Wed, Apr 24, 2024
Volume 14, Issue 1 (Jan-Feb 2020)
mljgoums 2020, 14(1): 1-9 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
younesian O, younesian S, hosseinzadeh S, joshaghani H R. Association of Selenium and Risk of Esophageal Cancer: A Review. mljgoums 2020; 14 (1) :1-9
URL: http://mlj.goums.ac.ir/article-1-1232-en.html
URL: http://mlj.goums.ac.ir/article-1-1232-en.html
1- Metabolic disorders research center, Golestan University of Medical Sciences, Gorgan, Iran
2- Department of hematology and blood banking Department of Hematology and Blood Banking, Tehran University of Medical Sciences, Tehran, Iran
3- Laboratory Sciences Research Center, Golestan University of Medical Sciences, Gorgan, Iran
4- Laboratory Sciences Research Center, Golestan University of Medical Sciences, Gorgan, Iran , joshaghani@goums.ac.ir
2- Department of hematology and blood banking Department of Hematology and Blood Banking, Tehran University of Medical Sciences, Tehran, Iran
3- Laboratory Sciences Research Center, Golestan University of Medical Sciences, Gorgan, Iran
4- Laboratory Sciences Research Center, Golestan University of Medical Sciences, Gorgan, Iran , joshaghani@goums.ac.ir
Abstract: (3671 Views)
ABSTRACT
Esophageal cancer (EC) is one of the most common types of cancer, especially in Asia. Esophageal squamous cell cancer (ESCC) is the most important histological subtype of EC, which accounts for 90% of all EC cases worldwide. ESCC is highly prevalent in Turkey, Iran, Kazakhstan and northern and central parts of China. Selenium is an essential micronutrient that is required for cellular functioning and synthesis of several selenoproteins. It also modulates the antioxidant defense system, cell cycle and apoptosis. This article reviews the most important molecular mechanisms of EC and investigates the association between selenium level and incidence of EC in high-risk areas.
Keywords: Esophageal cancer, selenium, selenoprotein.
Esophageal cancer (EC) is one of the most common types of cancer, especially in Asia. Esophageal squamous cell cancer (ESCC) is the most important histological subtype of EC, which accounts for 90% of all EC cases worldwide. ESCC is highly prevalent in Turkey, Iran, Kazakhstan and northern and central parts of China. Selenium is an essential micronutrient that is required for cellular functioning and synthesis of several selenoproteins. It also modulates the antioxidant defense system, cell cycle and apoptosis. This article reviews the most important molecular mechanisms of EC and investigates the association between selenium level and incidence of EC in high-risk areas.
Keywords: Esophageal cancer, selenium, selenoprotein.
Research Article: Review Article |
Subject:
Biochemistry
Received: 2019/07/18 | Accepted: 2019/08/19 | Published: 2019/10/30 | ePublished: 2019/10/30
Received: 2019/07/18 | Accepted: 2019/08/19 | Published: 2019/10/30 | ePublished: 2019/10/30
References
1. Bray F, Ferlay J, Soerjomataram I, Siegel RL, Torre LA, Jemal A. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2018; 68(6): 394-424. doi: 10.3322/caac.21492. [DOI:10.3322/caac.21492]
2. Torre LA, Bray F, Siegel RL, Ferlay J, Lortet-Tieulent J, Jemal A. Global cancer statistics, 2012. CA Cancer J Clin. 2015; 65(2): 87-108. doi: 10.3322/caac.21262. [DOI:10.3322/caac.21262]
3. Pennathur A, Gibson MK, Jobe BA, Luketich JD. Oesophageal carcinoma. Lancet. 2013; 381(9864): 400-12. [DOI:10.1016/S0140-6736(12)60643-6]
4. Sadjadi A, Nouraie M, Mohagheghi MA, Mousavi-Jarrahi A, Malekezadeh R, Parkin DM. Cancer occurrence in Iran in 2002, an international perspective. Asian Pac J Cancer Prev. 2005; 6(3): 359-63.
5. Yu Y, Taylor PR, Li J-Y, Dawsey SM, Wang G-Q, Guo W-D, et al. Retrospective cohort study of risk-factors for esophageal cancer in Linxian, People's Republic of China. Cancer Causes & Control. 1993;4(3):195-202.
6. Palladino-Davis A, Mendez B, Fisichella P, Davis C. Dietary habits and esophageal cancer. Dis Esophagus. 2015; 28(1): 59-67. doi: 10.1111/dote.12097. [DOI:10.1111/dote.12097]
7. Joshaghani H, Badiei F, Roshandel G, Sedaghat M, Tazik A, Kiaei M, et al. Vitamin D Deficiency in High and Low Risk Populations for Esophageal Cancer in Northern Iran. Basic Clin Cancer Res. 2018; 10(4): 26-31.
8. Keszei AP, Goldbohm RA, Schouten LJ, Jakszyn P, van den Brandt PA. Dietary N-nitroso compounds, endogenous nitrosation, and the risk of esophageal and gastric cancer subtypes in the Netherlands Cohort Study. Am J Clin Nutr. 2013; 97(1): 135-46. doi: 10.3945/ajcn.112.043885. [DOI:10.3945/ajcn.112.043885]
9. Joshaghani H, Amiriani T, Vaghari G, Besharat S, Molana A, Badeleh M, et al. Effects of omeprazole consumption on serum levels of trace elements. J Trace Elem Med Biol. 2012; 26(4): 234-7. doi: 10.1016/j.jtemb.2012.02.002. [DOI:10.1016/j.jtemb.2012.02.002]
10. Taherizadeh M, Khoshnia M, Shams S, Joshaghani H. Comparison of Plasma Taurine Levels between Patients with Esophageal Cancer and Healthy Controls. mljgoums. 2017; 11(2) :1-4. DOI: 10.18869/acadpub.mlj.11.2.1.
11. Ghasemi-Kebria F, Joshaghani H, Taheri NS, Semnani S, Aarabi M, Salamat F, et al. Aflatoxin contamination of wheat flour and the risk of esophageal cancer in a high risk area in Iran. Cancer Epidemiol. 2013; 37(3): 290-3. doi: 10.1016/j.canep.2013.01.010. [DOI:10.1016/j.canep.2013.01.010]
12. Namjoo M, Salamat F, Rajabli N, HAJIHOSEEINI R, Niknejad F, Kohsar F, et al. Quantitative determination of aflatoxin by high performance liquid chromatography in wheat silos in Golestan province, north of Iran. Iran J Public Health. 2016; 45(7): 905-10.
13. Joshaghani H, Mirkarimi H-s, Besharat S, Roshandel G, Sanaei O, Nejabat M. Comparison of the serum levels of trace elements in areas with high or low rate of esophageal cancer. Middle East J Dig Dis. 2017; 9(2): 81-85. doi: 10.15171/mejdd.2017.55. [DOI:10.15171/mejdd.2017.55]
14. Chung CS, Lee YC, Wu MS. Prevention strategies for esophageal cancer: Perspectives of the East vs. West. Best Pract Res Clin Gastroenterol. 2015; 29(6): 869-83. doi: 10.1016/j.bpg.2015.09.010. [DOI:10.1016/j.bpg.2015.09.010]
15. Domper Arnal MJ, Ferrandez Arenas A, Lanas Arbeloa A. Esophageal cancer: Risk factors, screening and endoscopic treatment in Western and Eastern countries. World J Gastroenterol. 2015; 21(26): 7933-43. doi: 10.3748/wjg.v21.i26.7933. [DOI:10.3748/wjg.v21.i26.7933]
16. Arnold M, Soerjomataram I, Ferlay J, Forman D. Global incidence of oesophageal cancer by histological subtype in 2012. Gut. 2015; 64(3): 381-7. doi: 10.1136/gutjnl-2014-308124. [DOI:10.1136/gutjnl-2014-308124]
17. Islami F, Kamangar F, Aghcheli K, Fahimi S, Semnani S, Taghavi N, et al. Epidemiologic features of upper gastrointestinal tract cancers in Northeastern Iran. Br J Cancer. 2004; 90(7): 1402-6. [DOI:10.1038/sj.bjc.6601737]
18. Mark SD, Qiao YL, Dawsey SM, Wu YP, Katki H, Gunter EW, et al. Prospective study of serum selenium levels and incident esophageal and gastric cancers. J Natl Cancer Inst. 2000; 92(21): 1753-63. [DOI:10.1093/jnci/92.21.1753]
19. Wei WQ, Abnet CC, Qiao YL, Dawsey SM, Dong ZW, Sun XD, et al. Prospective study of serum selenium concentrations and esophageal and gastric cardia cancer, heart disease, stroke, and total death. Am J Clin Nutr. 2004; 79(1): 80-5. [DOI:10.1093/ajcn/79.1.80]
20. Hashemian M, Poustchi H, Abnet CC, Boffetta P, Dawsey SM, Brennan PJ, et al. Dietary intake of minerals and risk of esophageal squamous cell carcinoma: results from the Golestan Cohort Study-3. Am J Clin Nutr. 2015; 102(1): 102-8. doi: 10.3945/ajcn.115.107847. [DOI:10.3945/ajcn.115.107847]
21. Montesano R, Holestein M, Hainaui P. Genetic alterations in esophageal cancer and their relevance to etiology and pathogenesis: a review. International journal of cancer. 1996; 69(3): 225-35.
https://doi.org/10.1002/(SICI)1097-0215(19960621)69:3<225::AID-IJC13>3.0.CO;2-6 [DOI:10.1002/(SICI)1097-0215(19960621)69:33.0.CO;2-6]
22. Ahmadian N, Pashaei-Asl R, Samadi N, Rahmati-Yamchi M, Rashidi M-R, Ahmadian M, et al. Hesa-a effects on cell cycle signaling in esophageal carcinoma cell line. Middle East J Dig Dis. 2016; 8(4): 297-302. [DOI:10.15171/mejdd.2016.39]
23. Yue Y, Song M, Qiao Y, Li P, Yuan Y, Lian J, et al. Gene function analysis and underlying mechanism of esophagus cancer based on microarray gene expression profiling. Oncotarget. 2017; 8(62): 105222-105237. doi: 10.18632/oncotarget.22160. [DOI:10.18632/oncotarget.22160]
24. Wang H, Zhang Y, Yun H, Chen S, Chen Y, Liu Z. ERK expression and its correlation with STAT1 in esophageal squamous cell carcinoma. Oncotarget. 2017; 8(28): 45249-45258. doi: 10.18632/oncotarget.16902. [DOI:10.18632/oncotarget.16902]
25. Cui X, Li S, Li T, Pang X, Zhang S, Jin J, et al. Significance of elevated ERK expression and its positive correlation with EGFR in Kazakh patients with esophageal squamous cell carcinoma. Int J Clin Exp Pathol. 2014; 7(5): 2382-2391.
26. Handlogten ME, Hong S-P, Zhang L, Vander AW, Steinbaum ML, Campbell-Thompson M, et al. Expression of the ammonia transporter proteins Rh B glycoprotein and Rh C glycoprotein in the intestinal tract. Am J Physiol Gastrointest Liver Physiol. 2005; 288(5): G1036-47. [DOI:10.1152/ajpgi.00418.2004]
27. Chen B-S, Xu Z-X, Xu X, Cai Y, Han Y-L, Wang J, et al. RhCG is downregulated in oesophageal squamous cell carcinomas, but expressed in multiple squamous epithelia. Eur J Cancer. 2002; 38(14): 1927-36. [DOI:10.1016/S0959-8049(02)00190-9]
28. Wang F, He W, Fanghui P, Wang L, Fan Q. NF‐κ BP 65 promotes invasion and metastasis of oesophageal squamous cell cancer by regulating matrix metalloproteinase‐9 and epithelial‐to‐mesenchymal transition. Cell biology international. 2013; 37(8): 780-8. [DOI:10.1002/cbin.10089]
29. Liu M, Hu Y, Zhang M-F, Luo K-J, Xie X-Y, Wen J, et al. MMP1 promotes tumor growth and metastasis in esophageal squamous cell carcinoma. Cancer letters. 2016; 377(1): 97-104. [DOI:10.1016/j.canlet.2016.04.034]
30. Ming X-Y, Zhang X, Cao T-T, Zhang L-Y, Qi J-L, Kam N-W, et al. RHCG Suppresses Tumorigenicity and Metastasis in Esophageal Squamous Cell Carcinoma via Inhibiting NF-κB Signaling and MMP1 Expression. Theranostics. 2018; 8(1): 185. [DOI:10.7150/thno.21383]
31. Bravi F, Edefonti V, Randi G, Garavello W, La Vecchia C, Ferraroni M, et al. Dietary patterns and the risk of esophageal cancer. Ann Oncol. 2012; 23(3): 765-70. doi: 10.1093/annonc/mdr295. [DOI:10.1093/annonc/mdr295]
32. Seitz HK, Stickel F. Molecular mechanisms of alcohol-mediated carcinogenesis. Nat Rev Cancer. 2007; 7(8): 599-612. [DOI:10.1038/nrc2191]
33. Hoshimoto S, Takeuchi H, Ono S, Sim MS, Huynh JL, Huang SK, et al. Genome-Wide Hypomethylation and Specific Tumor-Related Gene Hypermethylation are Associated with Esophageal Squamous Cell Carcinoma Outcome. J Thorac Oncol. 2015 Mar;10(3):509-17. doi: 10.1097/JTO.0000000000000441. [DOI:10.1097/JTO.0000000000000441]
34. Baba Y, Watanabe M, Murata A, Shigaki H, Miyake K, Ishimoto T, et al. LINE-1 hypomethylation, DNA copy number alterations, and CDK6 amplification in esophageal squamous cell carcinoma. Clin Cancer Res. 2014; 20(5): 1114-24. doi: 10.1158/1078-0432.CCR-13-1645. [DOI:10.1158/1078-0432.CCR-13-1645]
35. Iwagami S, Baba Y, Watanabe M, Shigaki H, Miyake K, Ishimoto T, et al. LINE-1 hypomethylation is associated with a poor prognosis among patients with curatively resected esophageal squamous cell carcinoma. Ann Surg. 2013; 257(3): 449-55. doi: 10.1097/SLA.0b013e31826d8602. [DOI:10.1097/SLA.0b013e31826d8602]
36. Gibb EA, Brown CJ, Lam WL. The functional role of long non-coding RNA in human carcinomas. Molecular cancer. 2011; 10(1): 38. doi: 10.1186/1476-4598-10-38. [DOI:10.1186/1476-4598-10-38]
37. Chen Z, Hu X, Wu Y, Cong L, He X, Lu J, et al. Long non-coding RNA XIST promotes the development of esophageal cancer by sponging miR-494 to regulate CDK6 expression. Biomed Pharmacother. 2019; 109: 2228-2236. doi: 10.1016/j.biopha.2018.11.049. [DOI:10.1016/j.biopha.2018.11.049]
38. Sclafani R, Holzen T. Cell cycle regulation of DNA replication. Annu Rev Genet. 2007; 41: 237-80. doi: 10.1146/annurev.genet.41.110306.130308. [DOI:10.1146/annurev.genet.41.110306.130308]
39. Labib K. How do Cdc7 and cyclin-dependent kinases trigger the initiation of chromosome replication in eukaryotic cells? Genes Dev. 2010; 24(12): 1208-19. doi: 10.1101/gad.1933010. [DOI:10.1101/gad.1933010]
40. Cao J-X, Lu Y. Targeting CDC7 improves sensitivity to chemotherapy of esophageal squamous cell carcinoma. Onco Targets Ther. 2019; 12: 63-74.doi: 10.2147/OTT.S183629. [DOI:10.2147/OTT.S183629]
41. Franke KW. A new toxicant occurring naturally in certain samples of plant foodstuffs. 1. Results obtained in preliminary feeding trials. Journal of Nutrition. 1934; 8(5): 597-608. [DOI:10.1093/jn/8.5.597]
42. Schwarz K, Foltz CM. Selenium as an integral part of factor 3 against dietary necrotic liver degeneration. Nutrition. 1999; 15(3): 255.
43. Harbison RD, Bourgeois MM, Johnson GT. Hamilton and Hardy's industrial toxicology: John Wiley & Sons; 2015. [DOI:10.1002/9781118834015]
44. Ohta Y, Suzuki KT. Methylation and demethylation of intermediates selenide and methylselenol in the metabolism of selenium. Toxicol Appl Pharmacol. 2008; 226(2): 169-77. [DOI:10.1016/j.taap.2007.09.011]
45. Gladyshev VN, Arner ES, Berry MJ, Brigelius-Flohe R, Bruford EA, Burk RF, et al. Selenoprotein Gene Nomenclature. J Biol Chem. 2016 Nov 11;291(46):24036-24040. [DOI:10.1074/jbc.M116.756155]
46. Roman M, Jitaru P, Barbante C. Selenium biochemistry and its role for human health. Metallomics. 2014; 6(1): 25-54. doi: 10.1039/c3mt00185g. [DOI:10.1039/C3MT00185G]
47. Hsueh YM, Su CT, Shiue HS, Chen WJ, Pu YS, Lin YC, et al. Levels of plasma selenium and urinary total arsenic interact to affect the risk for prostate cancer. Food Chem Toxicol. 2017; 107(Pt A): 167-175. doi: 10.1016/j.fct.2017.06.031. [DOI:10.1016/j.fct.2017.06.031]
48. Wu M, Kang MM, Schoene NW, Cheng W-H. Selenium compounds activate early barriers of tumorigenesis. J Biol Chem. 2010; 285(16): 12055-12062. doi: 10.1074/jbc.M109.088781. [DOI:10.1074/jbc.M109.088781]
49. Barrett CW, Short SP, Williams CS. Selenoproteins and oxidative stress-induced inflammatory tumorigenesis in the gut. Cell Mol Life Sci. 2017; 74(4): 607-616. doi: 10.1007/s00018-016-2339-2. [DOI:10.1007/s00018-016-2339-2]
50. Dreher D, Junod AF. Role of oxygen free radicals in cancer development. Eur J Cancer. 1996; 32(1): 30-8. [DOI:10.1016/0959-8049(95)00531-5]
51. Cooke MS, Evans MD, Dizdaroglu M, Lunec J. Oxidative DNA damage: mechanisms, mutation, and disease. FASEB J. 2003;17(10):1195-214. [DOI:10.1096/fj.02-0752rev]
52. Takebe G, Yarimizu J, Saito Y, Hayashi T, Nakamura H, Yodoi J, et al. A comparative study on the hydroperoxide and thiol specificity of the glutathione peroxidase family and selenoprotein P. J Biol Chem. 2002; 277(43): 41254-8. [DOI:10.1074/jbc.M202773200]
53. Huang Z, Rose AH, Hoffmann PR. The role of selenium in inflammation and immunity: from molecular mechanisms to therapeutic opportunities. Antioxid Redox Signal. 2012; 16(7): 705-43. doi: 10.1089/ars.2011.4145. [DOI:10.1089/ars.2011.4145]
54. Mattmiller S, Carlson BA, Sordillo L. Regulation of inflammation by selenium and selenoproteins: impact on eicosanoid biosynthesis. J Nutr Sci. 2013; 2: e28. doi: 10.1017/jns.2013.17. [DOI:10.1017/jns.2013.17]
55. Margis R, Dunand C, Teixeira FK, Margis‐Pinheiro M. Glutathione peroxidase family-an evolutionary overview. FEBS J. 2008; 275(15): 3959-70. doi: 10.1111/j.1742-4658.2008.06542.x. [DOI:10.1111/j.1742-4658.2008.06542.x]
56. Maiorino FM, Brigelius-Flohé R, Aumann K, Roveri A, Schomburg D, Flohé L. Diversity of glutathione peroxidases. Methods Enzymol. 1995; 252: 38-53. [DOI:10.1016/0076-6879(95)52007-4]
57. Lubos E, Loscalzo J, Handy DE. Glutathione peroxidase-1 in health and disease: from molecular mechanisms to therapeutic opportunities. Antioxid Redox Signal. 2011; 15(7): 1957-97. doi: 10.1089/ars.2010.3586. [DOI:10.1089/ars.2010.3586]
58. Barnes KM, Evenson JK, Raines AM, Sunde RA. Transcript analysis of the selenoproteome indicates that dietary selenium requirements of rats based on selenium-regulated selenoprotein mRNA levels are uniformly less than those based on glutathione peroxidase activity. J Nutr. 2008; 139(2): 199-206. [DOI:10.3945/jn.108.098624]
59. Baliga MS, Wang H, Zhuo P, Schwartz JL, Diamond AM. Selenium and GPx-1 overexpression protect mammalian cells against UV-induced DNA damage. Biol Trace Elem Res. 2007; 115(3): 227-41. [DOI:10.1007/BF02685998]
60. Chu F-F, Doroshow J, and, Esworthy R. Expression, characterization, and tissue distribution of a new cellular selenium-dependent glutathione peroxidase, GSHPx-GI. J Biol Chem. 1993; 268(4): 2571-6.
61. Brigelius-Flohé R. Tissue-specific functions of individual glutathione peroxidases. Free Radic Biol Med. 1999; 27(9-10): 951-65. [DOI:10.1016/S0891-5849(99)00173-2]
62. Serewko MM, Popa C, Dahler AL, Smith L, Strutton GM, Coman W, et al. Alterations in gene expression and activity during squamous cell carcinoma development. Cancer res. 2002; 62(13): 3759-65.
63. Mörk H, Scheurlen M, Al‐Taie O, Zierer A, Kraus M, Schöttker K, et al. Glutathione peroxidase isoforms as part of the local antioxidative defense system in normal and Barrett's esophagus. Int J Cancer. 2003; 105(3): 300-4. [DOI:10.1002/ijc.11087]
64. Lei Z, Tian D, Zhang C, Zhao S, Su M. Clinicopathological and prognostic significance of GPX2 protein expression in esophageal squamous cell carcinoma. BMC cancer. 2016; 16(1): 410. [DOI:10.1186/s12885-016-2462-3]
65. Zhu X, Wang J, Li L, Deng L, Wang J, Liu L, et al. GPX3 suppresses tumor migration and invasion via the FAK/AKT pathway in esophageal squamous cell carcinoma. Am J Transl Res. 2018; 10(6): 1908.
66. Wingler K, Böcher M, Flohé L, Kollmus H, Brigelius‐Flohé R. mRNA stability and selenocysteine insertion sequence efficiency rank gastrointestinal glutathione peroxidase high in the hierarchy of selenoproteins. Euro J Biochem. 1999; 259(1‐2): 149-57. [DOI:10.1046/j.1432-1327.1999.00012.x]
67. Björnstedt M, Kumar S, Holmgren A. Selenodiglutathione is a highly efficient oxidant of reduced thioredoxin and a substrate for mammalian thioredoxin reductase. J Biol Chem. 1992; 267(12): 8030-4.
68. Gromer S, Gross JH. Methylseleninate is a substrate rather than an inhibitor of mammalian thioredoxin reductase Implications for the antitumor effects of selenium. Journal of Biological Chemistry. 2002; 277(12): 9701-6. [DOI:10.1074/jbc.M109234200]
69. Kumar S, Björnstedt M, Holmgren A. Selenite is a substrate for calf thymus thioredoxin reductase and thioredoxin and elicits a large non‐stoichiometric oxidation of NADPH in the presence of oxygen. European journal of biochemistry. 1992; 207(2): 435-9. [DOI:10.1111/j.1432-1033.1992.tb17068.x]
70. Kahlos K, Zhang J, Block ER, Patel JM. Thioredoxin restores nitric oxide-induced inhibition of protein kinase C activity in lung endothelial cells. Molecular and cellular biochemistry. 2003; 254(1-2): 47-54. [DOI:10.1023/A:1027380828645]
71. Lee S-R, Yang K-S, Kwon J, Lee C, Jeong W, Rhee SG. Reversible inactivation of the tumor suppressor PTEN by H2O2. J Biol Chem. 2002; 277(23): 20336-42. [DOI:10.1074/jbc.M111899200]
72. Moos PJ, Edes K, Cassidy P, Massuda E, Fitzpatrick FA. Electrophilic prostaglandins and lipid aldehydes repress redox-sensitive transcription factors p53 and hypoxia-inducible factor by impairing the selenoprotein thioredoxin reductase. Journal of Biological Chemistry. 2003; 278(2): 745-50. [DOI:10.1074/jbc.M211134200]
73. Jeong D-w, Kim TS, Chung YW, Lee BJ, Kim IY. Selenoprotein W is a glutathione‐dependent antioxidant in vivo. FEBS Lett. 2002; 517(1-3): 225-8. [DOI:10.1016/S0014-5793(02)02628-5]
74. Tula-Sanchez AA, Havas AP, Alonge PJ, Klein ME, Doctor SR, Pinkston W, et al. A model of sensitivity and resistance to histone deacetylase inhibitors in diffuse large B cell lymphoma: Role of cyclin-dependent kinase inhibitors. Cancer biology & therapy. 2013; 14(10): 949-61. [DOI:10.4161/cbt.25941]
75. Wang K, Fu X-t, Li Y, Hou Y-j, Yang M-f, Sun J-y, et al. Induction of s-phase arrest in human glioma cells by selenocysteine, a natural selenium-containing agent via triggering reactive oxygen species-mediated DNA damage and modulating MAPKs and AKT pathways. Neurochem Res. 2016; 41(6): 1439-47. doi: 10.1007/s11064-016-1854-8. [DOI:10.1007/s11064-016-1854-8]
76. Hawkes WC, Wang TT, Alkan Z, Richter BD, Dawson K. Selenoprotein W modulates control of cell cycle entry. Biol Trace Elem Res. 2009; 131(3): 229-44. doi: 10.1007/s12011-009-8367-0. [DOI:10.1007/s12011-009-8367-0]
77. Park YH, Jeon YH, Kim IY. Selenoprotein W promotes cell cycle recovery from G2 arrest through the activation of CDC25B. Biochimica et Biophysica Acta (BBA)-Molecular Cell Research. 2012; 1823(12): 2217-26. [DOI:10.1016/j.bbamcr.2012.09.001]
78. Hawkes WC, Printsev I, Alkan Z. Selenoprotein W depletion induces a p53‐and p21‐dependent delay in cell cycle progression in RWPE‐1 prostate epithelial cells. J Cell Biochem. 2012; 113(1): 61-9. doi: 10.1002/jcb.23328. [DOI:10.1002/jcb.23328]
79. Banning A, Kipp A, Schmitmeier S, Löwinger M, Florian S, Krehl S, et al. Glutathione peroxidase 2 inhibits cyclooxygenase-2-mediated migration and invasion of HT-29 adenocarcinoma cells but supports their growth as tumors in nude mice. Cancer Res. 2008; 68(23): 9746-53. doi: 10.1158/0008-5472.CAN-08-1321. [DOI:10.1158/0008-5472.CAN-08-1321]
80. Yoo M-H, Xu X-M, Carlson BA, Gladyshev VN, Hatfield DL. Thioredoxin reductase 1 deficiency reverses tumor phenotype and tumorigenicity of lung carcinoma cells. J Biol Chem. 2006; 281(19): 13005-8. [DOI:10.1074/jbc.C600012200]
81. Irons R, Tsuji PA, Carlson BA, Ouyang P, Yoo M-H, Xu X-M, et al. Deficiency in the 15-kDa selenoprotein inhibits tumorigenicity and metastasis of colon cancer cells. Cancer Prev Res (Phila). 2010; 3(5): 630-9. doi: 10.1158/1940-6207.CAPR-10-0003. [DOI:10.1158/1940-6207.CAPR-10-0003]
82. Bang J, Huh JH, Na J-W, Lu Q, Carlson BA, Tobe R, et al. Cell proliferation and motility are inhibited by G1 phase arrest in 15-kDa selenoprotein-deficient Chang liver cells. Mol Cells. 2015; 38(5): 457-65. doi: 10.14348/molcells.2015.0007. [DOI:10.14348/molcells.2015.0007]
83. Bertz M, Kühn K, Koeberle SC, Müller MF, Hoelzer D, Thies K, et al. Selenoprotein H controls cell cycle progression and proliferation of human colorectal cancer cells. Free Radic Biol Med. 2018; 127: 98-107. doi: 10.1016/j.freeradbiomed.2018.01.010. [DOI:10.1016/j.freeradbiomed.2018.01.010]
84. Nakanishi M, Adami GR, Robetorye RS, Noda A, Venable SF, Dimitrov D, et al. Exit from G0 and entry into the cell cycle of cells expressing p21Sdi1 antisense RNA. PNAS. 1995; 92(10): 4352-6. [DOI:10.1073/pnas.92.10.4352]
85. Gladyshev VN, Jeang K-T, Wootton JC, Hatfield DL. A new human selenium-containing protein purification, characterization, and cDNA sequence. J Biol Chem. 1998; 273(15): 8910-5. [DOI:10.1074/jbc.273.15.8910]
86. Nasr M, Hu Y, Diamond A. Allelic loss at the Sep15 locus in breast cancer. Cancer Ther. 2004; 1: 293-8.
87. Kumaraswamy E, Malykh A, Korotkov KV, Kozyavkin S, Hu Y, Kwon SY, et al. Structure-expression relationships of the 15-kDa selenoprotein gene possible role of the protein in cancer etiology. J Biol Chem. 2000; 275(45): 35540-7. [DOI:10.1074/jbc.M004014200]
88. Tsuji PA, Carlson BA, Naranjo-Suarez S, Yoo M-H, Xu X-M, Fomenko DE, et al. Knockout of the 15 kDa selenoprotein protects against chemically-induced aberrant crypt formation in mice. PLoS One. 2012; 7(12): e50574. [DOI:10.1371/journal.pone.0050574]
89. Tsuji PA, Naranjo-Suarez S, Carlson BA, Tobe R, Yoo M-H, Davis CD. Deficiency in the 15 kDa selenoprotein inhibits human colon cancer cell growth. Nutrients. 2011; 3(9): 805-17. doi: 10.3390/nu3090805. [DOI:10.3390/nu3090805]
90. Sherr CJ, Roberts JM. CDK inhibitors: positive and negative regulators of G1-phase progression. Genes dev. 1999; 13(12): 1501-12. [DOI:10.1101/gad.13.12.1501]
91. Fan C, Jiang J, Yin X, Wong K-H, Zheng W, Chen T. Purification of selenium-containing allophycocyanin from selenium-enriched Spirulina platensis and its hepatoprotective effect against t-BOOH-induced apoptosis. Food chemistry. 2012; 134(1): 253-61. [DOI:10.1016/j.foodchem.2012.02.130]
92. Fan C, Chen J, Wang Y, Wong Y-S, Zhang Y, Zheng W, et al. Selenocystine potentiates cancer cell apoptosis induced by 5-fluorouracil by triggering reactive oxygen species-mediated DNA damage and inactivation of the ERK pathway. Free Radic Biol Med. 2013; 65: 305-316. doi: 10.1016/j.freeradbiomed.2013.07.002. [DOI:10.1016/j.freeradbiomed.2013.07.002]
93. Fan C, Zheng W, Fu X, Li X, Wong Y, Chen T. Enhancement of auranofin-induced lung cancer cell apoptosis by selenocystine, a natural inhibitor of TrxR1 in vitro and in vivo. Cell Death Dis. 2014; 5: e1191. doi: 10.1038/cddis.2014.132. [DOI:10.1038/cddis.2014.132]
94. Chen T, Wong Y-S. Selenocystine induces reactive oxygen species-mediated apoptosis in human cancer cells. Int J Biochem Cell Biol. 2009; 41(3): 666-76. doi: 10.1016/j.biocel.2008.07.014. [DOI:10.1016/j.biocel.2008.07.014]
95. Chen T, Wong Y-S. Selenocystine induces caspase-independent apoptosis in MCF-7 human breast carcinoma cells with involvement of p53 phosphorylation and reactive oxygen species generation. Int J Biochem Cell Biol. 2009; 41(3): 666-76. doi: 10.1016/j.biocel.2008.07.014. [DOI:10.1016/j.biocel.2008.07.014]
96. Chen T, Wong Y. Selenocystine induces apoptosis of A375 human melanoma cells by activating ROS-mediated mitochondrial pathway and p53 phosphorylation. Cell Mol Life Sci. 2008; 65(17): 2763-75. doi: 10.1007/s00018-008-8329-2. [DOI:10.1007/s00018-008-8329-2]
97. Lanfear J, Fleming J, Wu L, Webster G, Harrison PR. The selenium metabolite selenodiglutathione induces p53 and apoptosis: relevance to the chemopreventive effects of selenium? Carcinogenesis. 1994; 15(7): 1387-92. [DOI:10.1093/carcin/15.7.1387]
98. Jiang C, Hu H, Malewicz B, Wang Z, Lü J. Selenite-induced p53 Ser-15 phosphorylation and caspase-mediated apoptosis in LNCaP human prostate cancer cells. Molecular cancer therapeutics. 2004; 3(7): 877-84.
99. Goel A, Fuerst F, Hotchkiss E, Boland CR. Selenomethionine induces p53 mediated cell cycle arrest and apoptosis in human colon cancer cells. Cancer biology & therapy. 2006; 5(5): 529-35. [DOI:10.4161/cbt.5.5.2654]
100. Guan L, Huang F, Li Z, Han B, Jiang Q, Ren Y, et al. P53 transcription-independent activity mediates selenite-induced acute promyelocytic leukemia NB4 cell apoptosis. BMB Rep. 2008; 41(10): 745-50. [DOI:10.5483/BMBRep.2008.41.10.745]
101. Zhang T, Zhao G, Zhu X, Jiang K, Wu H, Deng G, et al. Sodium selenite induces apoptosis via ROS-mediated NF-kappaB signaling and activation of the Bax-caspase-9-caspase-3 axis in 4T1 cells. J Cell Physiol. 2019; 234(3): 2511-2522. doi: 10.1002/jcp.26783. [DOI:10.1002/jcp.26783]
102. Korbut E, Ptak-Belowska A, Brzozowski T. Inhibitory effect of selenomethionine on carcinogenesis in the model of human colorectal cancer in vitro and its link to the Wnt/beta-catenin pathway. Acta Biochim Pol. 2018; 65(3): 359-366. doi: 10.18388/abp.2018_2628. [DOI:10.18388/abp.2018_2628]
103. Zhang W, Yan S, Liu M, Zhang G, Yang S, He S, et al. β-catenin/TCF pathway plays a vital role in selenium induced-growth inhibition and apoptosis in esophageal squamous cell carcinoma (ESCC) cells. Cancer letters. 2010; 296(1): 113-22. [DOI:10.1016/j.canlet.2010.04.001]
104. Semnani S, Roshandel G, Zendehbad A, Keshtkar A, Rahimzadeh H, Abdolahi N, et al. Soils selenium level and esophageal cancer: An ecological study in a high risk area for esophageal cancer. J Trace Elem Med Biol. 2010; 24(3): 174-7. doi: 10.1016/j.jtemb.2010.03.002. [DOI:10.1016/j.jtemb.2010.03.002]
105. Keshavarzi B, Moore F, Najmeddin A, Rahmani F. The role of selenium and selected trace elements in the etiology of esophageal cancer in high risk Golestan province of Iran. Sci Total Environ. 2012; 433: 89-97. doi: 10.1016/j.scitotenv.2012.04.033. [DOI:10.1016/j.scitotenv.2012.04.033]
106. Rahimzadeh-Barzoki H, Joshaghani H, Beirami S, Mansurian M, Semnani S, Roshandel G. Selenium levels in rice samples from high and low risk areas for esophageal cancer. Saudi Medical Journal. 2014; 35(6): 617-20.
107. Steevens J, van den Brandt PA, Goldbohm RA, Schouten LJ. Selenium status and the risk of esophageal and gastric cancer subtypes: the Netherlands cohort study. Gastroenterology. 2010;138(5):1704-13. [DOI:10.1053/j.gastro.2009.12.004]
108. Hashemian M, Murphy G, Etemadi A, Poustchi H, Brockman JD, Kamangar F, et al. Toenail mineral concentration and risk of esophageal squamous cell carcinoma, results from the Golestan Cohort Study. Cancer medicine. 2017;6(12):3052-9. [DOI:10.1002/cam4.1247]
109. Lin T, Liu T, Lin Y, Zhang C, Yan L, Chen Z, et al. Serum levels of chemical elements in esophageal squamous cell carcinoma in Anyang, China: a case-control study based on machine learning methods. BMJ open. 2017; 7(9): e015443. [DOI:10.1136/bmjopen-2016-015443]
110. Cai L, Mu L-N, Lu H, Lu Q-Y, You N-CY, Yu S-Z, et al. Dietary selenium intake and genetic polymorphisms of the GSTP1 and p53 genes on the risk of esophageal squamous cell carcinoma. Cancer Epidemiol Biomarkers Prev. 2006; 15(2): 294-300. [DOI:10.1158/1055-9965.EPI-05-0680]
111. Hashemi SM, Mashhadi M, Moghaddam AA, Yousefi J, Mofrad AD, Sadeghi M, et al. The relationship between serum selenium and zinc with gastroesophageal cancers in the southeast of Iran. Indian J Med Paediatr Oncol. 2017; 38(2): 169-172. doi: 10.4103/ijmpo.ijmpo_83_16..
112. Pritchett NR, Burgert SL, Murphy GA, Brockman JD, White RE, Lando J, et al. Cross sectional study of serum selenium concentration and esophageal squamous dysplasia in western Kenya. BMC cancer. 2017; 17(1): 835. doi: 10.1186/s12885-017-3837-9. [DOI:10.1186/s12885-017-3837-9]
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
Enamad
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.