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Retraction
Retraction: Comparison of As2O3 and As4O6 in the Detection of SiHa Cervical Cancer Cell G rowth Inhibition Pathway
Yong Wook Kim, Su Mi Bae, Keun Ho Lee, Joon Mo Lee, Sung Eun Namkoong, Insu P. Lee, Chong Kook Kim, Jeong-Sun Seo, Jeong-Im Sin, Yong-Wan Kim, Woong Shick Ahn
Cancer Res Treat. 2007;39(1):47-47.   Published online March 31, 2007
DOI: https://doi.org/10.4143/crt.2007.39.1.47
Retracts: Cancer Res Treat 2004;36(4):255
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Original Articles
Activity of Green Tea Polyphenol Epigallocatechin-3-gallate Against Ovarian Carcinoma Cell Lines
Yong Wook Kim, Su Mi Bae, Joon Mo Lee, Sung Eun Namkoong, Sei Jun Han, Byoung Rai Lee, Insu P. Lee, Sang Hee Kim, Young Joo Lee, Chong Kook Kim, Yong-Wan Kim, Woong Shick Ahn
Cancer Res Treat. 2004;36(5):315-323.   Published online October 31, 2004
DOI: https://doi.org/10.4143/crt.2004.36.5.315
AbstractAbstract PDFPubReaderePub
Purpose

A constituent of green tea, (-)-epigallocatechin-3-gallate (EGCG), is known to possess anti-cancer properties. In this study, the time-course of the anticancer effects of EGCG on human ovarian cancer cells were investigated to provide insights into the molecular-level understanding of the growth suppression mechanism involved in EGCG-mediated apoptosis and cell cycle arrest.

Materials and Methods

Three human ovarian cancer cell lines (p53 negative, SKOV-3 cells; mutant type p53, OVCAR-3 cells; and wild type p53, PA-1 cells) were used. The effect of EGCG treatment was studied via a cell count assay, cell cycle analysis, FACS, Western blot and macroarray assay.

Results

EGCG exerts a significant role in suppressing ovarian cancer cell growth, showed dose dependent growth inhibitory effects in each cell line and induced apoptosis and cell cycle arrest. The cell cycle was arrested at the G1 phase by EGCG in SKOV-3 and OVCAR-3 cells.

In contrast, the cell cycle was arrested in the G1/S phase in PA-1 cells. EGCG differentially regulated the expression of genes and proteins (Bax, p21, Retinoblastoma, cyclin D1, CDK4 and Bcl-XL) more than 2 fold, showing a possible gene regulatory role for EGCG. The continual expression in p21WAF1 suggests that EGCG acts in the same way with p53 proteins to facilitate apoptosis after EGCG treatment. Bax, PCNA and Bcl-X are also important in EGCG-mediated apoptosis. In contrast, CDK4 and Rb are not important in ovarian cancer cell growth inhibition.

Conclusion

EGCG can inhibit ovarian cancer cell growth through the induction of apoptosis and cell cycle arrest, as well as in the regulation of cell cycle related proteins. Therefore, EGCG-mediated apoptosis could be applied to an advanced strategy in the development of a potential drug against ovarian cancer.

Citations

Citations to this article as recorded by  
  • Role of Epigallocatechin Gallate in Selected Malignant Neoplasms in Women
    Anna Markowska, Michał Antoszczak, Janina Markowska, Adam Huczyński
    Nutrients.2025; 17(2): 212.     CrossRef
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    Yuanyuan Zhao, Lichao Lu, Xingying Chen, Qiaozhi Yin
    Pharmacological Research.2025; 215: 107729.     CrossRef
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    Manzar Alam, Sabeeha Ali, Ghulam Md. Ashraf, Anwar L. Bilgrami, Dharmendra Kumar Yadav, Md. Imtaiyaz Hassan
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    Sabrina Bimonte, Marco Cascella
    Drug Design, Development and Therapy.2020; Volume 14: 4245.     CrossRef
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    S Xinqiang, Z Mu, C Lei, LY Mun
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    Sumit Bansal, Navneet Syan, Pooja Mathur, Shivani Choudhary
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    Salvatore Chirumbolo
    Journal of the Science of Food and Agriculture.2012; 92(8): 1573.     CrossRef
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    Dominique Trudel, David P. Labbé, Isabelle Bairati, Vincent Fradet, Laurent Bazinet, Bernard Têtu
    Gynecologic Oncology.2012; 126(3): 491.     CrossRef
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    Sarah J. Oppeneer, Kim Robien
    Nutrition and Cancer.2011; 63(6): 817.     CrossRef
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Comparison of As2O3 and As4O6 in the Detection of SiHa Cervical Cancer Cell Growth Inhibition Pathway
Yong Wook Kim, Su Mi Bae, Keun Ho Lee, Joon Mo Lee, Sung Eun Namkoong, Insu P. Lee, Chong Kook Kim, Jeong-Sun Seo, Jeong-Im Sin, Yong-Wan Kim, Woong Shick Ahn
Cancer Res Treat. 2004;36(4):255-262.   Published online August 31, 2004
DOI: https://doi.org/10.4143/crt.2004.36.4.255
Retraction in: Cancer Res Treat 2007;39(1):47
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  • 45 Download
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