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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 treatment did not affect the capillary density (3270 ± 162 vs. 3103 ± 226 #/mm^2; n = 8; P = 0.5215), and VEGF expression (261 ± 22 vs. 245 ± 19 pg/mg; n = 8; P = 0.4517) in the mouse heart, compared to the control group (Panel A), respectively. There was no significant difference in the capillary density (370 ± 55 vs. 381 ± 44 #/mm^2; n = 8; P = 0.5401), and VEGF expression (225 ± 16 vs. 214 ± 20 pg/mg; n = 8; P = 0.7825) in the limb skeletal muscles between the EGCG-treated mice and the control mice (Panel B), respectively. The digital images show CD31 immunohistochemistry staining in OCT-embedded cryosections of the heart (Panel A) and the limb muscle (Panel B) of control mouse and EGCG-treated mouse, respectively.
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Figure 5: EGCG treatment did not affect the capillary density (3270 ± 162 vs. 3103 ± 226 #/mm^2; n = 8; P = 0.5215), and VEGF expression (261 ± 22 vs. 245 ± 19 pg/mg; n = 8; P = 0.4517) in the mouse heart, compared to the control group (Panel A), respectively. There was no significant difference in the capillary density (370 ± 55 vs. 381 ± 44 #/mm^2; n = 8; P = 0.5401), and VEGF expression (225 ± 16 vs. 214 ± 20 pg/mg; n = 8; P = 0.7825) in the limb skeletal muscles between the EGCG-treated mice and the control mice (Panel B), respectively. The digital images show CD31 immunohistochemistry staining in OCT-embedded cryosections of the heart (Panel A) and the limb muscle (Panel B) of control mouse and EGCG-treated mouse, respectively.

Mentions: The data showed that there was no significant difference in the body weight (22.38.25 ± 0.51 vs. 22.94 ± 0.57; n = 8; P = 0.9437), heart weight (84.7 ± 11.2 vs. 85.1 vs. 10.6 mg; n = 8; P = 0.3546), or kidney weight (237.5 ± 9.2 vs. 240.1 ± 8.9 mg; n = 8; P = 0.3735) between the EGCG-treated mice and the control mice. Figure 5A showed that EGCG treatment did not affect the capillary density (number of capillary/mm^2 area) (3270 ± 162 vs. 3103 ± 226 #/mm^2; n = 8; P = 0.5215) analyzed by CD31 immunochemistry and morphometric analysis, and VEGF expression (261 ± 22 vs. 245 ± 19 pg/mg; n = 8; P = 0.4517) determined by ELISA in the mouse heart, compared to the control group, respectively. Figure 5B showed that there was no significant difference in the capillary density (370 ± 55 vs. 381 ± 44 #/mm^2; n = 8; P = 0.5401), and VEGF expression (225 ± 16 vs. 214 ± 20 pg/mg; n = 8; P = 0.7825) in the limb skeletal muscles between the EGCG-treated mice and the control mice, respectively. These findings illustrate that EGCG does not significantly affect angiogenesis and VEGF expression in the normal tissues such as the heart and skeletal muscles.


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 treatment did not affect the capillary density (3270 ± 162 vs. 3103 ± 226 #/mm^2; n = 8; P = 0.5215), and VEGF expression (261 ± 22 vs. 245 ± 19 pg/mg; n = 8; P = 0.4517) in the mouse heart, compared to the control group (Panel A), respectively. There was no significant difference in the capillary density (370 ± 55 vs. 381 ± 44 #/mm^2; n = 8; P = 0.5401), and VEGF expression (225 ± 16 vs. 214 ± 20 pg/mg; n = 8; P = 0.7825) in the limb skeletal muscles between the EGCG-treated mice and the control mice (Panel B), respectively. The digital images show CD31 immunohistochemistry staining in OCT-embedded cryosections of the heart (Panel A) and the limb muscle (Panel B) of control mouse and EGCG-treated mouse, respectively.
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Related In: Results  -  Collection

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Figure 5: EGCG treatment did not affect the capillary density (3270 ± 162 vs. 3103 ± 226 #/mm^2; n = 8; P = 0.5215), and VEGF expression (261 ± 22 vs. 245 ± 19 pg/mg; n = 8; P = 0.4517) in the mouse heart, compared to the control group (Panel A), respectively. There was no significant difference in the capillary density (370 ± 55 vs. 381 ± 44 #/mm^2; n = 8; P = 0.5401), and VEGF expression (225 ± 16 vs. 214 ± 20 pg/mg; n = 8; P = 0.7825) in the limb skeletal muscles between the EGCG-treated mice and the control mice (Panel B), respectively. The digital images show CD31 immunohistochemistry staining in OCT-embedded cryosections of the heart (Panel A) and the limb muscle (Panel B) of control mouse and EGCG-treated mouse, respectively.
Mentions: The data showed that there was no significant difference in the body weight (22.38.25 ± 0.51 vs. 22.94 ± 0.57; n = 8; P = 0.9437), heart weight (84.7 ± 11.2 vs. 85.1 vs. 10.6 mg; n = 8; P = 0.3546), or kidney weight (237.5 ± 9.2 vs. 240.1 ± 8.9 mg; n = 8; P = 0.3735) between the EGCG-treated mice and the control mice. Figure 5A showed that EGCG treatment did not affect the capillary density (number of capillary/mm^2 area) (3270 ± 162 vs. 3103 ± 226 #/mm^2; n = 8; P = 0.5215) analyzed by CD31 immunochemistry and morphometric analysis, and VEGF expression (261 ± 22 vs. 245 ± 19 pg/mg; n = 8; P = 0.4517) determined by ELISA in the mouse heart, compared to the control group, respectively. Figure 5B showed that there was no significant difference in the capillary density (370 ± 55 vs. 381 ± 44 #/mm^2; n = 8; P = 0.5401), and VEGF expression (225 ± 16 vs. 214 ± 20 pg/mg; n = 8; P = 0.7825) in the limb skeletal muscles between the EGCG-treated mice and the control mice, respectively. These findings illustrate that EGCG does not significantly affect angiogenesis and VEGF expression in the normal tissues such as the heart and skeletal muscles.

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