Systematic Review of the Anti-Cancer Activity of Green Tea (Camellia sinensis)-Derived Compounds in Breast Cancer In Vitro
Abstract
Breast cancer is the most common type of cancer occurring in women with increasing prevalence in these past few years. Although many targeted therapies have been developed to increase the specificity of the treatment, many patients still suffer from cancer resistance and relapse. Green tea, a common beverage derived from natural plants, has been shown to induce chemopreventive effects and exhibit anti-cancer activity through its catechins and polyphenols content. The main well-known compound that induces these effects is epigallocatechin-3-gallate (EGCG). Green tea also contains other naturally occurring compounds such as catechin (C), epicatechin (EC), epigallocatechin (EGC), epicatechin-3-gallate (ECG), and others. In this study, we assessed and compared the anti-cancer activity of these green tea-derived compounds towards different types of breast cancer cell lines. A total of 15 original research papers from PubMed, Google Scholar, and DOAJ databases were collected and evaluated for the data extraction. The results showed that EGCG was the most potent compound in green tea that was able to reduce cell viability, wound closure, and induce apoptosis even in highly aggressive MDA-MB-231 and lower grade MCF-7 cell lines with ranging concentration. The second potent compound was ECG, followed by EGC and EC that exhibited intermediate effects. Lastly, catechin was shown to have the lowest anti-cancer activity among all other compounds. Flavonols were also shown to exert cytotoxic effects toward breast cancer cells. Moreover, further study is needed to discover the exact mechanism of each compound and determine its relationship toward different types of breast cancer cell lines.
Downloads
References
Braicu, C., Gherman, C., Irimie, A., & Berindan-Neagoe, I. (2013). Epigallocatechin-3-Gallate (EGCG) Inhibits Cell Proliferation and Migratory Behaviour of Triple Negative Breast Cancer Cells. Journal Of Nanoscience And Nanotechnology, 13(1), 632-637. doi: 10.1166/jnn.2013.6882
Choudhary, S., Sood, S., Donnell, R., & Wang, H. (2012). Intervention of human breast cell carcinogenesis chronically induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine. Carcinogenesis, 33(4), 876-885. doi: 10.1093/carcin/bgs097
Das, A., Banik, N., & Ray, S. (2006). Mechanism of apoptosis with the involvement of calpain and caspase cascades in human malignant neuroblastoma SH-SY5Y cells exposed to flavonoids. International Journal Of Cancer, 119(11), 2575-2585. doi: 10.1002/ijc.22228
De Amicis, F., Russo, A., Avena, P., Santoro, M., Vivacqua, A., & Bonofiglio, D. et al. (2013). In vitro mechanism for downregulation of ER-α expression by epigallocatechin gallate in ER+/PR+ human breast cancer cells. Molecular Nutrition & Food Research, 57(5), 840-853. doi: 10.1002/mnfr.201200560
Deb, G., Thakur, V., Limaye, A., & Gupta, S. (2014). Epigenetic induction of tissue inhibitor of matrix metalloproteinase-3 by green tea polyphenols in breast cancer cells. Molecular Carcinogenesis, 54(6), 485-499. doi: 10.1002/mc.22121
Delgado, L., Fernandes, I., González-Manzano, S., de Freitas, V., Mateus, N., & Santos-Buelga, C. (2014). Anti-proliferative effects of quercetin and catechin metabolites. Food & function, 5(4), 797-803.
Farhan, M., Khan, H., Oves, M., Al-Harrasi, A., Rehmani, N., & Arif, H. et al. (2016). Cancer Therapy by Catechins Involves Redox Cycling of Copper Ions and Generation of Reactive Oxygen Species. Toxins, 8(2), 37. doi: 10.3390/toxins8020037
Garg, A., Buchholz, T., & Aggarwal, B. (2005). Chemosensitization and Radiosensitization of Tumors by Plant Polyphenols. Antioxidants & Redox Signaling, 7(11-12), 1630-1647. doi: 10.1089/ars.2005.7.1630
Granci, V., Dupertuis, Y., & Pichard, C. (2010). Angiogenesis as a potential target of pharmaconutrients in cancer therapy. Current Opinion In Clinical Nutrition And Metabolic Care, 13(4), 417-422. doi: 10.1097/mco.0b013e3283392656
Hastak, K., Gupta, S., Ahmad, N., Agarwal, M., Agarwal, M., & Mukhtar, H. (2003). Role of p53 and NF-κB in epigallocatechin-3-gallate-induced apoptosis of LNCaP cells. Oncogene, 22(31), 4851-4859. doi: 10.1038/sj.onc.1206708
Ho, J., Choue, R., & Lee, J. (2013). Green tea seed extract inhibits cell migration by suppressing the epithelial-to-mesenchymal transition (EMT) process in breast cancer cells. Food Science And Biotechnology, 22(4), 1125-1129. doi: 10.1007/s10068-013-0193-7
Khan, N., & Mukhtar, H. (2013). Tea and Health: Studies in Humans. Current Pharmaceutical Design, 19(34), 6141-6147. doi: 10.2174/1381612811319340008
Kim, H. S., Kim, M. H., Jeong, M., Hwang, Y. S., Lim, S. H., Shin, B. A., Ahn, B. W., & Jung, Y. D. (2004). EGCG blocks tumor promoter-induced MMP-9 expression via suppression of MAPK and AP-1 activation in human gastric AGS cells. Anticancer research, 24(2B), 747–753.
Kim, M., Murakami, A., Kawabata, K., & Ohigashi, H. (2005). (−)-Epigallocatechin-3-gallate promotes pro-matrix metalloproteinase-7 production via activation of the JNK1/2 pathway in HT-29 human colorectal cancer cells. Carcinogenesis, 26(9), 1553-1562. doi: 10.1093/carcin/bgi104
Kuban-Jankowska, A., Kostrzewa, T., Musial, C., Barone, G., Lo-Bosco, G., Lo-Celso, F., & Gorska-Ponikowska, M. (2020). Green Tea Catechins Induce Inhibition of PTP1B Phosphatase in Breast Cancer Cells with Potent Anti-Cancer Properties: In Vitro Assay, Molecular Docking, and Dynamics Studies. Antioxidants, 9(12), 1208. doi: 10.3390/antiox9121208
Kürbitz, C., Heise, D., Redmer, T., Goumas, F., Arlt, A., & Lemke, J. et al. (2011). Epicatechin gallate and catechin gallate are superior to epigallocatechin gallate in growth suppression and anti-inflammatory activities in pancreatic tumor cells. Cancer Science, 102(4), 728-734. doi: 10.1111/j.1349-7006.2011.01870.x
Lim, Y., & Cha, Y. (2011). Epigallocatechin-3-gallate induces growth inhibition and apoptosis of human anaplastic thyroid carcinoma cells through suppression of EGFR/ERK pathway and cyclin B1/CDK1 complex. Journal Of Surgical Oncology, 104(7), 776-780. doi: 10.1002/jso.21999
Lim, Y., Lee, S., Song, M., Yamaguchi, K., Yoon, J., Choi, E., & Baek, S. (2006). Growth inhibition and apoptosis by (−)-epicatechin gallate are mediated by cyclin D1 suppression in head and neck squamous carcinoma cells. European Journal Of Cancer, 42(18), 3260-3266. doi: 10.1016/j.ejca.2006.07.014
Mackenzie, G., & Oteiza, P. (2006). Modulation of transcription factor NF-κB in Hodgkin's lymphoma cell lines: Effect of (−)-epicatechin. Free Radical Research, 40(10), 1086-1094. doi: 10.1080/10715760600788396
Maeda-Yamamoto, M., Suzuki, N., Sawai, Y., Miyase, T., Sano, M., Hashimoto-Ohta, A., & Isemura, M. (2003). Association of Suppression of Extracellular Signal-Regulated Kinase Phosphorylation by Epigallocatechin Gallate with the Reduction of Matrix Metalloproteinase Activities in Human Fibrosarcoma HT1080 Cells. Journal Of Agricultural And Food Chemistry, 51(7), 1858-1863. doi: 10.1021/jf021039l
Masuda, M., Suzui, M., Lim, J., Deguchi, A., Soh, J., & Weinstein, I. (2002). Epigallocatechin-3-gallate decreases VEGF production in head and neck and breast carcinoma cells by inhibiting EGFR-related pathways of signal transduction. Journal Of Experimental Therapeutics And Oncology, 2(6), 350-359. doi: 10.1046/j.1359-4117.2002.01062.x
Meeran, S., Patel, S., Chan, T., & Tollefsbol, T. (2011). A Novel Prodrug of Epigallocatechin-3-gallate: Differential Epigenetic hTERT Repression in Human Breast Cancer Cells. Cancer Prevention Research, 4(8), 1243-1254. doi: 10.1158/1940-6207.capr-11-0009
Min, K., & Kwon, T. (2014). Anticancer effects and molecular mechanisms of epigallocatechin-3-gallate. Integrative Medicine Research, 3(1), 16-24. doi: 10.1016/j.imr.2013.12.001
Mineva, N., Paulson, K., Naber, S., Yee, A., & Sonenshein, G. (2013). Epigallocatechin-3-Gallate Inhibits Stem-Like Inflammatory Breast Cancer Cells. Plos ONE, 8(9), e73464. doi: 10.1371/journal.pone.0073464
Moradzadeh, M., Hosseini, A., Erfanian, S., & Rezaei, H. (2017). Epigallocatechin-3-gallate promotes apoptosis in human breast cancer T47D cells through down-regulation of PI3K/AKT and Telomerase. Pharmacological Reports, 69(5), 924-928. doi: 10.1016/j.pharep.2017.04.008
Ouzzani, M., Hammady, H., Fedorowicz, Z., & Elmagarmid, A. (2016). Rayyan—a web and mobile app for systematic reviews. Systematic Reviews, 5(1). doi: 10.1186/s13643-016-0384-4
Papież, M., Baran, J., Bukowska-Straková, K., & Wiczkowski, W. (2010). Antileukemic action of (−)-epicatechin in the spleen of rats with acute myeloid leukemia. Food And Chemical Toxicology, 48(12), 3391-3397. doi: 10.1016/j.fct.2010.09.010
QIN, J., WANG, Y., BAI, Y., YANG, K., MAO, Q., & LIN, Y. et al. (2012). Epigallocatechin-3-gallate inhibits bladder cancer cell invasion via suppression of NF-κB-mediated matrix metalloproteinase-9 expression. Molecular Medicine Reports, 6(5), 1040-1044. doi: 10.3892/mmr.2012.1054
Ramos, S. (2008). Cancer chemoprevention and chemotherapy: Dietary polyphenols and signalling pathways. Molecular Nutrition & Food Research, 52(5), 507-526. doi: 10.1002/mnfr.200700326
Rathore, K., Choudhary, S., Odoi, A., & Wang, H. (2011). Green tea catechin intervention of reactive oxygen species-mediated ERK pathway activation and chronically induced breast cell carcinogenesis. Carcinogenesis, 33(1), 174-183. doi: 10.1093/carcin/bgr244
Ravindranath, M., Saravanan, T., Monteclaro, C., Presser, N., Ye, X., Selvan, S., & Brosman, S. (2006). Epicatechins Purified from Green Tea (Camellia sinensis) Differentially Suppress Growth of Gender-Dependent Human Cancer Cell Lines. Evidence-Based Complementary And Alternative Medicine, 3(2), 237-247. doi: 10.1093/ecam/nel003
Rha, C., Jeong, H., Park, S., Lee, S., Jung, Y., & Kim, D. (2019). Antioxidative, Anti-Inflammatory, and Anticancer Effects of Purified Flavonol Glycosides and Aglycones in Green Tea. Antioxidants, 8(8), 278. doi: 10.3390/antiox8080278
Schneider, K., Schwarz, M., Burkholder, I., Kopp-Schneider, A., Edler, L., & Kinsner-Ovaskainen, A. et al. (2009). “ToxRTool”, a new tool to assess the reliability of toxicological data. Toxicology Letters, 189(2), 138-144. doi: 10.1016/j.toxlet.2009.05.013
Seely, D., Mills, E., Wu, P., Verma, S., & Guyatt, G. (2005). The Effects of Green Tea Consumption on Incidence of Breast Cancer and Recurrence of Breast Cancer: A Systematic Review and Meta-analysis. Integrative Cancer Therapies, 4(2), 144-155. doi: 10.1177/1534735405276420
Shay, J., Elbaz, H., Lee, I., Zielske, S., Malek, M., & Hüttemann, M. (2015). Molecular Mechanisms and Therapeutic Effects of (−)-Epicatechin and Other Polyphenols in Cancer, Inflammation, Diabetes, and Neurodegeneration. Oxidative Medicine And Cellular Longevity, 2015, 1-13. doi: 10.1155/2015/181260
Sheng, J., Shi, W., Guo, H., Long, W., Wang, Y., & Qi, J. et al. (2019). The Inhibitory Effect of (−)-Epigallocatechin-3-Gallate on Breast Cancer Progression via Reducing SCUBE2 Methylation and DNMT Activity. Molecules, 24(16), 2899. doi: 10.3390/molecules24162899
Siddique, H., Liao, D., Mishra, S., Schuster, T., Wang, L., & Matter, B. et al. (2012). Epicatechin-rich cocoa polyphenol inhibits Kras-activated pancreatic ductal carcinoma cell growth in vitro and in a mouse model. International Journal Of Cancer, 131(7), 1720-1731. doi: 10.1002/ijc.27409
Stout, N., Baima, J., Swisher, A., Winters-Stone, K., & Welsh, J. (2017). A Systematic Review of Exercise Systematic Reviews in the Cancer Literature (2005-2017). PM&R, 9, S347-S384. doi: 10.1016/j.pmrj.2017.07.074
Sun, H., Yin, M., Hao, D., & Shen, Y. (2020). Anti-Cancer Activity of Catechin against A549 Lung Carcinoma Cells by Induction of Cyclin Kinase Inhibitor p21 and Suppression of Cyclin E1 and P–AKT. Applied Sciences, 10(6), 2065. doi: 10.3390/app10062065
Sun, Y., Zhao, Z., Yang, Z., Xu, F., Lu, H., & Zhu, Z. et al. (2017). Risk Factors and Preventions of Breast Cancer. International Journal Of Biological Sciences, 13(11), 1387-1397. doi: 10.7150/ijbs.21635
Surh, Y. (2003). Cancer chemoprevention with dietary phytochemicals. Nature Reviews Cancer, 3(10), 768-780. doi: 10.1038/nrc1189
Tao, Z., Shi, A., Lu, C., Song, T., Zhang, Z., & Zhao, J. (2014). Breast Cancer: Epidemiology and Etiology. Cell Biochemistry And Biophysics, 72(2), 333-338. doi: 10.1007/s12013-014-0459-6
Thangapazham, R., Singh, A., Sharma, A., Warren, J., Gaddipati, J., & Maheshwari, R. (2007). Green tea polyphenols and its constituent epigallocatechin gallate inhibits proliferation of human breast cancer cells in vitro and in vivo. Cancer Letters, 245(1-2), 232-241. doi: 10.1016/j.canlet.2006.01.027
Wei, R., Mao, L., Xu, P., Zheng, X., Hackman, R., Mackenzie, G., & Wang, Y. (2018). Suppressing glucose metabolism with epigallocatechin-3-gallate (EGCG) reduces breast cancer cell growth in preclinical models. Food & Function, 9(11), 5682-5696. doi: 10.1039/c8fo01397g
Wu, A., & Butler, L. (2011). Green tea and breast cancer. Molecular Nutrition & Food Research, 55(6), 921-930. doi: 10.1002/mnfr.201100006
Xu, P., Yan, F., Zhao, Y., Chen, X., Sun, S., Wang, Y., & Ying, L. (2020). Green Tea Polyphenol EGCG Attenuates MDSCs-mediated Immunosuppression through Canonical and Non-Canonical Pathways in a 4T1 Murine Breast Cancer Model. Nutrients, 12(4), 1042. doi: 10.3390/nu12041042
Yang, J., Wei, D., & Liu, J. (2005). Repressions of MMP-9 expression and NF-κB localization are involved in inhibition of lung carcinoma 95-D cell invasion by (–)-epigallocatechin-3-gallate. Biomedicine & Pharmacotherapy, 59(3), 98-103. doi: 10.1016/j.biopha.2005.01.004
Zeng, L., Holly, J., & Perks, C. (2014). Effects of Physiological Levels of the Green Tea Extract Epigallocatechin-3-Gallate on Breast Cancer Cells. Frontiers In Endocrinology, 5. doi: 10.3389/fendo.2014.00061
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
Articles published in Indonesian Journal Life of Sciences are licensed under a Creative Commons Attribution-ShareAlike 4.0 International license. You are free to copy, transform, or redistribute articles for any lawful purpose in any medium, provided you give appropriate credit to the original author(s) and Indonesian Journal Life of Sciences, link to the license, indicate if changes were made, and redistribute any derivative work under the same license. Copyright on articles is retained by the respective author(s), without restrictions. A non-exclusive license is granted to Indonesian Journal Life of Sciences to publish the article and identify itself as its original publisher, along with the commercial right to include the article in a hardcopy issue for sale to libraries and individuals. By publishing in Indonesian Journal Life of Sciences, authors grant any third party the right to use their article to the extent provided by the Creative Commons Attribution-ShareAlike 4.0 International license.