Green tea polyphenols and its constituent epigallocatechin gallate inhibits proliferation of human breast cancer cells in vitro and in vivo

Thangapazham, Rajesh L.; Singh, Anoop; Sharma, Anuj; Warren, James W.; Gaddipati, Jaya P.; Maheshwari, Radha K.

doi:10.1016/j.canlet.2006.01.027

Cited by 279 publications

(196 citation statements)

References 36 publications

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“…Other studies have also shown that EGCG or green tea extract has a modest inhibitory effect on ER-negative tumour growth (Landis-Piwowar et al, 2007;Thangapazham et al, 2007;Somers-Edgar et al, 2008). For example, EGCG (50 mg kg À1 , s.c.) was minimally effective at reducing tumour growth in a MDA-MB-231 xenograft model, but acetylating EGCG and thus turning it into a pro-drug enhanced its efficacy (Landis-Piwowar et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

“…was based on our previous study, which demonstrated that this dose was non-toxic and elicited a modest decrease in MDA-MB-231 tumour growth (Somers-Edgar et al, 2008). This dose is also twofold lower than that recently used in other ER-negative xenograft experiments with EGCG (Landis-Piwowar et al, 2007;Thangapazham et al, 2007). On the basis of our in vitro experiments with EGCG þ tamoxifen, we wanted to use a very low dose of tamoxifen.…”

Section: Animals and Treatmentmentioning

confidence: 99%

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A new role for tamoxifen in oestrogen receptor-negative breast cancer when it is combined with epigallocatechin gallate

et al. 2008

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We have previously shown that tamoxifen þ epigallocatechin gallate (EGCG) is synergistically cytotoxic towards oestrogen receptor (ER)-negative breast cancer cells. To determine if this response would correlate with significant tumour suppression in vivo, athymic nude female mice were implanted with MDA-MB-231 cells and treated with tamoxifen, EGCG, EGCG þ tamoxifen, or vehicle control for 10 weeks. Tumour volume in EGCG-(25 mg kg À1 ) þ tamoxifen (75 mg kg À1 )-treated mice decreased by 71% as compared with vehicle control (Po0.05), whereas tumour weight was decreased by 80% compared with control (Po0.01). Epigallocatechin gallate treatment did not alter ER protein expression in MDA-MB-231 cells and thus was not a mechanism for the observed tumour suppression. However, western blotting of tumour extracts demonstrated that epidermal growth factor receptor (EGFR; 85% lower than control), pEGFR (78% lower than control), mammalian target of rapamycin (mTOR; 78% lower than control), and CYP1B1 (75% lower than control) were significantly lower after the combination treatment as compared with all other treatments. Nuclear factor-kB (NF-kB), b-Raf, p-MEK, S6K, 4EBP1, Akt, vascular EGFR-1 (VEGFR-1) and VEGF expressions were decreased in control but not in the individual treatments, whereas MEK, phospholipase D 1/2, TGFa, and ERK expressions were not changed after any treatment. The results demonstrate that tamoxifen at realistic doses (75 mg kg À1 ) can suppress the growth of ERnegative breast cancer when combined with EGCG. In addition, the dominant mechanism for tumour suppression is the concomitant decrease in tumour protein expressions of mTOR and the EGFR.

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Section: Discussionmentioning

confidence: 99%

Section: Animals and Treatmentmentioning

confidence: 99%

A new role for tamoxifen in oestrogen receptor-negative breast cancer when it is combined with epigallocatechin gallate

et al. 2008

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“…Epigallocatechin gallate (EGCG, 29) was described in many reviews as an inhibitor of carcinogenesis in different animal models [52,62,64]. Its mechanism of action has also been reviewed and the specific inhibition of protein kinases was discussed (Table 3), including inhibition of MEK1/2, ERK1/2, c-Jun, Akt, Dyrk1A, CDK1 and CDK2 in various types of cancer cells [52,[61][62][63][64]66]. In addition, activation of ERK and JNK was observed and it was dependent on the concentration of EGCG [61].…”

Section: Group Iii: Flavonoids and Their Analoguesmentioning

confidence: 99%

Natural Polyphenols that Display Anticancer Properties through Inhibition of Kinase Activity

Lamoral-Theys¹,

Pottier

Dufrasne³

et al. 2010

CMC

124

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Over eleven hundred publications reporting anticancer activities of polyphenols have appeared in the peerreviewed literature. In addition, a search of the PubMed database using "polyphenols -cancer -review" as keywords produced over 320 hits for review articles (July 2009). Polyphenol anticancer activities include, among others, anti-oxidative, pro-apoptotic, DNA damaging, anti-angiogenic, and immunostimulatory effects. Targeting specific protein kinases to combat cancer represents a major focus of oncology research within the so-called targeted therapy approach. An exhaustive search of the PubMed database (July 2009) using "polyphenols -cancer -kinases" as keywords resulted in more than 130 hits, half of them having been published within the past five years. Furthermore, the PubMed database contains 25 reviews on the subject of anti-kinase activity of some specific polyphenols, including mainly curcumin and the green tea polyphenol (-)-epigallocatechin 3-gallate (EGCG). However, no attempt has been made yet to review this area of research in a comprehensive, general manner. The current review therefore aims to highlight those anticancer polyphenols that target specific kinases in various types of cancer. The present review also provides an in-depth analysis of polyphenol structure-activity relationships in relation to their anticancer activities and specific kinase targeting. Lastly, a number of polyphenols are identified as potential antitumor agents that could be used to combat biologically aggressive cancers, including metastasizing cancers, through the targeting of specific kinases.

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“…(-)-Epi-gallocatechin-3-gallate (EGCG, structure shown in Figure 1), one of the most abundant bioactive components in leaves of green tea, has received increasing attention for its various physiological activities, such as antioxidant activity [2,3] and anti-tumor properties [4][5][6] . The effects of EGCG on tumor cell proliferation and apoptosis have been well documented [7] .…”

Section: Introductionmentioning

confidence: 99%

Prostanoid EP1 receptor as the target of (−)-epigallocatechin-3-gallate in suppressing hepatocellular carcinoma cells in vitro

et al. 2012

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Aim: To investigate the effects of (-)-epigallocatechin-3-gallate (EGCG), an active compound in green tea, on prostaglandin E 2 (PGE 2 )-induced proliferation and migration, and the expression of prostanoid EP 1 receptors in hepatocellular carcinoma (HCC) cells. Methods: HCC cell line HepG2, human hepatoma cell lines MHCC-97L, MHCC-97H and human hepatocyte cell line L02 were used. Cell viability was analyzed using MTT assay. PGE 2 production was determined with immunoassay. Wound healing assay and transwell filter assay were employed to assess the extent of HCC cell migration. The expression of EP 1 receptor and Gq protein were examined using Western blot assay. Results: PGE 2 (4-40000 nmol/L) or the EP 1 receptor agonist ONO-DI-004 (400-4000 nmol/L) increased the viability and migration of HepG2 cells in concentration-dependent manners. EGCG (100 μg/mL) significantly inhibited the viability and migration of HepG2 cells induced by PGE 2 or ONO-DI-004. HepG2 cells secreted an abundant amount of PGE 2 into the medium, and EGCG (100 μg/mL) significantly inhibited the PGE 2 production and EP 1 receptor expression in HepG2 cells. EGCG (100 μg/mL) also inhibited the viability of MHCC-97L cells, but not that of MHCC-97H cells. Both EGCG (100 μg/mL) and EP 1 receptor antagonist ONO-8711 inhibited PGE 2 4 μmol/L and ONO-DI-004 400 nmol/L-induced growth and migration of HepG2 cells. Both EGCG (100 μg/mL) and ONO-8711 210 nmol/L inhibited PGE 2 -and ONO-DI-004-induced EP 1 expression. EGCG and ONO-8711 had synergistic effects in inhibiting EP 1 receptor expression. PGE 2 , ONO-DI-004, ONO-8711, and EGCG had no effects on Gq expression in HepG2 cells, respectively. Conclusion: These findings suggest that the anti-HCC effects of EGCG might be mediated, at least partially, through the suppressing EP 1 receptor expression and PGE 2 production.

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Green tea polyphenols and its constituent epigallocatechin gallate inhibits proliferation of human breast cancer cells in vitro and in vivo

Cited by 279 publications

References 36 publications

A new role for tamoxifen in oestrogen receptor-negative breast cancer when it is combined with epigallocatechin gallate

A new role for tamoxifen in oestrogen receptor-negative breast cancer when it is combined with epigallocatechin gallate

Natural Polyphenols that Display Anticancer Properties through Inhibition of Kinase Activity

Prostanoid EP1 receptor as the target of (−)-epigallocatechin-3-gallate in suppressing hepatocellular carcinoma cells in vitro

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