Involvement of Impaired Interaction with .BETA.1 Integrin in Epigallocatechin Gallate-Mediated Inhibition of Fibrosarcoma HT-1080 Cell Adhesion to Fibronectin

Suzuki, Yasuo; Suzuki, Takuji; Minami, Takeshi; Isemura, Mamoru

doi:10.1248/jhs.52.103

Cited by 7 publications

(4 citation statements)

References 32 publications

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“…An earlier study from our laboratory has shown similar results in another human breast cancer cell line, MCF-7 [11]. Other reports have also shown that EGCG inhibits the adhesion of fibrosarcoma HT1080 cells to fibronectin by involving the fibronectin receptor a5b1 [23]. We have also shown that EGCG treatment considerably reduces the mRNA expression of the integrin receptors, a5b1 and avb3, in MDA-MB-231 cells.…”

Section: Discussionsupporting

confidence: 86%

Epigallocatechin-3-gallate (EGCG) downregulates gelatinase-B (MMP-9) by involvement of FAK/ERK/NFκB and AP-1 in the human breast cancer cell line MDA-MB-231

2010

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Epigallocatechin-3-gallate (EGCG) is effective against the initiation, progression, and invasion of carcinogenesis.Matrix-metalloproteinases (MMPs) are a family of endopeptidases that hydrolyze the majority of extracellular proteins. MMP-9 is one of the most important members of the family and we observed the effect of EGCG on MMP-9 in the human breast cancer cell line, MDA-MB-231.The effect of EGCG on MMP-9 was studied by gelatin zymography, western blot, quantitative and semiquantitative real-time RT-PCR, immunoflourescence, cell adhesion assay, enzyme-linked immunosorbent assay,and electrophoretic mobility shift assay. EGCG treatment reduced the activity, protein, and mRNA expression ofMMP-9 and enhanced the expression of the tissue inhibitor of MMP 1 (TIMP-1). EGCG downregulated the activation of focal adhesion kinase (FAK) and extracellular regulated kinase (ERK), reduced the adhesion of MDA-MB-231 cells to fibronectin and vitronectin, and reduced the mRNA expression of the integrin receptors alpha5beta1 and alphavbeta3. The expression of the nuclear factor kappa B (NFjB), and the DNA binding activity of NFjB and activator protein 1 (AP1)to MMP-9 promoter were noticeably reduced on EGCG treatment. Upregulation of TIMP-1 and disruption of the functional status of integrin receptors may indicate decreased MMP-9 activation; inhibition of FAK andERK activation might indicate disruption in the FAK/ERK-induced MMP-9 secretion and induction. Decreased DNA binding activity of NFjB and AP1 to MMP-9 promoter might indicate transcriptional deregulation of MMP-9 gene on EGCG treatment. We propose EGCG as a potential inhibitor of the expression and activity of MMP-9 by a process involving FAK/ERK and transcription factorsin MDA-MB-231.

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Section: Discussionsupporting

confidence: 86%

Epigallocatechin-3-gallate (EGCG) downregulates gelatinase-B (MMP-9) by involvement of FAK/ERK/NFκB and AP-1 in the human breast cancer cell line MDA-MB-231

2010

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“…These MMPs were identified as MMP2 and MMP9 ( Table 1 ) which have roles in the invasion and metastasis of cancer cells. Our research group has similarly demonstrated the binding interaction between EGCG and cell surface Fas protein [ 34 ], laminin, fibrinogen subunits, and integrin β1 [ 35 , 36 , 37 ]. These proteins are related to cancer, and EGCG binding would cause impairments in cancer development, which may be responsible for EGCG’s beneficial effects on cancer.…”

Section: Affinity Gel Chromatography (Agc) and Other Conventional mentioning

confidence: 99%

In Vitro and In Silico Studies of the Molecular Interactions of Epigallocatechin-3-O-gallate (EGCG) with Proteins That Explain the Health Benefits of Green Tea

et al. 2018

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Green tea has been shown to have beneficial effects on many diseases such as cancer, obesity, inflammatory diseases, and neurodegenerative disorders. The major green tea component, epigallocatechin-3-O-gallate (EGCG), has been demonstrated to contribute to these effects through its anti-oxidative and pro-oxidative properties. Furthermore, several lines of evidence have indicated that the binding affinity of EGCG to specific proteins may explain its mechanism of action. This review article aims to reveal how EGCG-protein interactions can explain the mechanism by which green tea/EGCG can exhibit health beneficial effects. We conducted a literature search, using mainly the PubMed database. The results showed that several methods such as dot assays, affinity gel chromatography, surface plasmon resonance, computational docking analyses, and X-ray crystallography have been used for this purpose. These studies have provided evidence to show how EGCG can fit or occupy the position in or near functional sites and induce a conformational change, including a quaternary conformational change in some cases. Active site blocking, steric hindrance by binding of EGCG near an active site or induced conformational change appeared to cause inhibition of enzymatic activity and other biological activities of proteins, which are related to EGCG’s biological oligomer and formation of their toxic aggregates, leading to the prevention of neurodegenerative diseases and amyloidosis. In conclusion, these studies have provided useful information on the action of green tea/catechins and would lead to future studies that will provide further evidence for rational EGCG therapy and use EGCG as a lead compound for drug design.

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“…Streptococcus mutans and Streptococcus salivarius have wall-associated protein A (wapA) in their outer membrane that allows them to bind collagen and a wide range of extracellular matrix molecules including type I collagen, laminin, keratin and Fn [22,23]. Tea catechins, such as EGCg, have been reported to impair the adhesion promoting ability of Fn [24], and inhibit the interactions between Fn and attaching cells by binding to the Fn receptor integrin β1 [25]. These catechins should theoretically inhibit attachment but this was not the case in our study.…”

Section: Resultsmentioning

confidence: 99%

Inhibition of attachment of oral bacteria to immortalized human gingival fibroblasts (HGF-1) by tea extracts and tea components

et al. 2013

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BackgroundTea has been suggested to promote oral health by inhibiting bacterial attachment to the oral cavity. Most studies have focused on prevention of bacterial attachment to hard surfaces such as enamel.FindingsThis study investigated the effect of five commercial tea (green, oolong, black, pu-erh and chrysanthemum) extracts and tea components (epigallocatechin gallate and gallic acid) on the attachment of five oral pathogens (Streptococcus mutans ATCC 25175, Streptococcus mutans ATCC 35668, Streptococcus mitis ATCC 49456, Streptococcus salivarius ATCC 13419 and Actinomyces naeslundii ATCC 51655) to the HGF-1 gingival cell line. Extracts of two of the teas (pu-erh and chrysanthemum) significantly (p < 0.05) reduced attachment of all the Streptococcus strains by up to 4 log CFU/well but effects of other teas and components were small.ConclusionsPu-erh and chrysanthemum tea may have the potential to reduce attachment of oral pathogens to gingival tissue and improve the health of oral soft tissues.

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Involvement of Impaired Interaction with .BETA.1 Integrin in Epigallocatechin Gallate-Mediated Inhibition of Fibrosarcoma HT-1080 Cell Adhesion to Fibronectin

Cited by 7 publications

References 32 publications

Epigallocatechin-3-gallate (EGCG) downregulates gelatinase-B (MMP-9) by involvement of FAK/ERK/NFκB and AP-1 in the human breast cancer cell line MDA-MB-231

Epigallocatechin-3-gallate (EGCG) downregulates gelatinase-B (MMP-9) by involvement of FAK/ERK/NFκB and AP-1 in the human breast cancer cell line MDA-MB-231

In Vitro and In Silico Studies of the Molecular Interactions of Epigallocatechin-3-O-gallate (EGCG) with Proteins That Explain the Health Benefits of Green Tea

Inhibition of attachment of oral bacteria to immortalized human gingival fibroblasts (HGF-1) by tea extracts and tea components

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