Ethanol Modulates the Growth of Human Breast Cancer Cells In Vitro

Izevbigie, Ernest B.; Ekunwe, Stephen I.N.; Jordan, Jennifer; Howard, Carolyn B.

doi:10.1177/153537020222700406

Cited by 43 publications

(46 citation statements)

References 37 publications

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“…These data are supported by experimental studies using animal models and cell culture systems, which show that ethanol promotes mammary tumorigenesis and stimulates proliferation as well as invasion of breast cancer cells (9)(10)(11)(12)(13)(14).…”

Section: Introductionsupporting

confidence: 61%

“…These epidemiological data suggest that ethanol may enhance tumor development and the metastatic spread of breast cancer cells. This is confirmed by in vitro and in vivo studies showing that ethanol stimulates not only proliferation but also invasion and migration of breast cancer cells (9)(10)(11)(12)(13)(14). Many studies have been realized in order to elucidate these effects.…”

Section: Discussionmentioning

confidence: 59%

See 1 more Smart Citation

Ethanol stimulates the secretion of matrix metalloproteinases 2 and 9 in MCF-7 human breast cancer cells

Etique¹,

Grillier-Vuissoz²,

Flament³

2006

Oncol Rep

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Abstract. Alcohol consumption is a well-established risk factor for hormone-dependent breast cancer. In vitro studies performed to understand the mechanisms by which ethanol acts on breast cancer cells have shown that this compound stimulates both proliferation and migration. In the present study, we show by gelatin zymography that, when exposed to ethanol, MCF-7 human breast cancer cells display a higher amount of active metalloproteinases (MMP) 2 and 9 in their culture medium. This increase is somewhat higher than those observed in the case of 17ß-estradiol (E 2 ) exposure. As expected, anti-estrogen ICI 182,780 inhibits the E 2 -induced overexpression of a well-known estrogen responsive gene, the progesterone receptor, in MCF-7 cells. ICI 182,780 also inhibits the E 2 -induced increase in MMP-2 and -9 secretion. Nevertheless, in the case of ethanol exposure, this ER antagonist was only efficient on MMP-9 secretion. In addition, although MMP-9 transcription was not sensitive to E 2 or ethanol, MMP-2 transcription was stimulated in MCF-7 cells exposed to ethanol. Collectively, these results give new insights into the effects of alcohol on breast cancer cell migration, which are not due solely to an estrogen-like activity of alcohol.

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Section: Introductionsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 59%

Ethanol stimulates the secretion of matrix metalloproteinases 2 and 9 in MCF-7 human breast cancer cells

Etique¹,

Grillier-Vuissoz²,

Flament³

2006

Oncol Rep

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“…These epidemiological data are supported by recent experimental studies using animal models and cell culture systems. These experimental studies show that ethanol can induce mammary tumor and stimulate proliferation as well as invasion of breast tumor cells (Singletary, 1997;Luo and Miller, 2000;Meng et al, 2000;Watabiki et al, 2000;Izevbigie et al, 2002). The data imply that the most likely mechanism of ethanol action involves tumor growth and metastasis.…”

Section: Introductionmentioning

confidence: 82%

“…This stimulation, however, is independent of ErbB2 levels. Previous studies show that ethanol promotes proliferation of breast cancer cells in vitro Izevbigie et al, 2002). It appears that the stimulation is dependent on the status of estrogen receptors and is mediated by ERK activation, that is, ethanol-mediated growth promotion only occurs in estrogen receptor-positive cells Izevbigie et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of ErbB2 enhances ethanol-stimulated intracellular signaling and invasion of human mammary epithelial and breast cancer cells in vitro

Lin

Leonard

et al. 2003

Oncogene

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Both epidemiological and experimental studies indicate that ethanol is a tumor promoter and may promote metastasis of breast cancer. However, the molecular mechanisms underlying ethanol-mediated tumor promotion remain unknown. Overexpression of ErbB proteins in breast cancer patients is generally associated with poor prognosis. The ErbB proteins are a family of receptor kinases that include four closely related members: epidermal growth factor receptor (EGFR/ErbB1), ErbB2/neu, ErbB3, and ErbB4. Particularly, ErbB2 plays a pivotal role in ErbB-mediated activities. Here we demonstrated that amplification of ErbB2 expression sensitized a specific cellular response to ethanol. Human breast cancer cells or mammary epithelial cells with a high expression of ErbB2 exhibited an enhanced response to ethanol-stimulated cell invasion in vitro. Ethanol also stimulated cell proliferation; however, this stimulation was independent of ErbB2 levels. Ethanol triggered divergent intracellular signaling among cells expressing different ErbB2 levels. In the cells overexpressing ErbB2, ethanol was more effective in the activation of c-Jun NH 2 terminal protein kinases (JNKs) and p38 mitogen-activated protein kinase (p38 MAPK) as well as the induction of reactive oxygen species (ROS) than the cells with normal ErbB2 expression. Blockage of either JNKs or p38 MAPK activation eliminated ethanol-mediated cell invasion. In contrast, the reduction of hydrogen peroxide concentration by catalase exposure had little effect on ethanolinduced cell invasion. These results indicated that ethanolinduced cell invasion was primarily mediated by JNKs and p38 MAPK, whereas the involvement of ROS formation might be minimal. Our study suggests that overexpression of ErbB2 may augment ethanol-elicited signaling and promote ethanol-stimulated tumor metastasis.

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“…It also seems reasonable to exclude the presence of ethanol solvate (some concentration as complex, i.e. 9.5 µM) as a factor in the higher toxicity of the present VO (dipic) complex towards PC9 cells as mM concentrations of ethanol have been found to promote cell growth of breast cancer cell line MCF-7 [DeCupis et al, 1998, Przylipiak, et al, 1996, Izevbigie, et al 2002. When VO (dipic) was screened on the MCF-7 cancer cell line, its IC 50 was slightly higher, at 16 µM.…”

Section: Cell Viability Assaymentioning

confidence: 99%

Oxovanadium (IV) Dipicolinate: Structure Nucleolytic and Anticancer Property

Guan¹,

Hee²,

Lai³

et al. 2008

MAS

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Diaqua(dipicolinato)oxovanadium (IV) ethanol solvate crystallizes in the triclinic space group P1. The complex was characterized by FTIR, elemental analysis, thermal gravimetric analysis, and solution visible spectral analysis. The complex alone cleaved DNA in the absence of hydrogen peroxide and its nucleolytic efficiency is greater than that of VOSO 4 . Its nucleolytic efficiency is affected by the choice of buffer used and pH. DNA cleavage can be inhibited by DMSO, NaN 3 and catalase, implying involvement of ROS. An MTT assay, involving the lung cancer cell line PC9, gave IC 50 values of 9.5 µM and 16 µM for the complex and VOSO 4 respectively. For breast cancer cell line MCF-7, this complex is less cytotoxic, with an IC 50 of 16 µM.

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Ethanol Modulates the Growth of Human Breast Cancer Cells In Vitro

Cited by 43 publications

References 37 publications

Ethanol stimulates the secretion of matrix metalloproteinases 2 and 9 in MCF-7 human breast cancer cells

Ethanol stimulates the secretion of matrix metalloproteinases 2 and 9 in MCF-7 human breast cancer cells

Overexpression of ErbB2 enhances ethanol-stimulated intracellular signaling and invasion of human mammary epithelial and breast cancer cells in vitro

Oxovanadium (IV) Dipicolinate: Structure Nucleolytic and Anticancer Property

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