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Article

Theaflavin-3, 3'-digallate decreases human ovarian carcinoma OVCAR-3 cell-induced angiogenesis via Akt and Notch-1 pathways, not via MAPK pathways

  • Authors:
    • Ying Gao
    • Gary O. Rankin
    • Youying Tu
    • Yi Charlie Chen
  • View Affiliations / Copyright

    Affiliations: Department of Tea Science, Zhejiang University, Hangzhou 310058, P.R. China, Department of Pharmacology, Physiology and Toxicology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USA, College of Science, Technology and Mathematics, Alderson Broaddus University, Philippi, WV 26416, USA
  • Pages: 281-292
    |
    Published online on: November 20, 2015
       https://doi.org/10.3892/ijo.2015.3257
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Abstract

Theaflavin-3, 3'-digallate (TF3) is a black tea polyphenol produced from polymerization and oxidization of the green tea ployphenols epicatechin gallate and (-)-epigallocatechin-3-gallate (EGCG) during fermentation of fresh tea leaves. TF3 has been reported to have anticancer properties. However, the effect of TF3 on tumor angiogenesis and the underlying mechanisms are not clear. In the present study, TF3 was verified to inhibit tumor angiogenesis. Compared with EGCG, TF3 was more potent. TF3 inhibited human ovarian carcinoma OVCAR-3 cell-induced angiogenesis in human umbilical vein endothelial cell model and in chick chorioallantoic membrane model. TF3 reduced tumor angiogenesis by downregulating HIF-1α and VEGF. One of the mechanisms was TF3 inactivated Akt/mTOR/p70S6K/4E-BP1 pathway and Akt/c-Myc pathway. Besides, TF3 suppressed the cleavage of Notch-1, subsequently decreased the expression of c-Myc, HIF-1α and VEGF, and finally the impaired cancer cells induced angiogenesis. Nevertheless, TF3 did not have any influence on the MAPK pathways. Taken together, these findings suggest that TF3 might serve as a potential anti-angiogenic agent for cancer treatment.
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Copy and paste a formatted citation
Spandidos Publications style
Gao Y, Rankin GO, Tu Y and Chen YC: Theaflavin-3, 3'-digallate decreases human ovarian carcinoma OVCAR-3 cell-induced angiogenesis via Akt and Notch-1 pathways, not via MAPK pathways. Int J Oncol 48: 281-292, 2016.
APA
Gao, Y., Rankin, G.O., Tu, Y., & Chen, Y.C. (2016). Theaflavin-3, 3'-digallate decreases human ovarian carcinoma OVCAR-3 cell-induced angiogenesis via Akt and Notch-1 pathways, not via MAPK pathways. International Journal of Oncology, 48, 281-292. https://doi.org/10.3892/ijo.2015.3257
MLA
Gao, Y., Rankin, G. O., Tu, Y., Chen, Y. C."Theaflavin-3, 3'-digallate decreases human ovarian carcinoma OVCAR-3 cell-induced angiogenesis via Akt and Notch-1 pathways, not via MAPK pathways". International Journal of Oncology 48.1 (2016): 281-292.
Chicago
Gao, Y., Rankin, G. O., Tu, Y., Chen, Y. C."Theaflavin-3, 3'-digallate decreases human ovarian carcinoma OVCAR-3 cell-induced angiogenesis via Akt and Notch-1 pathways, not via MAPK pathways". International Journal of Oncology 48, no. 1 (2016): 281-292. https://doi.org/10.3892/ijo.2015.3257
Copy and paste a formatted citation
x
Spandidos Publications style
Gao Y, Rankin GO, Tu Y and Chen YC: Theaflavin-3, 3'-digallate decreases human ovarian carcinoma OVCAR-3 cell-induced angiogenesis via Akt and Notch-1 pathways, not via MAPK pathways. Int J Oncol 48: 281-292, 2016.
APA
Gao, Y., Rankin, G.O., Tu, Y., & Chen, Y.C. (2016). Theaflavin-3, 3'-digallate decreases human ovarian carcinoma OVCAR-3 cell-induced angiogenesis via Akt and Notch-1 pathways, not via MAPK pathways. International Journal of Oncology, 48, 281-292. https://doi.org/10.3892/ijo.2015.3257
MLA
Gao, Y., Rankin, G. O., Tu, Y., Chen, Y. C."Theaflavin-3, 3'-digallate decreases human ovarian carcinoma OVCAR-3 cell-induced angiogenesis via Akt and Notch-1 pathways, not via MAPK pathways". International Journal of Oncology 48.1 (2016): 281-292.
Chicago
Gao, Y., Rankin, G. O., Tu, Y., Chen, Y. C."Theaflavin-3, 3'-digallate decreases human ovarian carcinoma OVCAR-3 cell-induced angiogenesis via Akt and Notch-1 pathways, not via MAPK pathways". International Journal of Oncology 48, no. 1 (2016): 281-292. https://doi.org/10.3892/ijo.2015.3257
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