2017
DOI: 10.1080/09637486.2017.1401980
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Epigallocatechin-3-O-gallate alleviates the malignant phenotype in A-431 epidermoid and SK-BR-3 breast cancer cell lines

Abstract: In this study, we evaluated the effects of epigallocatechin-3-O-gallate (EGCG) in two cancer cell lines, A-431 overexpressing ErbB1 and SK-BR-3, overexpressing ErbB2. EGCG treatment showed dose-dependent collapse of mitochondrial membrane potential (Δψ), increase in reactive oxygen species (ROS) production, changes in nuclear morphology and reduced viability. Flow cytometry data indicated that EGCG partially decreases the phosphorylation of several proteins involved in cell proliferation and survival: pErbB1(Y… Show more

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Cited by 12 publications
(9 citation statements)
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“…EGCG is able to stop growth of MCF-7Tam cells, a breast carcinoma cell line resistant to tamoxifen, through downregulation of EGFR, EMMPRIM and other molecules implicated in an aggressive biological behavior [31]. This catechin inhibits EGFR signaling pathway, mainly by direct inhibition of ERK1/2 and Akt kinases, which supports the role of EGCG as an inhibitor of breast cancer cell proliferation since this pathway is intrinsically related to the control of cell proliferation [32].…”
Section: Induction Of Cell Cycle Arrest (Table 2)mentioning
confidence: 55%
See 1 more Smart Citation
“…EGCG is able to stop growth of MCF-7Tam cells, a breast carcinoma cell line resistant to tamoxifen, through downregulation of EGFR, EMMPRIM and other molecules implicated in an aggressive biological behavior [31]. This catechin inhibits EGFR signaling pathway, mainly by direct inhibition of ERK1/2 and Akt kinases, which supports the role of EGCG as an inhibitor of breast cancer cell proliferation since this pathway is intrinsically related to the control of cell proliferation [32].…”
Section: Induction Of Cell Cycle Arrest (Table 2)mentioning
confidence: 55%
“…Similarly, Hong et al proved that EGCG decreases MDA-MB-231 cell viability through downregulation of the expression of β-catenin, cyclin D1, and p-AKT [39]. Moreover, Filippi et al demonstrated that EGCG was able to reduce the viability of SK-BR-3 cells, a human breast cancer cell line that overexpresses the Her2 (Neu/ErbB-2) gene product [32]. Finally, EGCG was found to be the most effective inhibitor of MCF-7 cell proliferation and viability, as compared to other epicatechin derivatives such as (-)epicatechin (EC), (-)-epicatechin gallate (ECG), (-)epigallocatechin (EGC) [24].…”
Section: Induction Of Cell Cycle Arrest (Table 2)mentioning
confidence: 98%
“…Lipid rafts are rich in tyrosine kinase receptors (RTKs), such as EGFR [116,117,118], IGF1R [119], and HER2 [120]. These receptors have been found to be inhibited by EGCG in several in vitro and in vivo cancer models (e.g., colon, lung, liver and breast cancers) [92,121,122,123]. The functional proteins recruited by lipid rafts allow these structures to play complex roles.…”
Section: 67-kda Laminin Receptor Signalling Pathwaysmentioning
confidence: 99%
“…As reported, under some external causes, cells will suffer from serious depletion of mitochondrial membrane potential, thus inducing apoptosis [ 27 ]. The cells treated with 50 µM EGCG for 0.5–24 hours in human glioblastoma cells [ 28 ], or 50–100 µM EGCG for 72 hours in epidermoid carcinoma and breast adenocarcinoma cells both observed a decrease in mitochondrial membrane potential [ 29 ]. Our results also confirmed that EGCG can reduce MMP and induce depolarization through a mitochondrial-dependent pathway, leading to increased apoptosis (Figures 1 and 2 ).…”
Section: Discussionmentioning
confidence: 99%