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Green tea catechin, epigallocatechin-3-gallate, attenuates the cell viability of human non-small-cell lung cancer A549 cells via reducing Bcl-xL expression.

Sonoda JI, Ikeda R, Baba Y, Narumi K, Kawachi A, Tomishige E, Nishihara K, Takeda Y, Yamada K, Sato K, Motoya T - Exp Ther Med (2014)

Bottom Line: The MTT assay revealed that cell proliferation was significantly reduced by EGCg in a dose-dependent manner (3-100 μM).The mRNA expression level of B-cell lymphoma-extra large (Bcl-xL) was decreased in A549 cells following 24 h incubation with 100 μM EGCg.Therefore, the results indicated that the inhibition of cell proliferation by EGCg may be achieved via suppressing the expression of the cell death-inhibiting gene, Bcl-xL.

View Article: PubMed Central - PubMed

Affiliation: First Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Kyushu University of Health & Welfare, Nobeoka, Miyazaki 882-8508, Japan.

ABSTRACT
Clinical and epidemiological studies have indicated that the consumption of green tea has a number of beneficial effects on health. Epigallocatechin-3-gallate (EGCg), the major polyphenolic compound present in green tea, has received much attention as an active ingredient. Among the numerous promising profiles of EGCg, the present study focused on the anticancer effects. Apoptosis induced by EGCg and subsequent cell growth suppression have been demonstrated in a number of cell culture studies. However, the underlying mechanism of apoptotic cell death remains unclear. Thus, the aim of the present study was to identify the major molecule that mediates proapoptotic cell death by EGCg. The effect of EGCg on cell proliferation and the induction of mRNA that modulates apoptotic cell death was evaluated in the A549 human non-small-cell lung cancer cell line. In addition, morphological changes were assessed by microscopy in A549 cells that had been treated with 100 μM EGCg for 24 h. The MTT assay revealed that cell proliferation was significantly reduced by EGCg in a dose-dependent manner (3-100 μM). The mRNA expression level of B-cell lymphoma-extra large (Bcl-xL) was decreased in A549 cells following 24 h incubation with 100 μM EGCg. Therefore, the results indicated that the inhibition of cell proliferation by EGCg may be achieved via suppressing the expression of the cell death-inhibiting gene, Bcl-xL.

No MeSH data available.


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Chemical structures of green tea catechins.
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f1-etm-08-01-0059: Chemical structures of green tea catechins.

Mentions: Green tea (Camellia sinensis) is one of the most popular beverages worldwide, and contains a large amount of flavonoids, predominantly catechins, including epicatechin, its hydroxyl derivative epigallocatechin, and their gallic acid esters, epicatechin-3-gallate and epigallocatechin-3-gallate (EGCg; Fig. 1). Among these catechins, EGCg is an abundant constituent of green tea (leaf) and has been shown to exhibit antioxidative, anticarcinogenic and anticancer effects in vitro. The polyphenolic structure of these compounds exerts antioxidative effects by trapping reactive oxygen species (ROS). It was previously demonstrated that daily intake of green tea reduced oxidative stress in vivo (1). In addition, against a background of increasing public health concerns, it has been hypothesized that green tea consumption has beneficial effects against various pathological conditions, including cardiovascular disease, diabetes and cancer.


Green tea catechin, epigallocatechin-3-gallate, attenuates the cell viability of human non-small-cell lung cancer A549 cells via reducing Bcl-xL expression.

Sonoda JI, Ikeda R, Baba Y, Narumi K, Kawachi A, Tomishige E, Nishihara K, Takeda Y, Yamada K, Sato K, Motoya T - Exp Ther Med (2014)

Chemical structures of green tea catechins.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061191&req=5

f1-etm-08-01-0059: Chemical structures of green tea catechins.
Mentions: Green tea (Camellia sinensis) is one of the most popular beverages worldwide, and contains a large amount of flavonoids, predominantly catechins, including epicatechin, its hydroxyl derivative epigallocatechin, and their gallic acid esters, epicatechin-3-gallate and epigallocatechin-3-gallate (EGCg; Fig. 1). Among these catechins, EGCg is an abundant constituent of green tea (leaf) and has been shown to exhibit antioxidative, anticarcinogenic and anticancer effects in vitro. The polyphenolic structure of these compounds exerts antioxidative effects by trapping reactive oxygen species (ROS). It was previously demonstrated that daily intake of green tea reduced oxidative stress in vivo (1). In addition, against a background of increasing public health concerns, it has been hypothesized that green tea consumption has beneficial effects against various pathological conditions, including cardiovascular disease, diabetes and cancer.

Bottom Line: The MTT assay revealed that cell proliferation was significantly reduced by EGCg in a dose-dependent manner (3-100 μM).The mRNA expression level of B-cell lymphoma-extra large (Bcl-xL) was decreased in A549 cells following 24 h incubation with 100 μM EGCg.Therefore, the results indicated that the inhibition of cell proliferation by EGCg may be achieved via suppressing the expression of the cell death-inhibiting gene, Bcl-xL.

View Article: PubMed Central - PubMed

Affiliation: First Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Kyushu University of Health & Welfare, Nobeoka, Miyazaki 882-8508, Japan.

ABSTRACT
Clinical and epidemiological studies have indicated that the consumption of green tea has a number of beneficial effects on health. Epigallocatechin-3-gallate (EGCg), the major polyphenolic compound present in green tea, has received much attention as an active ingredient. Among the numerous promising profiles of EGCg, the present study focused on the anticancer effects. Apoptosis induced by EGCg and subsequent cell growth suppression have been demonstrated in a number of cell culture studies. However, the underlying mechanism of apoptotic cell death remains unclear. Thus, the aim of the present study was to identify the major molecule that mediates proapoptotic cell death by EGCg. The effect of EGCg on cell proliferation and the induction of mRNA that modulates apoptotic cell death was evaluated in the A549 human non-small-cell lung cancer cell line. In addition, morphological changes were assessed by microscopy in A549 cells that had been treated with 100 μM EGCg for 24 h. The MTT assay revealed that cell proliferation was significantly reduced by EGCg in a dose-dependent manner (3-100 μM). The mRNA expression level of B-cell lymphoma-extra large (Bcl-xL) was decreased in A549 cells following 24 h incubation with 100 μM EGCg. Therefore, the results indicated that the inhibition of cell proliferation by EGCg may be achieved via suppressing the expression of the cell death-inhibiting gene, Bcl-xL.

No MeSH data available.


Related in: MedlinePlus