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Volume 10, Issue 3 (Vol.10 No.3 Oct 2021)
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Alizadeh M, Nafari A, Safarzadeh A, Veiskarami S, Almasian M, Kiani A A. The Impact of EGCG and RG108 on SOCS1 Promoter DNA Methylation and Expression in U937 Leukemia Cells. rbmb.net 2021; 10 (3) :455-461
URL: http://rbmb.net/article-1-702-en.html
URL: http://rbmb.net/article-1-702-en.html
The Impact of EGCG and RG108 on SOCS1 Promoter DNA Methylation and Expression in U937 Leukemia Cells
Mohsen Alizadeh 
, Amirhossein Nafari , Ali Safarzadeh , Saeed Veiskarami , Mohammad Almasian , Ali Asghar Kiani *
, Amirhossein Nafari , Ali Safarzadeh , Saeed Veiskarami , Mohammad Almasian , Ali Asghar Kiani *
Department of Medical Laboratory Sciences, School of Allied Medical Sciences, Lorestan University of Medical Sciences, Khorramabad, Iran
Abstract: (3026 Views)
Background: The available evidence has increasingly demonstrated that a combination of genetic and epigenetic factors, such as DNA methylation, could be considered as causing leukemia. Epigenetic changes and methylation of the suppressor of the cytokine signaling 1 promoter (SOCS1) CpG region silence SOCS1 expression in cancer. In the current study, we evaluated the impact of epigallocatechin gallate (EGCG) and RG108 on SOCS1 promoter methylation and expression in U937 cells.
Methods: In the current study, U937 leukemic cells were treated with EGCG and RG108 for 12, 24, 48, and 72 h and SOCS1 promoter methylation and its expression were measured by methylationspecific PCR (MSP) and quantitative real-time PCR, respectively.
Results: The outcomes indicated that the SOCS1 promoter is methylated in U937 cells, and treatment of these cells with either EGCG or RG108 reduced its methylation. Moreover, we observed that SOCS1 expression was significantly upregulated in a time-dependent manner by both EGCG and RG108 in U937
cells compared with control cells. In the RG108-treated group at 12, 24, 48, and 72 h, SOCS1 expression was upregulated by 1, 4.2, 16.6, and 32.6 -fold respectively, and in the EGCG-treated group, by 0.5, 3.2, 10.8, and 22.3 -fold, respectively.
Conclusions: Treatment with either EGCG or RG108 reduced SOCS1 promoter methylation and increased SOCS1 expression in U937 cells in a time-dependent manner, which may play a role in leukemia therapy.
Methods: In the current study, U937 leukemic cells were treated with EGCG and RG108 for 12, 24, 48, and 72 h and SOCS1 promoter methylation and its expression were measured by methylationspecific PCR (MSP) and quantitative real-time PCR, respectively.
Results: The outcomes indicated that the SOCS1 promoter is methylated in U937 cells, and treatment of these cells with either EGCG or RG108 reduced its methylation. Moreover, we observed that SOCS1 expression was significantly upregulated in a time-dependent manner by both EGCG and RG108 in U937
cells compared with control cells. In the RG108-treated group at 12, 24, 48, and 72 h, SOCS1 expression was upregulated by 1, 4.2, 16.6, and 32.6 -fold respectively, and in the EGCG-treated group, by 0.5, 3.2, 10.8, and 22.3 -fold, respectively.
Conclusions: Treatment with either EGCG or RG108 reduced SOCS1 promoter methylation and increased SOCS1 expression in U937 cells in a time-dependent manner, which may play a role in leukemia therapy.
Type of Article: Original Article |
Subject:
Cell Biology
Received: 2021/05/9 | Accepted: 2021/07/15 | Published: 2021/12/5
Received: 2021/05/9 | Accepted: 2021/07/15 | Published: 2021/12/5
References
1. Kim Y, Jekarl DW, Kim J, Kwon A, Choi H, Lee S, et al. Genetic and epigenetic alterations of bone marrow stromal cells in myelodysplastic syndrome and acute myeloid leukemia patients. Stem cell research. 2015;14(2):177-84. [DOI:10.1016/j.scr.2015.01.004] [PMID]
2. Zahedpanah M, Shaiegan M, Ghaffari SH, Nikbakht M, Nikugoftar M, Mohammadi S. Parthenolide induces apoptosis in committed progenitor AML cell line U937 via reduction in osteopontin. Rep Biochem Mol Biol. 2016;4(2):82-8.
3. Gholami M, Bayat S, Manoochehrabadi S, Pashaiefar H, Omrani MD, Jalaeikhoo H, et al. Investigation of CEBPA and CEBPA-AS genes expression in acute myeloid leukemia. Rep Biochem Mol Biol. 2019;7(2):136-141.
4. Oakes CC, Seifert M, Assenov Y, Gu L, Przekopowitz M, Ruppert AS, et al. DNA methylation dynamics during B cell maturation underlie a continuum of disease phenotypes in chronic lymphocytic leukemia. Nat Genet. 2016;48(3):253-64. [DOI:10.1038/ng.3488] [PMID] [PMCID]
5. Klutstein M, Nejman D, Greenfield R, Cedar H. DNA methylation in cancer and aging. Cancer Res. 2016;76(12):3446-50. [DOI:10.1158/0008-5472.CAN-15-3278] [PMID]
6. Ghaznavi H, Kiani AA, Soltanpour MS. Association study between DNA methylation and genetic variation of APOE gene with the risk of coronary artery disease. Mol Biol Res Commun. 2018;7(4):173-179.
7. Soltanpour MS, Soheili Z, Pourfathollah AA, Samiei S, Meshkani R, Kiani AA, et al. The A1298C mutation in methylenetetrahydrofolate reductase gene and its association with idiopathic venous thrombosis in an Iranian population. Laboratory Medicine. 2011;42(4):213-6. [DOI:10.1309/LM5LWXCHVZY9RFOM]
8. Schübeler D. Function and information content of DNA methylation. Nature. 2015;517(7534):321-326. [DOI:10.1038/nature14192] [PMID]
9. Villarino AV, Kanno Y, Ferdinand JR, O'Shea JJ. Mechanisms of Jak/STAT signaling in immunity and disease. J Immunol. 2015;194(1):21-7. [DOI:10.4049/jimmunol.1401867] [PMID] [PMCID]
10. Thomas S, Snowden J, Zeidler M, Danson S. The role of JAK/STAT signalling in the pathogenesis, prognosis and treatment of solid tumours. Br J Cancer. 2015;113(3):365-71. [DOI:10.1038/bjc.2015.233] [PMID] [PMCID]
11. Shen L, Evel-Kabler K, Strube R, Chen S-Y. Silencing of SOCS1 enhances antigen presentation by dendritic cells and antigen-specific anti-tumor immunity. Nat Biotechnol. 2004;22(12):1546-53. [DOI:10.1038/nbt1035] [PMID]
12. Jiang M, Zhang W-w, Liu P, Yu W, Liu T, Yu J. Dysregulation of SOCS-mediated negative feedback of cytokine signaling in carcinogenesis and its significance in cancer treatment. Front Immunol. 2017;8:70. [DOI:10.3389/fimmu.2017.00070] [PMID] [PMCID]
13. Liau NP, Laktyushin A, Lucet IS, Murphy JM, Yao S, Whitlock E, et al. The molecular basis of JAK/STAT inhibition by SOCS1. Nature communications. 2018;9(1):1558. [DOI:10.1038/s41467-018-04013-1] [PMID] [PMCID]
14. Beaurivage C, Champagne A, Tobelaim WS, Pomerleau V, Menendez A, Saucier C. SOCS1 in cancer: An oncogene and a tumor suppressor. Cytokine. 2016;82:87-94. [DOI:10.1016/j.cyto.2016.01.005] [PMID]
15. Yoshikawa H, Matsubara K, Qian G-S, Jackson P, Groopman JD, Manning JE, et al. SOCS-1, a negative regulator of the JAK/STAT pathway, is silenced by methylation in human hepatocellular carcinoma and shows growth-suppression activity. Nature genetics. 2001;28(1):29-35.
https://doi.org/10.1038/ng0501-29 [DOI:10.1038/88225] [PMID]
16. Nagai H, Naka T, Terada Y, Komazaki T, Yabe A, Jin E, et al. Hypermethylation associated with inactivation of the SOCS-1 gene, a JAK/STAT inhibitor, in human hepatoblastomas. Journal of human genetics. 2003;48(2):65-69. [DOI:10.1007/s100380300008] [PMID]
17. Galm O, Yoshikawa H, Esteller M, Osieka R, Herman JG. SOCS-1, a negative regulator of cytokine signaling, is frequently silenced by methylation in multiple myeloma. Blood. 2003;101(7):2784-8. [DOI:10.1182/blood-2002-06-1735] [PMID]
18. Chen CY, Tsay W, Tang JL, Shen HL, Lin SW, Huang SY, et al. SOCS1 methylation in patients with newly diagnosed acute myeloid leukemia. Genes Chromosomes Cancer. 2003;37(3):300-5. [DOI:10.1002/gcc.10222] [PMID]
19. Liu TC, Lin SF, Chang JG, Yang MY, Hung SY, Chang CS. Epigenetic alteration of the SOCS1 gene in chronic myeloid leukaemia. Br J Haematol. 2003;123(4):654-61. [DOI:10.1046/j.1365-2141.2003.04660.x] [PMID]
20. Watanabe D, Ezoe S, Fujimoto M, Kimura A, Saito Y, Nagai H, et al. Suppressor of cytokine signalling‐1 gene silencing in acute myeloid leukaemia and human haematopoietic cell lines. Br J Haematol. 2004;126(5):726-35. [DOI:10.1111/j.1365-2141.2004.05107.x] [PMID]
21. Mimoto J, Kiura K, Matsuo K, Yoshino T, Takata I, Ueoka H, et al. (-)-Epigallocatechin gallate can prevent cisplatin-induced lung tumorigenesis in A/J mice. Carcinogenesis. 2000;21(5):915-9. [DOI:10.1093/carcin/21.5.915] [PMID]
22. Chen J, Ye ZQ, Koo M. Growth inhibition and cell cycle arrest effects of epigallocatechin gallate in the NBT‐II bladder tumour cell line. BJU Int. 2004;93(7):1082-6. [DOI:10.1111/j.1464-410X.2004.04785.x] [PMID]
23. Mantena SK, Roy AM, Katiyar SK. Retracted: Epigallocatechin‐3‐Gallate Inhibits Photocarcinogenesis Through Inhibition of Angiogenic Factors and Activation of CD8+ T Cells in Tumors. Photochem Photobiol. 2005;81(5):1174-9. [DOI:10.1562/2005-04-11-RA-487] [PMID]
24. Stuart EC, Scandlyn MJ, Rosengren RJ. Role of epigallocatechin gallate (EGCG) in the treatment of breast and prostate cancer. Life Sci. 2006;79(25):2329-36. [DOI:10.1016/j.lfs.2006.07.036] [PMID]
25. Zhang Y, Wang X, Han L, Zhou Y, Sun S. Green tea polyphenol EGCG reverse cisplatin resistance of A549/DDP cell line through candidate genes demethylation. Biomed Pharmacother. 2015;69:285-90. [DOI:10.1016/j.biopha.2014.12.016] [PMID]
26. Tarhriz V, Wagner KD, Masoumi Z, Molavi O, Hejazi MS, Ghanbarian H. CDK9 regulates apoptosis of myoblast cells by modulation of microRNA‐1 expression. J Cell Biochem. 2018;119(1):547-554. [DOI:10.1002/jcb.26213] [PMID]
27. Kohram F, Fallah P, Shamsara M, Bolandi Z, Rassoulzadegan M, Soleimani M, et al. Cell type‐dependent functions of microRNA‐92a. Journal of cellular biochemistry. 2018;119(7):5798-804. [DOI:10.1002/jcb.26765] [PMID]
28. Jones PA, Baylin SB. The epigenomics of cancer. Cell. 2007;128(4):683-692. [DOI:10.1016/j.cell.2007.01.029] [PMID] [PMCID]
29. Ley TJ, Ding L, Walter MJ, McLellan MD, Lamprecht T, Larson DE, et al. DNMT3A mutations in acute myeloid leukemia. N Engl J Med. 2010;363(25):2424-33. [DOI:10.1056/NEJMoa1005143] [PMID] [PMCID]
30. Li Y, Tollefsbol TO. Impact on DNA methylation in cancer prevention and therapy by bioactive dietary components. Curr Med Chem. 2010;17(20):2141-51. [DOI:10.2174/092986710791299966] [PMID] [PMCID]
31. Zhong J, Xu C, Reece EA, Yang P. The green tea polyphenol EGCG alleviates maternal diabetes-induced neural tube defects by inhibiting DNA hypermethylation. Am J Obstet Gynecol. 2016;215(3):368.e1-368.e10. [DOI:10.1016/j.ajog.2016.03.009] [PMID] [PMCID]
32. Yoo J, Medina-Franco JL. Homology modeling, docking and structure-based pharmacophore of inhibitors of DNA methyltransferase. J Comput Aided Mol Des. 2011;25(6):555-67. [DOI:10.1007/s10822-011-9441-1] [PMID]
33. Nandakumar V, Vaid M, Katiyar SK. (−)-Epigallocatechin-3-gallate reactivates silenced tumor suppressor genes, Cip1/p21 and p 16 INK4a, by reducing DNA methylation and increasing histones acetylation in human skin cancer cells. Carcinogenesis. 2011;32(4):537-44. [DOI:10.1093/carcin/bgq285] [PMID] [PMCID]
34. Kato K, Long N, Makita H, Toida M, Yamashita T, Hatakeyama D, et al. Effects of green tea polyphenol on methylation status of RECK gene and cancer cell invasion in oral squamous cell carcinoma cells. Br J Cancer. 2008;99(4):647-654. [DOI:10.1038/sj.bjc.6604521] [PMID] [PMCID]
35. Meng J, Tong Q, Liu X, Yu Z, Zhang J, Gao B. Epigallocatechin-3-gallate inhibits growth and induces apoptosis in esophageal cancer cells through the demethylation and reactivation of the p16 gene. Oncol Lett. 2017;14(1):1152-1156. [DOI:10.3892/ol.2017.6248] [PMID] [PMCID]
36. Remely M, Ferk F, Sterneder S, Setayesh T, Roth S, Kepcija T, et al. EGCG prevents high fat diet-induced changes in gut microbiota, decreases of DNA strand breaks, and changes in expression and DNA methylation of Dnmt1 and MLH1 in C57BL/6J male mice. Oxid Med Cell Longev. 2017;2017:3079148. [DOI:10.1155/2017/3079148] [PMID] [PMCID]
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