The combination of raloxifene and epigallocatechin gallate suppresses growth and induces apoptosis in MDA-MB-231 cells

Stuart, Emma; Rosengren, Rhonda J.

doi:10.1016/j.lfs.2008.02.009

Cited by 27 publications

(30 citation statements)

References 35 publications

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“…With regard to our previous results, the data correlate well with the time-course over which apoptosis induction is observed. Specifically, the greatest reductions in the phosphorylation of EGFR, AKT, S6K and mTOR are observed between 12 and 18 h (with the exception of S6K, where the greatest suppression of phosphorylation occurred after 6 h) while the greatest increases in SAPK phosphorylation were observed after 18 h. Our previous report demonstrated that apoptosis induction was significantly increased versus all other treatments following 12, 18, 24 and 36 h (16). Importantly, pharmacological inhibition of EGFR, AKT and mTOR in MDA-MB-231 human breast cancer cells all result in the induction of apoptosis.…”

Section: Discussionmentioning

confidence: 74%

“…We demonstrated that this cytotoxicity was elicited as a result of enhanced apoptosis induction, occurring independently of changes in cell cycle progression (16). We further investigated the mechanism of this effect via Western blotting of total protein expression and phosphorylation of EGFR and AKT proteins, where we observed a significant reduction in the phosphorylation of both proteins following 18 h (16).…”

Section: Discussionmentioning

confidence: 89%

“…Our laboratory has previously demonstrated that the combination of raloxifene and EGCG is particularly cytotoxic toward the aggressive, basal-like (ER-negative/HER-2-negative) MDA-MB-231 cell line (16). Specifically, we have shown that the combination of EGCG and raloxifene elicited a strong apoptotic response, which occurred independently of cell cycle changes (16).…”

Section: Introductionmentioning

confidence: 79%

“…Specifically, we have shown that the combination of EGCG and raloxifene elicited a strong apoptotic response, which occurred independently of cell cycle changes (16). Therefore, the aim of the current study was to further investigate whether this treatment regime ONCOLOGY REPORTS 24: 779-785, 2010 …”

Section: Introductionmentioning

confidence: 96%

“…MDA-MB-231 or MCF-7 cells were plated in 100 mm culture dishes at a density of 2x10 6 cells per dish, in 20 ml of DMEM media supplemented with 10% FBS, 1% antibiotic/antimycotic solution and 0.2% NaHCO 3 . Cells were treated with EGCG (25 μM) raloxifene (4 μM), EGCG + raloxifene or DMSO (0.1%) for 0-18 h. Cell lysates were prepared as previously described (16). Protein concentration was determined using the BCA assay (17) and the samples were stored at -80˚C for a maximum of 6 months.…”

mentioning

confidence: 99%

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In vitro mechanism of action for the cytotoxicity elicited by the combination of epigallocatechin gallate and raloxifene in MDA-MB-231 cells

Stuart

Jarvis²,

Rosengren³

2010

Oncol Rep

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Abstract. The anticancer effects elicited by epigallocatechin gallate (EGCG) are well established in various models of cancer, while raloxifene is as an established selective estrogen receptor modulator (SERM), which is not yet clinically utilized for the treatment of breast cancer. Previous study from this laboratory has demonstrated that the combination of EGCG (25 μM) and raloxifene (4 μM) elicits a strong cytotoxic response in MDA-MB-231 human breast cancer cells, which lack the estrogen receptor (ER) and erbB-2/ Her-2 receptor. This study was therefore designed to probe the mechanism underlying this cytotoxic response, with an emphasis on determining how the combination treatment influenced the total expression and phosphorylation of key signaling proteins. Specifically, following 12 and 18 h of the combination treatment, we observed significant decreases in the phosphorylation of the epidermal growth factor receptor (EGFR), AKT, mammalian target of rapamycin (mTOR) and S-6-kinase (S6K), and significant increases in the phosphorylation of stress activated protein kinases (SAPKs). Furthermore, these changes were associated with a reduction in the nuclear localization of p65, a major subunit of NF-κB. These results demonstrate that the combination of EGCG and raloxifene effectively reduced the mitogenic and survival signaling in MDA-MB-231 cells. Thus, this combination warrants further experimentation as a potential treatment for ER-negative breast cancer.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 79%

Section: Introductionmentioning

confidence: 96%

mentioning

confidence: 99%

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In vitro mechanism of action for the cytotoxicity elicited by the combination of epigallocatechin gallate and raloxifene in MDA-MB-231 cells

Stuart

Jarvis²,

Rosengren³

2010

Oncol Rep

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Novel human breast cancer cell lines IBH‐4, IBH‐6, and IBH‐7 growing in nude mice

Bruzzone¹,

Vanzulli²,

Soldati³

et al. 2009

Journal Cellular Physiology

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Breast cancer is the most frequent cancer in women. However, in vivo hormone receptor positive and metastatic models are scarce. The aim of the present manuscript was to assess if the novel steroid receptor positive human cell lines IBH-4, IBH-6, and IBH-7 developed in our laboratory from primary infiltrant ductal carcinomas are good models to study in vivo human breast cancer. Cell lines or tumors were inoculated to nude mice in the presence or absence of hormone supplementation. Growth was analyzed by ANOVA followed by Tukey-Kramer's test. Steroid hormone expression was assessed by immunohistochemistry and Western blotting. The histology of the tumors was analyzed. IBH-4 and IBH-6 cells were inoculated to nude mice and 100% of the injected mice developed tumors in the presence or absence of hormone treatment, although tamoxifen inhibited growth. IBH-4 and IBH-6 cell lines in vivo gave rise to poorly differentiated carcinomas with areas of solid growth and sarcomatoid areas showing no morphological signs of epithelial differentiation. Distinct features of malignancy were observed. IBH-7 tumors in animals receiving estradiol were semi-differentiated adenocarcinomas. IBH-7 cells grew only in the presence of estradiol, but even with hormone addition, the tumor take was 20%. These tumors metastasized to the uterus and lung and vascular tumor emboli were evident. IBH-7 tumors were invasive and able to break through the peritoneum. As a conclusion, IBH-4 and IBH-6 are good models for studying tumor progression, whereas IBH-7 is a good model for tumor take, being metastatic and strictly estrogen-dependent.

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Tea polyphenol (−)‐epigallocatechin‐3‐gallate inhibits nicotine‐ and estrogen‐induced α9‐nicotinic acetylcholine receptor upregulation in human breast cancer cells

et al. 2010

Molecular Nutrition Food Res

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The combination of raloxifene and epigallocatechin gallate suppresses growth and induces apoptosis in MDA-MB-231 cells

Cited by 27 publications

References 35 publications

In vitro mechanism of action for the cytotoxicity elicited by the combination of epigallocatechin gallate and raloxifene in MDA-MB-231 cells

In vitro mechanism of action for the cytotoxicity elicited by the combination of epigallocatechin gallate and raloxifene in MDA-MB-231 cells

Novel human breast cancer cell lines IBH‐4, IBH‐6, and IBH‐7 growing in nude mice

Tea polyphenol (−)‐epigallocatechin‐3‐gallate inhibits nicotine‐ and estrogen‐induced α9‐nicotinic acetylcholine receptor upregulation in human breast cancer cells

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