Original Research Article:
Artichoke polyphenols induce
apoptosis and decrease the invasive potential of the human breast cancer cell
line MDA-MB231
- Anna
Maria Mileo1,
- Donato
Di Venere2,
- Vito
Linsalata2,
- Rocco
Fraioli3,
- Stefania
Miccadei4,*
Article first published online: 17 MAY 2012
DOI: 10.1002/jcp.24029
Abstract
The human breast cancer cell line, estrogen receptor
negative, MDA-MB231, was used to evaluate the antitumor effect of polyphenolic
extracts from the edible part of artichokes (AE s). Treatment of cancer cells
reduced cell viability and inhibited cell growth in a dose-dependent manner.
Importantly, AEs did not have any effect on normal breast epithelial cell line,
MCF10A. Chlorogenic acid (ChA), the most representative component of the
polyphenolic fraction of artichoke, had no prominent effects on the cell death
rate of MDA-MB231 cells. ，The addition of AEs to the cells, rather
than ChA, triggered apoptosis via a mitochondrial and a death-receptor pathway,
as shown by the activation of caspase-9 and caspase-8, respectively.
Furthermore, an increase of the Bax:Bcl2 ratio and up-regulation of
cyclin-dependent kinase inhibitor, p21WAF1, crucial apoptotic players,
were documented. According to our data on activation of caspase-9, a loss of
mitochondrial transmembrane potential (Ψm) was shown. Cell motility and
invasion capabilities were remarkably inhibited by AEs-treatment in highly
invasive MDA-MB231 cells. In addition, a significant decrease of proteolytic
activity of metalloproteinase-2 protein (MMP-2), involved in degrading components
of the extracellular matrix, was detected. Our findings indicate that AEs
reduced cell viability, inhibited cell growth, triggered apoptotic mechanisms,
and showed inhibitory properties against the invasive behavior of MDA-MB231
cancer cell line. Altogether, these data indicate the potential chemopreventive
activity of artichoke polyphenolic extracts. J. Cell. Physiol. 227: 3301–3309,
2012. © 2011 Wiley Periodicals, Inc.
朝鮮薊多酚誘導細胞凋亡和降低人類乳腺癌細胞株MDA-MB231的侵襲潛力
摘要
人類乳腺癌細胞株雌激素受體陰性，MDA-MB231，是用來評估的朝鮮薊可食部分（AES）的多酚提取物的抗腫瘤作用。癌細胞的治療是降低細胞活力和劑量依賴型抑制細胞生長。重要的是，AES不會影響任何正常乳腺上皮細胞系，MCF10A。綠原酸（CHA），朝鮮薊的多酚成份中最具代表性含量的一種，MDA-MB231細胞的細胞死亡率無顯著影響。當AES加入到該細胞中，而不是CHA，除了通過線粒體和死亡受體途徑引發細胞凋亡，如所示之分別活化caspase-9和caspase-8。此外，增加的Bax:Bcl2的比例和上調細胞週期蛋白依賴性激酶抑製劑，p21WAF1，被記錄為重要的細胞凋亡之成員。根據我們的數據在激活的caspase-9，結果表明線粒體跨膜電位（Ψm）的損失。由AES-治療高度侵襲MDA-MB231細胞的細胞運動和侵襲能力被明顯受到抑制。此外，一個顯著減少金屬蛋白酶2蛋白（MMP-2）的水解活性被檢測出，一種參與細胞外基質的降解成分。我們的研究結果表明，AES降低細胞活力，抑制細胞生長，引發細胞凋亡機制，並展示對入侵行為的MDA-MB231癌細胞株的抑制性能。總之，這些數據表明，朝鮮薊多酚提取物在化學預防活動的潛力。細胞研究。生理學。 227：3301-3309，2012。 ©2011威利公司
人類乳腺癌細胞株雌激素受體陰性，MDA-MB231，是用來評估的朝鮮薊可食部分（AES）的多酚提取物的抗腫瘤作用。癌細胞的治療是降低細胞活力和劑量依賴型抑制細胞生長。重要的是，AES不會影響任何正常乳腺上皮細胞系，MCF10A。綠原酸（CHA），朝鮮薊的多酚成份中最具代表性含量的一種，MDA-MB231細胞的細胞死亡率無顯著影響。當AES加入到該細胞中，而不是CHA，除了通過線粒體和死亡受體途徑引發細胞凋亡，如所示之分別活化caspase-9和caspase-8。此外，增加的Bax:Bcl2的比例和上調細胞週期蛋白依賴性激酶抑製劑，p21WAF1，被記錄為重要的細胞凋亡之成員。根據我們的數據在激活的caspase-9，結果表明線粒體跨膜電位（Ψm）的損失。由AES-治療高度侵襲MDA-MB231細胞的細胞運動和侵襲能力被明顯受到抑制。此外，一個顯著減少金屬蛋白酶2蛋白（MMP-2）的水解活性被檢測出，一種參與細胞外基質的降解成分。我們的研究結果表明，AES降低細胞活力，抑制細胞生長，引發細胞凋亡機制，並展示對入侵行為的MDA-MB231癌細胞株的抑制性能。總之，這些數據表明，朝鮮薊多酚提取物在化學預防活動的潛力。細胞研究。生理學。 227：3301-3309，2012。 ©2011威利公司
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