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Abstract 2323: The inhibitory role of Kaempferol-3-O-rutinoside induced AMPK activation on the growth of human breast cancer cell lines

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Abstract Solidago virga-aurea, herbaceous perennial plant of the family Asteraceae, has astringent, diuretic, and antiseptic assets. In our current study, we found that kaempferol-3- O -rutinoside (KR) from Solidago virga-aurea extract prompted cellular apoptosis in breast cancer cells. The present study was conducted to investigate its effects on MCF-7 cells with respect to the induction of inhibitory effect on cell viability against MDA-MB-231 and MCF-7 breast cancer cell lines. In addition, apoptotic protein, especially Bim, was also increased in KR treated MDA-MB-231 and MCF-7 cell line. However, an anti-apoptotic protein, Bcl-xL, was not changed by KR. To find out positive regulator of Bim expression, FOXO (forkhead-box transcription factor, group O) 3a and AMPK (5' AMP-activated protein kinase) protein expressions were examined in KR treated cells. Immunoblot analysis showed dramatically increased expressions of FOXO3a and AMPK in KR treated MDA-MB-231 and MCF-7 cells. In addition, cell cycle analysis indicated that G0/G1 arrest was intensely increased in KR treated MDA-MB-231 and MCF-7 cells. Moreover, phospho-AMPK (pT172) and phospho-FOXO3a (S472) expression were also increased in KR treated MDA-MB-231 and MCF-7 cells. Our results suggest that KR induces apoptosis by AMPK-FOXO3a mediated Bim expression. The mechanisms of KR mediated AMPK and FOXO3a regulation is not fully elucidated yet, but further studies about these molecular mechanisms between two proteins will give some ideas for cancer therapies for certain breast cancer patients. Citation Format: Chea Ha Kim. The inhibitory role of Kaempferol-3-O-rutinoside induced AMPK activation on the growth of human breast cancer cell lines [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2323. doi:10.1158/1538-7445.AM2017-2323
American Association for Cancer Research (AACR)
Title: Abstract 2323: The inhibitory role of Kaempferol-3-O-rutinoside induced AMPK activation on the growth of human breast cancer cell lines
Description:
Abstract Solidago virga-aurea, herbaceous perennial plant of the family Asteraceae, has astringent, diuretic, and antiseptic assets.
In our current study, we found that kaempferol-3- O -rutinoside (KR) from Solidago virga-aurea extract prompted cellular apoptosis in breast cancer cells.
The present study was conducted to investigate its effects on MCF-7 cells with respect to the induction of inhibitory effect on cell viability against MDA-MB-231 and MCF-7 breast cancer cell lines.
In addition, apoptotic protein, especially Bim, was also increased in KR treated MDA-MB-231 and MCF-7 cell line.
However, an anti-apoptotic protein, Bcl-xL, was not changed by KR.
To find out positive regulator of Bim expression, FOXO (forkhead-box transcription factor, group O) 3a and AMPK (5' AMP-activated protein kinase) protein expressions were examined in KR treated cells.
Immunoblot analysis showed dramatically increased expressions of FOXO3a and AMPK in KR treated MDA-MB-231 and MCF-7 cells.
In addition, cell cycle analysis indicated that G0/G1 arrest was intensely increased in KR treated MDA-MB-231 and MCF-7 cells.
Moreover, phospho-AMPK (pT172) and phospho-FOXO3a (S472) expression were also increased in KR treated MDA-MB-231 and MCF-7 cells.
Our results suggest that KR induces apoptosis by AMPK-FOXO3a mediated Bim expression.
The mechanisms of KR mediated AMPK and FOXO3a regulation is not fully elucidated yet, but further studies about these molecular mechanisms between two proteins will give some ideas for cancer therapies for certain breast cancer patients.
Citation Format: Chea Ha Kim.
The inhibitory role of Kaempferol-3-O-rutinoside induced AMPK activation on the growth of human breast cancer cell lines [abstract].
In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC.
Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2323.
doi:10.
1158/1538-7445.
AM2017-2323.

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