Желчные кислоты – фактор риска развития колоректального рака
Желчные кислоты – фактор риска развития колоректального рака
Крумс Л.М., Гудкова Р.Б., Индейкина Л.Х. и др. Желчные кислоты – фактор риска развития колоректального рака. Терапевтический архив. 2020; 92 (2): 93–96. DOI: 10.26442/00403660.2020.02.000457
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Krumz L.M., Gudkova R.B., Indejkina L.Kh., et al. Bile acids are a risk factor for colorectal cancer. Therapeutic Archive. 2020; 92 (2): 93–96. DOI:10.26442/00403660.2020.02.000457
Желчные кислоты – фактор риска развития колоректального рака
Крумс Л.М., Гудкова Р.Б., Индейкина Л.Х. и др. Желчные кислоты – фактор риска развития колоректального рака. Терапевтический архив. 2020; 92 (2): 93–96. DOI: 10.26442/00403660.2020.02.000457
________________________________________________
Krumz L.M., Gudkova R.B., Indejkina L.Kh., et al. Bile acids are a risk factor for colorectal cancer. Therapeutic Archive. 2020; 92 (2): 93–96. DOI:10.26442/00403660.2020.02.000457
Желчные кислоты (ЖК) впервые рассмотрены в качестве канцерогенов в 1939 г. С тех пор накопленные данные подтверждают, что высокие уровни ЖК в толстой кишке являются важным фактором риска развития колоректального рака (КРР) у людей, регулярно употребляющих жирную пищу. Вторичные ЖК, образующиеся в кишечнике под влиянием кишечной микрофлоры, вызывают образование реактивных форм кислорода и азота, повреждают клеточные мембраны, митохондрии и ДНК, нарушают апоптоз, вызывают мутации клеток и их озлокачествление. Таким образом, ЖК, диета с высоким содержанием жира и кишечная микрофлора относятся к факторам риска развития КРР.
Bile acids were first considered carcinogenic in 1939. Since then, accumulated data have associated colon cell changes with high levels of bile acids as an important risk factor for developing colorectal cancer, which is more common among people who consume large amounts of dietary fat. Secondary bile acids formed under the influence of the intestinal microbiota can cause the formation of reactive forms of oxygen and nitrogen, disruption of the cell membrane, mitochondria, DNA damage, reduction of apoptosis, increased cell mutation, turning them into cancer cells. High-fat diet, intestinal microflora, bile acids are a risk factors for colorectal cancer.
Keywords: colorectal cancer, bile acids, intestinal microflora, high fat diet, apoptosis.
Список литературы
1. Пасевич Д.М., Сушков С.А., Семенов В.М. Молекулярно-генетические аспекты злокачественных новообразований толстой кишки. Новости хирургии. 2016;24(2):184-92 [Pasevich DM, Sushkov SA, Semenov VM. Molecular Genetic Aspects of Malignant Colon Tumors. Novosti Khirurgii. 2016;24(2):184-92 (In Russ.)]. doi: 10.18484/2305-0647
2. Fearon ER. Molecular genetics of colorectal cancer. Ann Rev Patol. 2011;6:479-507. doi: 10.1146/annurev-patol-011110-130235
3. Thi Nguyen, Hong-Quan Duong. The molecular characteristics of colorectal cancer: implications for diagnosis and therahy. Oncol Lett. 2018;16(1):9-18. doi: 10.3892/ol.2018.8679
4. Berg A. Nutrition, development, and population growth. Popul Bull. 1973;29:36-7.
5. Kirkegaard H, Johnsen NF, Christensen J. Association of adherence to lifestyle recommendations and risk of colorectal cancer: a prospective Danish cohort study. BMJ. 2010;341:c5504. doi: 10.1136/bmj.c5504
6. Bayerdörffer E, Mannes GA, Richter WO, Ochsenkühn T, Wiebecke B, Köpcke W, Paumgartner G. Increased serum deoxycholic acid levels in men with colorectal adenomas. Gastroenterology. 1993;104:145-51.
7. Bayerdörffer E, Mannes GA, Ochsenkühn T, Dirschedl P, Wiebecke B, Paumgartner G. Unconjugated secondary bile acids in the serum of patients with colorectal adenomas. Gut. 1995;36:268-73. doi: 10.1136/gut.36.2.268
8. Nagengast FM, Grubben MJ, van Munster IP. Role of bile acids in colorеctal cancerogenesis. Eur J Cancer. 1995;31A(7-8):1067-70.
9. Tong JL, Ran ZH, Shen J, Fan GQ, Xiao SD. Association between fecal bile acids and colorectal cancer: a meta-analysis of observational studies. Yonset Med J. 2008;49:792-803. doi: 10.3349/ymj 2008 49.792
10. Imary CH, Radley S, Davis A, Barker G, Hendrickse CW, Donovan IA, et al. Faecal unconjugated bile acids in patients with colorectal cancer or polypos. Gut. 1992;33:1239-45.
11. Ou J, Delani JP, Zhang M, Sharma SO. Association between low colonic short-chain fattyn acids and high bile acids colon cancer risk populations. Nutr Cancer. 2012;64:34-40. doi: 10.1080/01635581
12. Ajouz H, Mukherji D, Shamseddine A. Secondary bile acids: underrecognized cause of colon cancer. World J Surg Onco. 2014;12:164. doi: 10.1186/1477-7819-12-164
13. Ou J, Carbonero F, Zoetendal E, De Lany P, et al. Diet, microbiota and microbial metabolites in colon cancer risk in rural Africans and African Americans. Am J Clin Nutr. 2013;98:111-20. doi: 10.3945/ajcn.112.056689
14. Farhana L, Nangia-Makker P, Arbit E, Shango K, Sarkar S, Mahmud H, et al. Bile acid: a potential inducer of colon cancer stem cells. Stem Cell Res Ther. 2016;7:181. doi: 10 1186/s13287-016-0439-4
15. Hofmann AF, Cravetto C, Molino G, Belforte G, Bona B. Simulation of the metabolism and enterohepatic circulation of endogenous deoxycholic acid in humans using a physiologic pharmacokinetic model for bile acid metabolism. Gastroenterology. 1987;93:693-709.
16. Li T, Cyiang JY. Bile acid signaling in metabolic disease and drag therapy. Pharmacol Rev. 2014;66:948-83. doi: 10.1124/pr113008201
17. Song KH, Li T, Owsley E, Strom S, Chiang JY. Bile acids activate fibroblast growth factor 19 signaling in human hepatocytes to inhibit cholesterol 7alpha-hydroxylase gene expression. Hepatology. 2009;49:297-305. doi: 10.1002/hep.22627
18. Lundasen T, Gälman C, Angelin B, Rudling M. Circulating intestinal fibroblast growth factor 19 has a pronounced diurnal variation and modulates hepatic bileacid synthesis in man. J Intern Med. 2006;260:530-6. doi: 10.1111/j.1365-2796.2006.017
19. Monte MJ, Marin JJ, Antelo A, Vazquez T, et al. Bile acids: chemistry, physiology, and patophisiology. World Gastroenterol. 2009;15:804-16. doi: 10.3748wjg 15804
20. Reddy BS. Role of bile metabolites in colon cancerogenesis. Animal models. Cancer. 1975;36:2401-6.
21. Ocvirk SL, O'Keefe SJ. Influence of Bile Acids on Colorectal Cancer Risk: Potential Mechanisms Mediated by Diet – Gut Microbiota Interactions. Curr Nutr Rep. 2017;6(4):315-22. doi: 10.1007/s13668-017-0219-5
22. Alexander J, Scott AJ, Pouncey A, et al. Colorecnal carcinogenesis; an archetype of gut microbiota-host interacnion. E-Cancer Med Sci. 2018;12:865. doi: 10.3332/ecancer.2018.865
23. O’Keefe SJD. Diet, microorganisms and their metabolites, and colon cancer. Nat Rev Gastrotnterol Hepatol. 2016;13:691-706. doi: 10.1038/nrgastro2016.165
24. Schulz MD, Atay C, Heringer J. High-fat-diet-mediated disbiosis promotes intestinal carcinogenesis independently of obesity. Nature. 2014;514:508-12. doi: 10.1038/nature13398
25. Degirolamo C, Modica S, Palasciano G, Moschetta A. Bile acids and colon cancer: Solving the puzzle with nuclear receptors. Trends Mol Med. 2011;17:564-72. doi: 10.1016/jmolmed.2011.05.10
26. Craciun S, Balskus EP. Microbial conversion of choline to trimethylamine requires a glicyl radical enzyme. Proc Natl Acad Sci USA. 2012;109(52):815-22. doi: 10.1073/pnas. 1215689109.24
27. Qiao D, Gaitonde SV, Qi W, Martinez JD. Deoxycholic acid suppresses p53 by stimulating proteasome-mediated p53 protein degradation. Carcinogenesis. 2001;22:957-64. doi: 10.1093/carcin/22.6.956
28. Shant J, Cheng K, Marasa BS, Wang JY, Raufman JP. Akt-dependent NF-kappaB activation is required for bile acids to rescue colon cancer cells from stress-induced apoptosis. Exp Cell Res. 2009;315:432-50. doi: 10.1016/jyekcr2008.11.003
29. Raufman JP, Shant J, Guo CY, Roy S, Cheng K. Deoxycholyltaurine rescues human colon cancer cells from apoptosis by activating EGFR-dependent PI3K/Akt signaling. J Cell Physiol. 2008;215:538-49. doi: 10.1002/jcp.21332
30. Turner DJ, Alaish SM, Zou T, Rao JN, Wang JY, Strauch ED. Bile salts induce resistance to apoptosis through NF-kappaB-mediated XIAP expression. Ann Surg. 2007;245:415-25. doi: 10.1097/01sia0000236631/72698/99
31. Arvind P, Papavassiliou ED, Tsioulias GJ, Duceman BW, Lovelace CI, Geng W, et al. Lithocholic acid inhibits the expression of HLA class I genes in colon adenocarcinoma cells. Differential effect on HLA-A, -B and -C loci. Mol Immunol. 1994;31:607-14.
32. Pai R, Tarnawski AS, Tran T. Deoxycholic acid activates beta-catenin signaling pathway and increases colon cell cancer growth and invasiveness. Mol Biol Cell. 2004;15:2156-63. doi: 10.1091/mbc.E03-12-0894
33. Oshio H, Abe T, Onogawa T, Ohtsuka H, Sato T, Ii T, et al. Peroxisome proliferator-activated receptor alpha activates cyclooxygenase-2 gene transcription through bile acid transport in human colorectal cancer cell lines. J Gastroenterol. 2008;43:538-49. doi: 10/1007/s00535-008-2188-3
34. Thi Thinh Nguyen, Trong Thuan Ung, Nam Ho Kim, Young Do Jung. Role of bile acids in colon carcinogenesis. World J Clin Cases. 2018 Nov 6;6(13):577-88. doi: 10.12998/wjcc.v6.i13.577
35. Nguyen TT, Lian S, Ung TT, Xia Y, Han JY, Jung YD. Lithocholic Acid Stimulates IL-8 Expression in Human Colorectal Cancer Cells Via Activation of Erk1/2 MAPK and Suppression of STAT3 Activity. J Cell Biochem. 2017;118:2958-67. doi: 10.1002/jcb2595
36. Tucker ON, Dannenberg AJ, Yang EK, Fahey TJ 3rd. Bile acids induce cyclooxygenase-2 expression in human pancreatic cancer cell lines. Carcinogenesis. 2004;25:419-23. doi: 10.1093/carcin/bgh 010
37. Mühlbauer M, Allard B, Bosserhoff AK, Kiessling S, Herfarth H, Rogler G, et al. Differential effects of deoxycholic acid and taurodeoxycholic acid on NF-kappa B signal transduction and IL-8 gene expression in colonic epithelial cells. Am J Physiol Gastrointest Liver Physiol. 2004;286:G1000-G1008. doi: 10.1152/ojpgi00338.2003
38. Hess LM, Krutzsch MF, Guillen J, Chow HH, et al. Result of a phase 1 multihple-dose clinical study of ursodeoxycholic. Acid Cancer Epidemiol Biomarkers Prev. 2004;13:861-7.
39. Kim EK, Cho JH, Kim E, Kim YJ. Ursodeoxicholic acid inhibits the proliferation of colon cancer cells by regulating oxidative stress and cancer stem-like cell growth. PLoS One. 2017;12:181-3. doi: 10.1371/journal.pone.0181183
40. Logan RE, Grainge MJ, Sheperd VC, et al. Aspirin and folic acid for prevention of recurrent colorectal adenomas. Gastroenterology. 2008;1:29-38.
41. Wu K, Peatz EA, Willett WC, et al. A randomized trial on folic acid of risk recurrent colorectal adenoma. Am J Clin Nutr. 2009;6:1623-31. doi: 10.3945/ajcn2009.283
________________________________________________
1. Pasevich DM, Sushkov SA, Semenov VM. Molecular Genetic Aspects of Malignant Colon Tumors. Novosti Khirurgii. 2016;24(2):184-92 (In Russ.) doi: 10.18484/2305-0647
2. Fearon ER. Molecular genetics of colorectal cancer. Ann Rev Patol. 2011;6:479-507. doi: 10.1146/annurev-patol-011110-130235
3. Thi Nguyen, Hong-Quan Duong. The molecular characteristics of colorectal cancer: implications for diagnosis and therahy. Oncol Lett. 2018;16(1):9-18. doi: 10.3892/ol.2018.8679
4. Berg A. Nutrition, development, and population growth. Popul Bull. 1973;29:36-7.
5. Kirkegaard H, Johnsen NF, Christensen J. Association of adherence to lifestyle recommendations and risk of colorectal cancer: a prospective Danish cohort study. BMJ. 2010;341:c5504. doi: 10.1136/bmj.c5504
6. Bayerdörffer E, Mannes GA, Richter WO, Ochsenkühn T, Wiebecke B, Köpcke W, Paumgartner G. Increased serum deoxycholic acid levels in men with colorectal adenomas. Gastroenterology. 1993;104:145-51.
7. Bayerdörffer E, Mannes GA, Ochsenkühn T, Dirschedl P, Wiebecke B, Paumgartner G. Unconjugated secondary bile acids in the serum of patients with colorectal adenomas. Gut. 1995;36:268-73. doi: 10.1136/gut.36.2.268
8. Nagengast FM, Grubben MJ, van Munster IP. Role of bile acids in colorеctal cancerogenesis. Eur J Cancer. 1995;31A(7-8):1067-70.
9. Tong JL, Ran ZH, Shen J, Fan GQ, Xiao SD. Association between fecal bile acids and colorectal cancer: a meta-analysis of observational studies. Yonset Med J. 2008;49:792-803. doi: 10.3349/ymj 2008 49.792
10. Imary CH, Radley S, Davis A, Barker G, Hendrickse CW, Donovan IA, et al. Faecal unconjugated bile acids in patients with colorectal cancer or polypos. Gut. 1992;33:1239-45.
11. Ou J, Delani JP, Zhang M, Sharma SO. Association between low colonic short-chain fattyn acids and high bile acids colon cancer risk populations. Nutr Cancer. 2012;64:34-40. doi: 10.1080/01635581
12. Ajouz H, Mukherji D, Shamseddine A. Secondary bile acids: underrecognized cause of colon cancer. World J Surg Onco. 2014;12:164. doi: 10.1186/1477-7819-12-164
13. Ou J, Carbonero F, Zoetendal E, De Lany P, et al. Diet, microbiota and microbial metabolites in colon cancer risk in rural Africans and African Americans. Am J Clin Nutr. 2013;98:111-20. doi: 10.3945/ajcn.112.056689
14. Farhana L, Nangia-Makker P, Arbit E, Shango K, Sarkar S, Mahmud H, et al. Bile acid: a potential inducer of colon cancer stem cells. Stem Cell Res Ther. 2016;7:181. doi: 10 1186/s13287-016-0439-4
15. Hofmann AF, Cravetto C, Molino G, Belforte G, Bona B. Simulation of the metabolism and enterohepatic circulation of endogenous deoxycholic acid in humans using a physiologic pharmacokinetic model for bile acid metabolism. Gastroenterology. 1987;93:693-709.
16. Li T, Cyiang JY. Bile acid signaling in metabolic disease and drag therapy. Pharmacol Rev. 2014;66:948-83. doi: 10.1124/pr113008201
17. Song KH, Li T, Owsley E, Strom S, Chiang JY. Bile acids activate fibroblast growth factor 19 signaling in human hepatocytes to inhibit cholesterol 7alpha-hydroxylase gene expression. Hepatology. 2009;49:297-305. doi: 10.1002/hep.22627
18. Lundasen T, Gälman C, Angelin B, Rudling M. Circulating intestinal fibroblast growth factor 19 has a pronounced diurnal variation and modulates hepatic bileacid synthesis in man. J Intern Med. 2006;260:530-6. doi: 10.1111/j.1365-2796.2006.017
19. Monte MJ, Marin JJ, Antelo A, Vazquez T, et al. Bile acids: chemistry, physiology, and patophisiology. World Gastroenterol. 2009;15:804-16. doi: 10.3748wjg 15804
20. Reddy BS. Role of bile metabolites in colon cancerogenesis. Animal models. Cancer. 1975;36:2401-6.
21. Ocvirk SL, O'Keefe SJ. Influence of Bile Acids on Colorectal Cancer Risk: Potential Mechanisms Mediated by Diet – Gut Microbiota Interactions. Curr Nutr Rep. 2017;6(4):315-22. doi: 10.1007/s13668-017-0219-5
22. Alexander J, Scott AJ, Pouncey A, et al. Colorecnal carcinogenesis; an archetype of gut microbiota-host interacnion. E-Cancer Med Sci. 2018;12:865. doi: 10.3332/ecancer.2018.865
23. O’Keefe SJD. Diet, microorganisms and their metabolites, and colon cancer. Nat Rev Gastrotnterol Hepatol. 2016;13:691-706. doi: 10.1038/nrgastro2016.165
24. Schulz MD, Atay C, Heringer J. High-fat-diet-mediated disbiosis promotes intestinal carcinogenesis independently of obesity. Nature. 2014;514:508-12. doi: 10.1038/nature13398
25. Degirolamo C, Modica S, Palasciano G, Moschetta A. Bile acids and colon cancer: Solving the puzzle with nuclear receptors. Trends Mol Med. 2011;17:564-72. doi: 10.1016/jmolmed.2011.05.10
26. Craciun S, Balskus EP. Microbial conversion of choline to trimethylamine requires a glicyl radical enzyme. Proc Natl Acad Sci USA. 2012;109(52):815-22. doi: 10.1073/pnas. 1215689109.24
27. Qiao D, Gaitonde SV, Qi W, Martinez JD. Deoxycholic acid suppresses p53 by stimulating proteasome-mediated p53 protein degradation. Carcinogenesis. 2001;22:957-64. doi: 10.1093/carcin/22.6.956
28. Shant J, Cheng K, Marasa BS, Wang JY, Raufman JP. Akt-dependent NF-kappaB activation is required for bile acids to rescue colon cancer cells from stress-induced apoptosis. Exp Cell Res. 2009;315:432-50. doi: 10.1016/jyekcr2008.11.003
29. Raufman JP, Shant J, Guo CY, Roy S, Cheng K. Deoxycholyltaurine rescues human colon cancer cells from apoptosis by activating EGFR-dependent PI3K/Akt signaling. J Cell Physiol. 2008;215:538-49. doi: 10.1002/jcp.21332
30. Turner DJ, Alaish SM, Zou T, Rao JN, Wang JY, Strauch ED. Bile salts induce resistance to apoptosis through NF-kappaB-mediated XIAP expression. Ann Surg. 2007;245:415-25. doi: 10.1097/01sia0000236631/72698/99
31. Arvind P, Papavassiliou ED, Tsioulias GJ, Duceman BW, Lovelace CI, Geng W, et al. Lithocholic acid inhibits the expression of HLA class I genes in colon adenocarcinoma cells. Differential effect on HLA-A, -B and -C loci. Mol Immunol. 1994;31:607-14.
32. Pai R, Tarnawski AS, Tran T. Deoxycholic acid activates beta-catenin signaling pathway and increases colon cell cancer growth and invasiveness. Mol Biol Cell. 2004;15:2156-63. doi: 10.1091/mbc.E03-12-0894
33. Oshio H, Abe T, Onogawa T, Ohtsuka H, Sato T, Ii T, et al. Peroxisome proliferator-activated receptor alpha activates cyclooxygenase-2 gene transcription through bile acid transport in human colorectal cancer cell lines. J Gastroenterol. 2008;43:538-49. doi: 10/1007/s00535-008-2188-3
34. Thi Thinh Nguyen, Trong Thuan Ung, Nam Ho Kim, Young Do Jung. Role of bile acids in colon carcinogenesis. World J Clin Cases. 2018 Nov 6;6(13):577-88. doi: 10.12998/wjcc.v6.i13.577
35. Nguyen TT, Lian S, Ung TT, Xia Y, Han JY, Jung YD. Lithocholic Acid Stimulates IL-8 Expression in Human Colorectal Cancer Cells Via Activation of Erk1/2 MAPK and Suppression of STAT3 Activity. J Cell Biochem. 2017;118:2958-67. doi: 10.1002/jcb2595
36. Tucker ON, Dannenberg AJ, Yang EK, Fahey TJ 3rd. Bile acids induce cyclooxygenase-2 expression in human pancreatic cancer cell lines. Carcinogenesis. 2004;25:419-23. doi: 10.1093/carcin/bgh 010
37. Mühlbauer M, Allard B, Bosserhoff AK, Kiessling S, Herfarth H, Rogler G, et al. Differential effects of deoxycholic acid and taurodeoxycholic acid on NF-kappa B signal transduction and IL-8 gene expression in colonic epithelial cells. Am J Physiol Gastrointest Liver Physiol. 2004;286:G1000-G1008. doi: 10.1152/ojpgi00338.2003
38. Hess LM, Krutzsch MF, Guillen J, Chow HH, et al. Result of a phase 1 multihple-dose clinical study of ursodeoxycholic. Acid Cancer Epidemiol Biomarkers Prev. 2004;13:861-7.
39. Kim EK, Cho JH, Kim E, Kim YJ. Ursodeoxicholic acid inhibits the proliferation of colon cancer cells by regulating oxidative stress and cancer stem-like cell growth. PLoS One. 2017;12:181-3. doi: 10.1371/journal.pone.0181183
40. Logan RE, Grainge MJ, Sheperd VC, et al. Aspirin and folic acid for prevention of recurrent colorectal adenomas. Gastroenterology. 2008;1:29-38.
41. Wu K, Peatz EA, Willett WC, et al. A randomized trial on folic acid of risk recurrent colorectal adenoma. Am J Clin Nutr. 2009;6:1623-31. doi: 10.3945/ajcn2009.283