metastatic cascade, including cell-cell attachment, tissue barrier degradation, migration, invasion, cell-matrix adhesion,and angiogenesis, it is essential that a bioactive compound prevent tumor cells from metastasizing. This review summarizes the effects of flavonoids on the metastatic cascade and the related proteins, the in vitro anti-invasive activity of flavonoids against cancer cells, and the effects of flavonoids on antiangiogenic and in vivo anti-metastatic models. The available scientific evidence indicates that flavonoids are a ubiquitous dietary phenolics subclass and exert extensive in vitro anti-invasive and in vivo anti-metastatic activities.

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Section: Egcg Egc Ecg and Ecmentioning

confidence: 99%

Flavonoids, a ubiquitous dietary phenolic subclass, exert extensive in vitro anti-invasive and in vivo anti-metastatic activities

Weng

Yen

2012

Cancer Metastasis Rev

191

128

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“…EGCG suppressed adhesion and invasion of hepatocarcinoma cells through antioxidant activity (6). EGCG inhibited the growth and metastasis of pancreatic cancer (7,8) and colorectal cancer (9), reduced the incidence of esophageal cancer (10) and improved the prognosis of breast cancer (11). It also inhibited the growth of HepG2 cells (12).…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-gallate inhibits cell growth, induces apoptosis and causes S phase arrest in hepatocellular carcinoma by suppressing the AKT pathway

Shen

Zhang

Yan

et al. 2014

International Journal of Oncology

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Abstract. Epigallocatechin-3-gallate (EGCG) has been shown to inhibit the growth and induce apoptosis of certain cancer cells. The aim of this study was to determine the role of EGCG in hepatocellular carcinoma (HCC) and the underlying mechanism(s) thereof. MTT assay was used to determine the cell growth inhibition by EGCG. Apoptosis induced by EGCG was investigated by both AO/EB staining and flow cytometry. The cell cycle distribution was analyzed by flow cytometry. The mRNA levels of the AKT pathway were analyzed by quantitative PCR. The expression of AKT and its phosphorylation at Ser473 were detected by western blotting. The IC 50 of EGCG at 48 h for HepG2, SMMC7721 and SK-hep1 cells were 74.7, 59.6 and 61.3 µg/ml, respectively. Significantly higher proportion of SMMC7721 cells entered the S phase upon treatment with EGCG for 48 h compared with control cells. EGCG decreased the mRNA levels of PI3K, AKT and NF-κB. The protein levels of AKT decreased and its phosphorylation at Ser473 was downregulated with EGCG treatment. EGCG inhibited growth by affecting the cell cycle and induced apoptosis in different HCC cells by downregulating PI3K/ AKT activity. The results suggest the potential of EGCG as an anticancer agent in the prevention or treatment of HCC.

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“…In the present study, we showed that EGCG exhibits anti-invasion and anti-migration effect on SGT cells at the concentrations showing little cytotoxicity. EGCG has been reported to inhibit invasion and metastasis of a variety of cancer cells (14)(15)(16)(17). Moreover, EGCG inhibited adhesion and migration of stromal cells such as fibroblasts (28).…”

Section: Discussionmentioning

confidence: 99%

“…EGCG is the most abundant polyphenol in green tea and has been found to inhibit growth of tumor cells by inducing apoptosis or inhibiting angiogenesis (12,13). In addition, EGCG inhibits invasion and metastasis of a variety of tumor cells (14)(15)(16)(17). Sakagami's group showed that EGCG induced apoptosis of human salivary gland tumor HSG (18,19).…”

Section: Introductionmentioning

confidence: 99%

(−)-Epigallocatechin-3-gallate inhibits invasion and migration of salivary gland adenocarcinoma cells

Park

Yoon²,

Kim³

et al. 2009

Oncol Rep

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Abstract. (-)-Epigallocatechin-3-gallate (EGCG) has inhibitory effect on a variety of cancers by inducing apoptosis and cell cycle arrest or inhibiting angiogenesis and metastasis. EGCG has been found to induce apoptosis in salivary gland carcinoma cells, however, it is not known whether EGCG affects invasion and migration. Thus, this study was performed to clarify whether EGCG affects invasion and migration of salivary gland tumors. Matrigel invasion assay, wound scratch assay and migration assay using commercial kit were performed. ß1 integrin expression and activation of its downstream molecules such as focal adhesion kinase (FAK), AKT and extracellular signal-regulated kinase (ERK) were examined by Western blot. Enzymatic activity of matrix metalloprotease (MMP)-2 and MMP-9 was examined by gelatin zymography. EGCG inhibited effectively invasion and migration of SGT cells in a dose-dependent manner. EGCG also inhibited the activation of ß1 integrin-downstream molecules such as FAK, AKT and ERK as well as the expression of ß1 integrin itself. Moreover, MMP-2 and MMP-9 expression and their enzymatic activity were reduced by EGCG in a dose-dependent manner. These results indicate that EGCG may effectively suppress salivary gland tumors by inhibiting metastasis through ß1 integrinmediated signaling.

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Inhibitory Effect of (-)-Epigallocatechin and (-)-Epigallocatechin Gallate against Heregulin .BETA.1-Induced Migration/Invasion of the MCF-7 Breast Carcinoma Cell Line

Cited by 37 publications

References 26 publications

Flavonoids, a ubiquitous dietary phenolic subclass, exert extensive in vitro anti-invasive and in vivo anti-metastatic activities

Flavonoids, a ubiquitous dietary phenolic subclass, exert extensive in vitro anti-invasive and in vivo anti-metastatic activities

Epigallocatechin-3-gallate inhibits cell growth, induces apoptosis and causes S phase arrest in hepatocellular carcinoma by suppressing the AKT pathway

(−)-Epigallocatechin-3-gallate inhibits invasion and migration of salivary gland adenocarcinoma cells

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