[1] BRAY F, LAVERSANNE M, SUNG H, et al. Global cancer statistics 2022: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries[J]. CA Cancer J Clin, 2024, 74(3): 229-263.
[2] HAN B F, ZHENG R S, ZENG H M, et al. Cancer incidence and mortality in China, 2022[J]. J Natl Cancer Cent, 2024, 4(1):47-53.
[3] LIU Y N, RONG Z H, XIANG D, et al. Detection technologies and metabolic profiling of bile acids: a comprehensive review[J]. Lipids Health Dis, 2018, 17(1): 1-13. doi:  10.1186/s12944-017-0646-8
[4] CHIANG J Y. Bile acid metabolism and signaling[J]. Compr Physiol, 2013, 3(3): 1191-1212.
[5] THAKARE R, ALAMOUDI J A, GAUTAM N, et al. Species differences in bile acids : II. bile acid metabolism[J]. J Appl Toxicol, 2018, 38(10): 1336-1352.
[6] THAKARE R, ALAMOUDI J A, GAUTAM N, et al. Species differences in bile acids : I. plasma and urine bile acid composition[J]. J Appl Toxicol, 2018, 38(10): 1323-1335.
[7] GREIM H, TRÜLZSCH D, CZYGAN P, et al. Mechanism of cholestasis[J]. Gastroenterology, 1972, 63(5): 846-850. doi:  10.1016/S0016-5085(19)33226-3
[8] HIGUCHI H, GORES G J. Ⅳ. Bile acids and death receptors[J]. Am J Physiol Gastrointest Liver Physiol, 2003, 284(5): G734-G738. doi:  10.1152/ajpgi.00491.2002
[9] HUANG J G, BATHENA S P R, CSANAKY I L, et al. Simultaneous characterization of bile acids and their sulfate metabolites in mouse liver, plasma, bile, and urine using LC-MS/MS[J]. J Pharm Biomed Anal, 2011, 55(5): 1111-1119. doi:  10.1016/j.jpba.2011.03.035
[10] TICHO A L, MALHOTRA P, DUDEJA P K, et al. Bile acid receptors and gastrointestinal functions[J]. Liver Res, 2019, 3(1): 31-39. doi:  10.1016/j.livres.2019.01.001
[11] VAVASSORI P, MENCARELLI A, RENGA B, et al. The bile acid receptor FXR is a modulator of intestinal innate immunity[J]. J Immunol, 2009, 183(10): 6251-6261. doi:  10.4049/jimmunol.0803978
[12] TICHO ALEXANDER L, POOJA M, DUDEJA PRADEEP K, et al. Intestinal absorption of bile acids in health and disease[J]. Compr Physiol, 2019, 10(1): 21-56.
[13] INAGAKI T, MOSCHETTA A, LEE Y K, et al. Regulation of antibacterial defense in the small intestine by the nuclear bile acid receptor[J]. Proc Natl Acad Sci USA, 2006, 103(10): 3920-3925. doi:  10.1073/pnas.0509592103
[14] D'ALDEBERT E, BIYEYEME BI MVE M J, MERGEY M, et al. Bile salts control the antimicrobial peptide cathelicidin through nuclear receptors in the human biliary epithelium[J]. Gastroenterology, 2009, 136(4): 1435-1443. doi:  10.1053/j.gastro.2008.12.040
[15] GADALETA R M, VAN ERPECUM K J, OLDENBURG B, et al. Farnesoid X receptor activation inhibits inflammation and preserves the intestinal barrier in inflammatory bowel disease[J]. Gut, 2011, 60(4): 463-472. doi:  10.1136/gut.2010.212159
[16] CIPRIANI S, MENCARELLI A, CHINI M G, et al. The bile acid receptor GPBAR-1(TGR5)modulates integrity of intestinal barrier and immune response to experimental colitis[J]. PLoS One, 2011, 6(10): e25637. doi:  10.1371/journal.pone.0025637
[17] HASELOW K, BODE J G, WAMMERS M, et al. Bile acids PKA-dependently induce a switch of the IL-10/IL-12 ratio and reduce proinflammatory capability of human macrophages[J]. J Leukoc Biol, 2013, 94(6): 1253-1264. doi:  10.1189/jlb.0812396
[18] BIAGIOLI M, CARINO A, CIPRIANI S, et al. The bile acid receptor GPBAR1 regulates the M1/M2 phenotype of intestinal macrophages and activation of GPBAR1 rescues mice from murine colitis[J]. J Immunol, 2017, 199(2): 718-733. doi:  10.4049/jimmunol.1700183
[19] ICHIKAWA R, TAKAYAMA T, YONENO K, et al. Bile acids induce monocyte differentiation toward interleukin-12 hypo-producing dendritic cells via a TGR5-dependent pathway[J]. Immunology, 2012, 136(2): 153-162. doi:  10.1111/j.1365-2567.2012.03554.x
[20] XIE W, RADOMINSKA-PANDYA A, SHI Y, et al. An essential role for nuclear receptors SXR/PXR in detoxification of cholestatic bile acids[J]. Proc Natl Acad Sci USA, 2001, 98(6): 3375-3380. doi:  10.1073/pnas.051014398
[21] OWEN B M, MILONA A, VAN MIL S, et al. Intestinal detoxification limits the activation of hepatic pregnane X receptor by lithocholic acid[J]. Drug Metab Dispos, 2010, 38(1): 143-149.
[22] DE AGUIAR VALLIM T Q, TARLING E J, EDWARDS P A. Pleiotropic roles of bile acids in metabolism[J]. Cell Metab, 2013, 17(5): 657-669. doi:  10.1016/j.cmet.2013.03.013
[23] KIM J H, YAMAORI S, TANABE T, et al. Implication of intestinal VDR deficiency in inflammatory bowel disease[J]. Biochim Biophys Acta, 2013, 1830(1): 2118-2128. doi:  10.1016/j.bbagen.2012.09.020
[24] LIU T Y, SONG X L, KHAN S, et al. The gut microbiota at the intersection of bile acids and intestinal carcinogenesis: an old story, yet mesmerizing[J]. Int J Cancer, 2020, 146(7): 1780-1790. doi:  10.1002/ijc.32563
[25] WU S P, YOON S, ZHANG Y G, et al. Vitamin D receptor pathway is required for probiotic protection in colitis[J]. Am J Physiol Gastrointest Liver Physiol, 2015, 309(5): G341-G349. doi:  10.1152/ajpgi.00105.2015
[26] VAR1ŞCCCL1 B, CAGLAYAN C, KANDEMIR F M, et al. Chrysin mitigates diclofenac-induced hepatotoxicity by modulating oxidative stress, apoptosis, autophagy and endoplasmic reticulum stress in rats[J]. Mol Biol Rep, 2023, 50(1): 433-442.
[27] ZHANG Q S, NONG Y Y, LIU Z Q, et al. Proteinase K combining two-step liquid-liquid extraction for plasma untargeted liquid chromatography-mass spectrometry-based metabolomics to discover the potential mechanism of colorectal adenoma[J]. Anal Chem, 2019, 91(22): 14458-14466.
[28] YACHIDA S, MIZUTANI S, SHIROMA H, et al. Metagenomic and metabolomic analyses reveal distinct stage-specific phenotypes of the gut microbiota in colorectal cancer[J]. Nat Med, 2019, 25(6): 968-976. doi:  10.1038/s41591-019-0458-7
[29] BROWN D G, RAO S, WEIR T L, et al. Metabolomics and metabolic pathway networks from human colorectal cancers, adjacent mucosa, and stool[J]. Cancer Metab, 2016, 4: 11. doi:  10.1186/s40170-016-0151-y
[30] YANG Y Z, MISRA B B, LIANG L, et al. Integrated microbiome and metabolome analysis reveals a novel interplay between commensal bacteria and metabolites in colorectal cancer[J]. Theranostics, 2019, 9(14): 4101-4114. doi:  10.7150/thno.35186
[31] LE GALL G, GUTTULA K, KELLINGRAY L, et al. Metabolite quantification of faecal extracts from colorectal cancer patients and healthy controls[J]. Oncotarget, 2018, 9(70): 33278-33289. doi:  10.18632/oncotarget.26022
[32] WANG X X, WANG J P, RAO B Q, et al. Gut flora profiling and fecal metabolite composition of colorectal cancer patients and healthy individuals[J]. Exp Ther Med, 2017, 13(6): 2848-2854. doi:  10.3892/etm.2017.4367
[33] BERNSTEIN H, BERNSTEIN C, PAYNE C M, et al. Bile acids as endogenous etiologic agents in gastrointestinal cancer[J]. World J Gastroenterol, 2009, 15(27): 3329-3340. doi:  10.3748/wjg.15.3329
[34] WILLIAMS M D, ZHANG X, PARK J J, et al. Characterizing metabolic changes in human colorectal cancer[J]. Anal Bioanal Chem, 2015, 407(16): 4581-4595. doi:  10.1007/s00216-015-8662-x
[35] CHETWYND A J, OGILVIE L A, NZAKIZWANAYO J, et al. The potential of nanoflow liquid chromatography-nano electrospray ionisation-mass spectrometry for global profiling the faecal metabolome[J]. J Chromatogr A, 2019, 1600: 127-136. doi:  10.1016/j.chroma.2019.04.028
[36] UCHIYAMA K, YAGI N, MIZUSHIMA K, et al. Serum metabolomics analysis for early detection of colorectal cancer[J]. J Gastroenterol, 2017, 52(6): 677-694. doi:  10.1007/s00535-016-1261-6
[37] DENG L L, GU H W, ZHU J J, et al. Combining NMR and LC/MS using backward variable elimination: metabolomics analysis of colorectal cancer, polyps, and healthy controls[J]. Anal Chem, 2016, 88(16): 7975-7983. doi:  10.1021/acs.analchem.6b00885
[38] BRIM H, YOOSEPH S, LEE E, et al. A microbiomic analysis in African Americans with colonic lesions reveals Streptococcus sp. VT162 as a marker of neoplastic transformation[J]. Genes, 2017, 8(11): 314. doi:  10.3390/genes8110314
[39] VAHABI F, SADEGHI S, ARJMAND M, et al. Staging of colorectal cancer using serum metabolomics with 1HNMR Spectroscopy[J]. Iran J Basic Med Sci, 2017, 20(7): 835-840.
[40] DJUKOVIC D, ZHANG J J, RAFTERY D. Colorectal cancer detection using targeted LC-MS metabolic profiling[M]. Colorectal Cancer. New York: Humana Press, 2018: 229-240.
[41] BIAN X Q, LI N, TAN B B, et al. Polarity-tuning derivatization-LC-MS approach for probing global carboxyl-containing metabolites in colorectal cancer[J]. Anal Chem, 2018, 90(19): 11210-11215. doi:  10.1021/acs.analchem.8b01873
[42] OSE J, GIGIC B, LIN T D, et al. Multiplatform urinary metabolomics profiling to discriminate cachectic from non-cachectic colorectal cancer patients: pilot results from the ColoCare study[J]. Metabolites, 2019, 9(9): 178.
[43] WAHӏSTOMӦM A, KOVATCHEVA-DATCHARY P, STAHӏMAN M, et al. Crosstalk between bile acids and gut microbiota and its impact on farnesoid X receptor signalling[J]. Dig Dis, 2017, 35(3): 246-250.
[44] LOUIS P, HOLD G L, FLINT H J. The gut microbiota, bacterial metabolites and colorectal cancer[J]. Nat Rev Microbiol, 2014, 12(10): 661-672. doi:  10.1038/nrmicro3344
[45] RIDLON J M, WOLF P G, GASKINS H R. Taurocholic acid metabolism by gut microbes and colon cancer[J]. Gut Microbes, 2016, 7(3): 201-215. doi:  10.1080/19490976.2016.1150414
[46] CROSS AJ, MOORE SC, BOCA S, et al. A prospective study of serum metabolites and colorectal cancer risk[J]. Cancer, 2014, 120(19): 3049-3057.
[47] ESTIÚ M C, FRAILUNA M A, OTERO C, et al. Relationship between early onset severe intrahepatic cholestasis of pregnancy and higher risk of meconium-stained fluid[J]. PLoS One, 2017, 12(4): e0176504. doi:  10.1371/journal.pone.0176504
[48] ZENG H W, CLAYCOMBE K J, REINDL K M. Butyrate and deoxycholic acid play common and distinct roles in HCT116 human colon cell proliferation[J]. J Nutr Biochem, 2015, 26(10): 1022-1028. doi:  10.1016/j.jnutbio.2015.04.007
[49] LULU F, PRATIMA N M, EVAN A, et al. Bile acid: a potential inducer of colon cancer stem cells[J]. Stem Cell Res Ther, 2016, 7(1): 181. doi:  10.1186/s13287-016-0439-4
[50] GADALETA R M, GARCIA-IRIGOYEN O, MOSCHETTA A. Bile acids and colon cancer: is FXR the solution of the conundrum?[J]. Mol Aspects Med, 2017, 56: 66-74. doi:  10.1016/j.mam.2017.04.002
[51] RIDLON J M, WOLF P G, GASKINS H R. Taurocholic acid metabolism by gut microbes and colon cancer[J]. Gut Microbes, 2016, 7(3): 201-215. doi:  10.1080/19490976.2016.1150414
[52] VAUGHN B P, KAISER T, STALEY C, et al. A pilot study of fecal bile acid and microbiota profiles in inflammatory bowel disease and primary sclerosing cholangitis[J]. Clin Exp Gastroenterol, 2019, 12: 9-19. doi:  10.2147/CEG.S186097
[53] ZENG H W, UMAR S, RUST B, et al. Secondary bile acids and short chain fatty acids in the colon: a focus on colonic microbiome, cell proliferation, inflammation, and cancer[J]. Int J Mol Sci, 2019, 20(5): 1214. doi:  10.3390/ijms20051214
[54] AMARAL J D, VIANA R J S, RAMALHO R M, et al. Bile acids: regulation of apoptosis by ursodeoxycholic acid[J]. J Lipid Res, 2009, 50(9): 1721-1734. doi:  10.1194/jlr.R900011-JLR200
[55] HARA E. Relationship between obesity, gut microbiome and hepatocellular carcinoma development[J]. Dig Dis, 2015, 33(3): 346-350. doi:  10.1159/000371679
[56] DEBRUYNE P R, BRUYNEEL E A, KARAGUNI I M, et al. Bile acids stimulate invasion and haptotaxis in human colorectal cancer cells through activation of multiple oncogenic signaling pathways[J]. Oncogene, 2002, 21(44): 6740-6750. doi:  10.1038/sj.onc.1205729
[57] KITAMURA T, SRIVASTAVA J, DIGIOVANNI J, et al. Bile acid accelerates erbB2-induced pro-tumorigenic activities in biliary tract cancer[J]. Mol Carcinog, 2015, 54(6): 459-472. doi:  10.1002/mc.22118
[58] FENG H Y, CHEN Y C. Role of bile acids in carcinogenesis of pancreatic cancer: an old topic with new perspective[J]. World J Gastroenterol, 2016, 22(33): 7463-7477. doi:  10.3748/wjg.v22.i33.7463
[59] RAUFMAN J P, DAWSON P A, RAO A, et al. Slc10a2-null mice uncover colon cancer-promoting actions of endogenous fecal bile acids[J]. Carcinogenesis, 2015, 36(10): 1193-1200. doi:  10.1093/carcin/bgv107
[60] LOKE MF, CHUA EG, GAN HM, et al. Metabolomics and 16S rRNA sequencing of human colorectal cancers and adjacent mucosa[J]. PLOS ONE, 2018, 13(12): e0208584. doi:  10.1371/journal.pone.0208584
[61] HANG S Y, PAIK D, YAO L N, et al. Bile acid metabolites control TH17 and Treg cell differentiation[J]. Nature, 2019, 576(7785): 143-148. doi:  10.1038/s41586-019-1785-z
[62] CAMPBELL C, MCKENNEY P T, KONSTANTINOVSKY D, et al. Bacterial metabolism of bile acids promotes generation of peripheral regulatory T cells[J]. Nature, 2020, 581(7809): 475-479. doi:  10.1038/s41586-020-2193-0
[63] Centuori S M, Martinez J D. Differential regulation of EGFR-MAPK signaling by deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA) in colon cancer[J]. Dig Dis Sci, 2014, 59(10): 2367-2380. doi:  10.1007/s10620-014-3190-7
[64] SINGH S, KHANNA S, PARDI D S, et al. Effect of ursodeoxycholic acid use on the risk of colorectal neoplasia in patients with primary sclerosing cholangitis and inflammatory bowel disease: a systematic review and meta-analysis[J]. Inflamm Bowel Dis, 2013, 19(8): 1631-1638. doi:  10.1097/MIB.0b013e318286fa61
[65] THOMPSON P A, WERTHEIM B C, ROE D J, et al. Gender modifies the effect of ursodeoxycholic acid in a randomized controlled trial in colorectal adenoma patients[J]. Cancer Prev Res, 2009, 2(12): 1023-1030. doi:  10.1158/1940-6207.CAPR-09-0234
[66] BROWN D G, BORRESEN E C, BROWN R J, et al. Heat-stabilised rice bran consumption by colorectal cancer survivors modulates stool metabolite profiles and metabolic networks: a randomised controlled trial[J]. Br J Nutr, 2017, 117(9): 1244-1256. doi:  10.1017/S0007114517001106
[67] SHEFLIN A M, BORRESEN E C, WDOWIK M J, et al. Pilot dietary intervention with heat-stabilized rice bran modulates stool microbiota and metabolites in healthy adults[J]. Nutrients, 2015, 7(2): 1282-1300. doi:  10.3390/nu7021282
[68] HANLEY M, ALADELOKUN O, KADAVERU K, et al. Methyl donor deficiency blocks colorectal cancer development by affecting key metabolic pathways[J]. Cancer Prev Res, 2019, 13: 1-14.
[69] SÁNCHEZ B. Bile acid-microbiota crosstalk in gastrointestinal inflammation and carcinogenesis: a role for bifidobacteria and lactobacilli?[J]. Nat Rev Gastroenterol Hepatol, 2018, 15(4): 205.