[1]Chen W, Zheng R, Baade PD, et al. Cancer Statistics in China, 2015[J]. CA Cancer J Clin, 2016, 66(2):115-132. [2]Houten SM, Watanabe M, Auwer XJ, et al. Endocrine functions of bile acids[J]. EMBO J, 2006, 25(7):1419-1425. [3]Li T, Apte U. Bile Acid Metabolism and Signaling in Cholestasis, Inflammation, and Cancer[J]. Adv Pharmacol, 2015, 74:263-302. [4] Takahashi S, Tanaka N, Fukami T, et al. Role of Farnesoid X Receptor and Bile Acids in Hepatic Tumor Development[J]. Hepatol Commun, 2018, 2(12):1567-1582. [5] Forman BM, Goode E, Chen J, et al. Identification of a nuclear receptor that is activated by farnesol metabolites[J]. Cell, 1995, 81(5):687-693. [6] Martinot E, Sedes L, Baptissart M, et al. Bile acids and their receptors [J]. Molecular Aspects of Medicine, 2017, (56):2-9. [7] Hylemon PB, Zhou H, Pandak WM, et al. Bile acids as regulatory molecules[J]. J Lipid Res, 2009, 50(8):1509-1520. [8] Zollner G, Wagner M, Trauner M. Nuclear receptors as drug targets in cholestasis and drug-induced hepatotoxicity. Pharmacol Ther, 2010, 126(3):228-243. [9] Hong J, Behar J, Wands J, et al. Role of a novel bile acid receptor TGR5 in the development of oesophageal adenocarcinoma[J]. Gut, 2010, 59(2): 170-180. [10] Cao WB, Tian W, Hong J, et al. Expression of bile acid receptor TGR5 in gastric adenocarcinoma[J]. Am J Physiol Gastrointest Liver Physiol, 2013, 304(4):G322-G327. [11] 王林,张楠,李闯等.胆酸通过其膜受体TGR5调控肝癌的发生发展[C].//中国生理学会第24届全国会员代表大会暨生理学学术大会论文集.%,2014:1-2. [12] Schaap FG, Trauner M, Jansen PL. Bile acid receptors as targets for drug development[J]. Nat Rev Gastroenterol Hepatol, 2014, 11(1):55-67. [13]Kawamata Y, Fujii R, Hosoya M, et al. A G protein-coupled receptor responsive to bile acids[J]. J Biol Chem, 2003, 278(11): 9435-9440. [14]Hodge R, Lin J, Vasist L, et al. Safety, pharmacokinetics, and pharmacodynamic eff ects of a selective TGR5 agonist, SB?756050, in type 2 diabetes[J]. Clin Pharmacol Drug Dev, 2013, 2(3): 213?222. [15]Ahmad NN, Pfalzer A, Kaplan LM. Roux-en-Y gastric bypass normalizes the blunted postprandial bile acid excursion associated with obesity[J]. Int J Obes (Lond), 2013, 37(12): 1553?1559. [16]Mobraten K, Haugbro T, Karlstrom E, et al. Activation of the bile acid receptor TGR5 enhances LPS-induced inflammatory responses in a human monocytic cell line[J]. J Recept Signal Transduct Res, 2015, 35(5): 402?409. [17]Martinot E,Sedes L,Baptissart M, et a1.Bile acids and their receptors [J].Molecular Aspects of Medicine, 2017, 56:2-9. [18]Pohl H, Wrobel K, Bojarski C, et al. Risk factors in the development of esophageal adenocarcinoma[J]. Am J Gastroenterol, 2013, 108(2):200-207. [19]Kahrilas PJ. The problems with surveillance of Barrett’s esophagus[J]. N Engl J Med, 2011, 365(15): 1437-1438. [20]Si J, Fu X, Behar J, et al. NADPH oxidase NOX5-S mediates acid-induced cyclooxygenase-2 expression via activation of NF-kappa B in Barrett''s esophageal adenocarcinoma cells[J]. J Biol Chem, 2007, 282:16244-16255. [21]Shivali Marketkar, Li D, Yang DF, et al. TGR5 expression in benign, preneoplastic and neoplastic lesions of Barrett’s esophagus: Case series and findings[J]. World J Gastroenterol , 2017, 23(8): 1338-1344. [22]Hong J, Jose Behar, Jack Wands,et al. Role of a novel bile acid receptor TGR5 in the development of oesophageal adenocarcinoma[J]. Gut, 2010, 59(2): 170-180. [23]Zhou Z, Xia Y, Bandla S, et al. Vitamin D receptor is highly expressed in precancerous lesions and esophageal adenocarcinoma with significant sex difference[J]. Hum Pathol, 2014, 45(8):1744-1751. [24]Pang CH, Amy LaLonde, Tony E Godfrey, et al. Bile salt receptor TGR5 is highly expressed in esophageal adenocarcinoma and precancerous lesions with significantly worse overall survival and gender differences[J]. Clinical and Experimental Gastroenterology, 2017, 10:29-37. [25] Wroblewski LE, Peek RM Jr, Wilson KT. Helicobacter pylori and gastric cancer: factors that modulate disease risk[J]. Clin Microbiol Rev, 2010, 23(4): 713-739. [26] McClain MS, Beckett AC, Cover TL. Helicobacter pylori Vacuolating Toxin and Gastric Cancer[J]. Toxins (Basel), 2017, 9(10): E316. [27] 张竹青,卢书明,陈美如,等.胃癌中STAT3、p-STAT3和Bcl-XL的表达及临床意义[J].肿瘤防治研究, 2014, 41(5):121-124. [28] Guo C, Su J, Li ZJ, et al. The G-protein-coupled bile acid receptor Gpbar1 (TGR5) suppresses gastric cancer cell proliferation and migration through antagonizing STAT3 signaling pathway [J]. Oncotarget, 2015, 6(33):34402-34413. [29] Kim MA, Lee HS, Lee HE, et al. Prognostic importance of epithelial-mesenchymal transition-related protein expression in gastric carcinoma[J]. Histopathology, 2009, 54(4): 442-451. [30] Adriana Carino, Luigina Graziosi, Claudio D’Amore1,et al. The bile acid receptor GPBAR1 (TGR5) is expressed in human gastric cancers and promotes epithelial-mesenchymal transition in gastric cancer cell lines[J]. Oncotarget, 2016, 7(38):61021-61035. [31] Baptissart M, Vega A, Maqdasy S, et al. Bile acids: from digestion to cancers[J]. Biochimie, 2013, 95(3):504-517. [32] Chen WD, Yu DN, Barry M. Forman, et al. Deficiency of G-Protein-Coupled Bile Acid Receptor Gpbar1 (TGR5) Enhances Chemically Induced Liver Carcinogenesis[J]. Hepatology, 2013, 57(2):656-666. [33] Jansen PL. Endogenous bile acids as carcinogens[J]. J Hepatol, 2007, 47(3):434-435. [34] He G, Karin M. NF-kappaB and STAT3: key players in liver inflammation and cancer[J]. Cell Res, 2011, 21(1):159-168. [35] Wang YD, Chen WD, Yu D, et al. The G-protein-coupled bile acid receptor, Gpbar1 (TGR5), negatively regulates hepatic inflammatory response through antagonizing nuclear factor κ light-chain enhancer of activated B cells (NF-κB) in mice[J]. Hepatology, 2011, 54(4):1421-1432. [36] Reich M, Klindt C, Deutschmann K, et al. Role of the G Protein-Coupled Bile Acid Receptor TGR5 in Liver Damage[J]. Dig Dis, 2017, 35(3):235-240. [37] Reich M, Deutschmann K, Sommerfeld A, et al. TGR5 is essential for bile acid-dependent cholangiocyte proliferation in vivo and in vitro[J]. Gut, 2016, 65(3):487-501. [38] Keitel V, Reich M, Reinehr R, et al. TGR5 has antiapoptotic and proliferative effects in isolated cholangiocytes and is overexpressed in human cholangiocarcinomas[A]. XXII International Bile Acid Meeting, 2012. [39] 李艾迪. TGR5在胆管癌发生发展中的作用及机制研究[D]. 河北医科大学, 2016. [40] De Almeida CV, de Camargo MR, Russo E,et al. Role of diet and gut microbiota on colorectal cancer immunomodulation[J]. World J Gastroenterol, 2019, 14;25(2):151-162. [41] Vargas AJ, Thompson PA. Diet and nutrient factors in colorectal cancer risk[J]. Nutr Clin Pract, 2012, 27(5):613-623. [42] Hofmann AF, Cravetto C, Molino G, et al. Simulation of the metabolism and enterohepatic circulation of endogenous deoxycholic acid in humans using a physiologic pharmacokinetic model for bile acid metabolism[J]. Gastroenterology, 1987, 93(4):693-709. [43] Haslam A, Robb S.W, Hébert J.R, et al. The association between Dietary Inflammatory Index scores and the prevalence of colorectal adenoma[J]. Public Health Nutr, 2017, 20(9):1609-1616. [44] Jensen DD, Godfrey CB, Niklas C, et al. The bile acid receptor TGR5 does not interact with beta-arrestins or traffic to endosomes but transmits sustained signals from plasma membrane rafts[J]. J Biol Chem, 2013, 288(32):22942-22960. [45] Kamada N, Seo SU, Chen GY, et al. Role of the gut microbiota in immunity and inflammatory disease[J]. Nat Rev Immunol, 2013, 13(5):321-335.
|