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EGCG, a major green tea catechin suppresses breast tumor angiogenesis and growth via inhibiting the activation of HIF-1α and NFκB, and VEGF expression.

Gu JW, Makey KL, Tucker KB, Chinchar E, Mao X, Pei I, Thomas EY, Miele L - (2013)

Bottom Line: EGCG treatment significantly reduced tumor weight over the control (0.37 ± 0.15 vs. 1.16 ± 0.30 g; P < 0.01), tumor CD (109 ± 20 vs. 156 ± 12 capillary #/mm^2; P < 0.01), tumor VEGF expression (45.72 ± 1.4 vs. 59.03 ± 3.8 pg/mg; P < 0.01), respectively.EGCG at 50 μg/ml significantly inhibited the activation of HIF-1α and NFκB as well as VEGF expression in cultured E0771 cells, compared to the control, respectively.These findings support the hypothesis that EGCG, a major green tea catechin, directly targets both tumor cells and tumor vasculature, thereby inhibiting tumor growth, proliferation, migration, and angiogenesis of breast cancer, which is mediated by the inhibition of HIF-1α and NFκB activation as well as VEGF expression.

View Article: PubMed Central - HTML - PubMed

Affiliation: Cancer Institute, University of Mississippi Medical Center, Jackson, Mississippi 39216, USA. jgu@umc.edu.

ABSTRACT
The role of EGCG, a major green tea catechin in breast cancer therapy is poorly understood. The present study tests the hypothesis that EGCG can inhibit the activation of HIF-1α and NFκB, and VEGF expression, thereby suppressing tumor angiogenesis and breast cancer progression. Sixteen eight-wk-old female mice (C57BL/6 J) were inoculated with 10^6 E0771 (mouse breast cancer) cells in the left fourth mammary gland fat pad. Eight mice received EGCG at 50-100 mg/kg/d in drinking water for 4 weeks. 8 control mice received drinking water only. Tumor size was monitored using dial calipers. At the end of the experiment, blood samples, tumors, heart and limb muscles were collected for measuring VEGF expression using ELISA and capillary density (CD) using CD31 immunohistochemistry. EGCG treatment significantly reduced tumor weight over the control (0.37 ± 0.15 vs. 1.16 ± 0.30 g; P < 0.01), tumor CD (109 ± 20 vs. 156 ± 12 capillary #/mm^2; P < 0.01), tumor VEGF expression (45.72 ± 1.4 vs. 59.03 ± 3.8 pg/mg; P < 0.01), respectively. But, it has no effects on the body weight, heart weight, angiogenesis and VEGF expression in the heart and skeletal muscle of mice. EGCG at 50 μg/ml significantly inhibited the activation of HIF-1α and NFκB as well as VEGF expression in cultured E0771 cells, compared to the control, respectively. These findings support the hypothesis that EGCG, a major green tea catechin, directly targets both tumor cells and tumor vasculature, thereby inhibiting tumor growth, proliferation, migration, and angiogenesis of breast cancer, which is mediated by the inhibition of HIF-1α and NFκB activation as well as VEGF expression.

No MeSH data available.


Related in: MedlinePlus

EGCG caused a dose-related inhibition in 3H-thymidine incorporation, decreasing by 22% at10 μg/ml and by 77% at 50 μg/ml (Panel A, n = 6, P < 0.01), and in migration (Panel B, n = 6, P < 0.01) in cultured E0771 cells, compared to the control group. In Panel C, EGCG at 50 μg/ml significantly inhibited the proliferation in cultured MCF-7 and MDA-MB-231 cells, compared to the control group (n = 6; P < 0.01), respectively.
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Figure 3: EGCG caused a dose-related inhibition in 3H-thymidine incorporation, decreasing by 22% at10 μg/ml and by 77% at 50 μg/ml (Panel A, n = 6, P < 0.01), and in migration (Panel B, n = 6, P < 0.01) in cultured E0771 cells, compared to the control group. In Panel C, EGCG at 50 μg/ml significantly inhibited the proliferation in cultured MCF-7 and MDA-MB-231 cells, compared to the control group (n = 6; P < 0.01), respectively.

Mentions: We used a 3H-thymidine incorporation assay to determine the effects of EGCG on the proliferation of cultured mouse breast cancer cells (E0771), human estrogen receptor positive breast cancer cells (MCF-7), and triple negative breast cancer cells (MDA-MB-231). Figure 3A showed that E0771 cells treated with EGCG caused a dose-related decrease in 3H-thymidine incorporation, decreasing by 22% at 10 μg/ml and by 77% at 50 μg/ml, compared to the control group (n = 6; P < 0.01). We examined the inhibitory effect of EGCG on E0771 cell migration using BD BioCoat Matrigel Invasion Chamber. Figure 3B demonstrates that EGCG at 10, 20, and 50 μg/ml caused a dose-dependent reduction of migrated breast cancer (E0771) cells, decreasing by 25%, 48%, and 71%, respectively, compared to the control group (n = 6; P < 0.01). In the another experiment, as shown in Figure 3C, we demonstrated that EGCG at 50 μg/ml significantly inhibited the proliferation of human estrogen receptor positive breast cancer cells (MCF-7) and triple negative breast cancer cells (MDA-MB-231) by 91% and 52%, respectively, compared to the control group (n = 6; P < 0.01), but not at 10 μg/ml. These in vitro findings illustrate that EGCG can directly target breast cancer cells by inhibiting the proliferation and migration.


EGCG, a major green tea catechin suppresses breast tumor angiogenesis and growth via inhibiting the activation of HIF-1α and NFκB, and VEGF expression.

Gu JW, Makey KL, Tucker KB, Chinchar E, Mao X, Pei I, Thomas EY, Miele L - (2013)

EGCG caused a dose-related inhibition in 3H-thymidine incorporation, decreasing by 22% at10 μg/ml and by 77% at 50 μg/ml (Panel A, n = 6, P < 0.01), and in migration (Panel B, n = 6, P < 0.01) in cultured E0771 cells, compared to the control group. In Panel C, EGCG at 50 μg/ml significantly inhibited the proliferation in cultured MCF-7 and MDA-MB-231 cells, compared to the control group (n = 6; P < 0.01), respectively.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3649947&req=5

Figure 3: EGCG caused a dose-related inhibition in 3H-thymidine incorporation, decreasing by 22% at10 μg/ml and by 77% at 50 μg/ml (Panel A, n = 6, P < 0.01), and in migration (Panel B, n = 6, P < 0.01) in cultured E0771 cells, compared to the control group. In Panel C, EGCG at 50 μg/ml significantly inhibited the proliferation in cultured MCF-7 and MDA-MB-231 cells, compared to the control group (n = 6; P < 0.01), respectively.
Mentions: We used a 3H-thymidine incorporation assay to determine the effects of EGCG on the proliferation of cultured mouse breast cancer cells (E0771), human estrogen receptor positive breast cancer cells (MCF-7), and triple negative breast cancer cells (MDA-MB-231). Figure 3A showed that E0771 cells treated with EGCG caused a dose-related decrease in 3H-thymidine incorporation, decreasing by 22% at 10 μg/ml and by 77% at 50 μg/ml, compared to the control group (n = 6; P < 0.01). We examined the inhibitory effect of EGCG on E0771 cell migration using BD BioCoat Matrigel Invasion Chamber. Figure 3B demonstrates that EGCG at 10, 20, and 50 μg/ml caused a dose-dependent reduction of migrated breast cancer (E0771) cells, decreasing by 25%, 48%, and 71%, respectively, compared to the control group (n = 6; P < 0.01). In the another experiment, as shown in Figure 3C, we demonstrated that EGCG at 50 μg/ml significantly inhibited the proliferation of human estrogen receptor positive breast cancer cells (MCF-7) and triple negative breast cancer cells (MDA-MB-231) by 91% and 52%, respectively, compared to the control group (n = 6; P < 0.01), but not at 10 μg/ml. These in vitro findings illustrate that EGCG can directly target breast cancer cells by inhibiting the proliferation and migration.

Bottom Line: EGCG treatment significantly reduced tumor weight over the control (0.37 ± 0.15 vs. 1.16 ± 0.30 g; P < 0.01), tumor CD (109 ± 20 vs. 156 ± 12 capillary #/mm^2; P < 0.01), tumor VEGF expression (45.72 ± 1.4 vs. 59.03 ± 3.8 pg/mg; P < 0.01), respectively.EGCG at 50 μg/ml significantly inhibited the activation of HIF-1α and NFκB as well as VEGF expression in cultured E0771 cells, compared to the control, respectively.These findings support the hypothesis that EGCG, a major green tea catechin, directly targets both tumor cells and tumor vasculature, thereby inhibiting tumor growth, proliferation, migration, and angiogenesis of breast cancer, which is mediated by the inhibition of HIF-1α and NFκB activation as well as VEGF expression.

View Article: PubMed Central - HTML - PubMed

Affiliation: Cancer Institute, University of Mississippi Medical Center, Jackson, Mississippi 39216, USA. jgu@umc.edu.

ABSTRACT
The role of EGCG, a major green tea catechin in breast cancer therapy is poorly understood. The present study tests the hypothesis that EGCG can inhibit the activation of HIF-1α and NFκB, and VEGF expression, thereby suppressing tumor angiogenesis and breast cancer progression. Sixteen eight-wk-old female mice (C57BL/6 J) were inoculated with 10^6 E0771 (mouse breast cancer) cells in the left fourth mammary gland fat pad. Eight mice received EGCG at 50-100 mg/kg/d in drinking water for 4 weeks. 8 control mice received drinking water only. Tumor size was monitored using dial calipers. At the end of the experiment, blood samples, tumors, heart and limb muscles were collected for measuring VEGF expression using ELISA and capillary density (CD) using CD31 immunohistochemistry. EGCG treatment significantly reduced tumor weight over the control (0.37 ± 0.15 vs. 1.16 ± 0.30 g; P < 0.01), tumor CD (109 ± 20 vs. 156 ± 12 capillary #/mm^2; P < 0.01), tumor VEGF expression (45.72 ± 1.4 vs. 59.03 ± 3.8 pg/mg; P < 0.01), respectively. But, it has no effects on the body weight, heart weight, angiogenesis and VEGF expression in the heart and skeletal muscle of mice. EGCG at 50 μg/ml significantly inhibited the activation of HIF-1α and NFκB as well as VEGF expression in cultured E0771 cells, compared to the control, respectively. These findings support the hypothesis that EGCG, a major green tea catechin, directly targets both tumor cells and tumor vasculature, thereby inhibiting tumor growth, proliferation, migration, and angiogenesis of breast cancer, which is mediated by the inhibition of HIF-1α and NFκB activation as well as VEGF expression.

No MeSH data available.


Related in: MedlinePlus