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Abstract 1851: Resveratrol impairs GLUT-1 mediated glucose uptake in ovarian cancer cells .
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Abstract
Resveratrol(RSV), a phytoalexin found in red wine, has drawn interest due to its anticancer effect through the modulation of cancer cell metabolism in in vitro and in vivo studies. Increased uptake of [18F] fluorodeoxyglucose (FDG) using positron emission tomography (PET) has been found to be effective diagnostic tool for ovarian cancer. Thus, the manipulation of the metabolic derangement could be an effective therapeutic target for ovarian cancer. In this study, we found that RSV inhibited glucose uptake via inhibition of Glut1 translocation to plasma membrane and induced apoptosis irrespective of p53-status, using four ovarian cancer cell lines, PA-1 (p53-wild), OVCAR3, MDAH 2774 (p53-mutant) and SKOV3 (p53-null). RSV (50 μM) treatment in ovarian cancer cells decreased glucose uptake in parallel with cell viability. The facilitative glucose uptake by glucose transporter1 (GLUT1) seems to be a primary step in ovarian cancer. Also in previous data, mRNA of GLUT1 was more highly expressed in tumor tissue than in normal tissue in patients with ovarian cancer. However, RSV did not affect the protein levels of GLUT1. To identify translocation of Glut1, we performed immunofluorescence and immunoblotting of total and membrane-bound proteins. GLUT1 translocation to plasma-membrane was found to be decreased. Furthermore, localization of GLUT1 in ovarian cancer was found to be associated with the inhibition of Akt activity by RSV. In conclusion, RSV induced apoptosis by impairing glucose uptake through modulating Akt-GLUT1 signaling axis in ovarian cancer cells.
Citation Format: HyeRan Gwak, Jae Hong No, Yong Sang Song. Resveratrol impairs GLUT-1 mediated glucose uptake in ovarian cancer cells . [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1851. doi:10.1158/1538-7445.AM2013-1851
American Association for Cancer Research (AACR)
Title: Abstract 1851: Resveratrol impairs GLUT-1 mediated glucose uptake in ovarian cancer cells .
Description:
Abstract
Resveratrol(RSV), a phytoalexin found in red wine, has drawn interest due to its anticancer effect through the modulation of cancer cell metabolism in in vitro and in vivo studies.
Increased uptake of [18F] fluorodeoxyglucose (FDG) using positron emission tomography (PET) has been found to be effective diagnostic tool for ovarian cancer.
Thus, the manipulation of the metabolic derangement could be an effective therapeutic target for ovarian cancer.
In this study, we found that RSV inhibited glucose uptake via inhibition of Glut1 translocation to plasma membrane and induced apoptosis irrespective of p53-status, using four ovarian cancer cell lines, PA-1 (p53-wild), OVCAR3, MDAH 2774 (p53-mutant) and SKOV3 (p53-null).
RSV (50 μM) treatment in ovarian cancer cells decreased glucose uptake in parallel with cell viability.
The facilitative glucose uptake by glucose transporter1 (GLUT1) seems to be a primary step in ovarian cancer.
Also in previous data, mRNA of GLUT1 was more highly expressed in tumor tissue than in normal tissue in patients with ovarian cancer.
However, RSV did not affect the protein levels of GLUT1.
To identify translocation of Glut1, we performed immunofluorescence and immunoblotting of total and membrane-bound proteins.
GLUT1 translocation to plasma-membrane was found to be decreased.
Furthermore, localization of GLUT1 in ovarian cancer was found to be associated with the inhibition of Akt activity by RSV.
In conclusion, RSV induced apoptosis by impairing glucose uptake through modulating Akt-GLUT1 signaling axis in ovarian cancer cells.
Citation Format: HyeRan Gwak, Jae Hong No, Yong Sang Song.
Resveratrol impairs GLUT-1 mediated glucose uptake in ovarian cancer cells .
[abstract].
In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC.
Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1851.
doi:10.
1158/1538-7445.
AM2013-1851.
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