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Journals / Turkish Journal of Biology / 2015 / Cilt: 39 - Sayı: 5

Epigallocatechin 3-gallate applications on HT-29 and MCF-7 cell lines andevaluation of tumor suppressor gene methylation

YUNUS KASIM TERZİ
ÖZGE ÖZER KAYA
ÖZLEM DARCANSOY İŞERİ
ZERRİN ÇELİK
FERİDE İFFET ŞAHİN
Pages
698–704
Publication Date
2015-12-04
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Our results suggest that methylation status of tumor suppressor genes did not change with different EGCG doses.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Abstract: Epigallocatechin 3-gallate (EGCG) is an antitumor molecule and shows this activity by binding to the active center of a methyltransferase enzyme (DNMT1).
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Key Findings & Data:In this study, we analyzed the effect of EGCG on the methylation status of 25 tumor suppressor genes in cancer cell lines HT-29 and MCF-7.
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Conclusion & Impact:Our results suggest that methylation status of tumor suppressor genes did not change with different EGCG doses.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Epigallocatechin 3-gallate · epigenetics · methylation

Abstract

Abstract: Epigallocatechin 3-gallate (EGCG) is an antitumor molecule and shows this activity by binding to the active center of a methyltransferase enzyme (DNMT1). The methylation of DNA sequences of tumor suppressor and DNA repair genes is observed in different stages of carcinogenesis. In this study, we analyzed the effect of EGCG on the methylation status of 25 tumor suppressor genes in cancer cell lines HT-29 and MCF-7. HT-29 and MCF-7 cells were incubated with 10 μM, 20 μM, and 50 μM and 1 μM, 5 μM, and 10 μM EGCG for 48 h, respectively. We found promoter hypermethylation of (1) CDH13, GATA5, and RARβ genes in MCF-7 cell line and (2) RARβ, ESR1, PAX6, WT1, CADM1, CHFR, CDH13, and GATA5 genes in HT-29 cell line. However, (3) after EGCG application, no changes in methylation status were detected in our samples. Our results suggest that methylation status of tumor suppressor genes did not change with different EGCG doses.

Özet

Abstract: Epigallocatechin 3-gallate (EGCG) is an antitumor molecule and shows this activity by binding to the active center of a methyltransferase enzyme (DNMT1). The methylation of DNA sequences of tumor suppressor and DNA repair genes is observed in different stages of carcinogenesis. In this study, we analyzed the effect of EGCG on the methylation status of 25 tumor suppressor genes in cancer cell lines HT-29 and MCF-7. HT-29 and MCF-7 cells were incubated with 10 μM, 20 μM, and 50 μM and 1 μM, 5 μM, and 10 μM EGCG for 48 h, respectively. We found promoter hypermethylation of (1) CDH13, GATA5, and RARβ genes in MCF-7 cell line and (2) RARβ, ESR1, PAX6, WT1, CADM1, CHFR, CDH13, and GATA5 genes in HT-29 cell line. However, (3) after EGCG application, no changes in methylation status were detected in our samples. Our results suggest that methylation status of tumor suppressor genes did not change with different EGCG doses.

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Cite This Article

TERZİ, Y. K., KAYA, Ö. Ö., İŞERİ, Ö. D., ÇELİK, Z., ŞAHİN, F. İ. (2015). Epigallocatechin 3-gallate applications on HT-29 and MCF-7 cell lines andevaluation of tumor suppressor gene methylation. Turkish Journal of Biology, Cilt: 39 - Sayı: 5, 698–704. https://ajindex.com/articles/181485

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References (13)

  1. Alvarez M, Robey R, Sandor V, Nishiyama K, Matsumoto Y, Paull K, Bates S, Fojo T (1998). Using the National Cancer Institute anticancer drug screen to assess the effect of MRP expression on drug sensitivity profiles. Mol Pharmacol 54: 802–814.
  2. Arai M, Yokosuka O, Hirasawa Y, Fukai K, Chiba T, Imazeki F, Kanda T, Yatomi M, Takiguchi Y, Seki N et al. (2006). Sequential gene expression changes in cancer cell lines after treatment with the demethylation agent 5-Aza-2’-deoxycytidine. Cancer 106: 2514–2525.
  3. Arends MJ (2013). Pathways of colorectal carcinogenesis. Appl Immunohistochem Mol Morphol 21: 97–102.
  4. Baylin SB, Herman JG (2000). DNA hypermethylation in tumorigenesis: epigenetics joins genetics. Trends Genet 16: 168–174.
  5. Brooks J, Cairns P, Zeleniuch-Jacquotte A (2009). Promoter methylation and the detection of breast cancer. Cancer Causes Control 20: 1539–1550.
  6. Chen D, Wan SB, Yang H, Yuan J, Chan TH, Dou QP (2011). EGCG, green tea polyphenols and their synthetic analogs and prodrugs for human cancer prevention and treatment. Adv Clin Chem 53: 155–177.
  7. Cho YH, Yazici H, Wu HC, Terry MB, Gonzalez K, Qu M, Dalay N, Santella RM (2010). Aberrant promoter hypermethylation and genomic hypomethylation in tumor, adjacent normal tissues and blood from breast cancer patients. Anticancer Res 30: 2489–2496.
  8. Chung J Y, Huang C, Meng X, Dong Z, Yang CS (1999). Inhibition of activator protein 1 activity and cell growth by purified green tea and black tea polyphenols in H-Ras-transformed cells: structure-activity relationship and mechanisms involved. Cancer Res 59: 4610–4617.
  9. Chung JY, Park JO, Phyu H, Dong Z, Yang CS (2001). Mechanisms of inhibition of the Ras-MAP kinase signaling pathway in 30.7b Ras 12 cells by tea polyphenols (-)-epigallocatechin-3-gallate and theaflavin-3,3’-digallate. FASEB J 15: 2022–2024.
  10. Colussi D, Brandi G, Bazzoli F, Ricciardiello L (2013). Molecular pathways involved in colorectal cancer: implications for disease behavior and prevention. Int J Mol Sci 14: 16365–16385.
  11. Fang MZ, Wang Y, Ai N, Hou Z, Sun Y, Lu H, Welsh W, Yang CS (2003). Tea polyphenol (-)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer cell lines. Cancer Res 63: 7563–7570.
  12. Gao Z, Xu Z, Hung MS, Lin YC, Wang T, Gong M, Zhi X, Jablon DM, You L (2009). Promoter demethylation of WIF-1 by epigallocatechin-3-gallate in lung cancer cells. Anticancer Res 29: 2025–2230.
  13. Hardy TM, Tollefsbol TO (2011). Epigenetic diet: impact