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  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
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We are analyzing https://link.springer.com/article/10.1007/s00018-022-04278-2.

Title:
The role of bile acids in carcinogenesis | Cellular and Molecular Life Sciences
Description:
Bile acids are soluble derivatives of cholesterol produced in the liver that subsequently undergo bacterial transformation yielding a diverse array of metabolites. The bulk of bile acid synthesis takes place in the liver yielding primary bile acids; however, other tissues have also the capacity to generate bile acids (e.g. ovaries). Hepatic bile acids are then transported to bile and are subsequently released into the intestines. In the large intestine, a fraction of primary bile acids is converted to secondary bile acids by gut bacteria. The majority of the intestinal bile acids undergo reuptake and return to the liver. A small fraction of secondary and primary bile acids remains in the circulation and exert receptor-mediated and pure chemical effects (e.g. acidic bile in oesophageal cancer) on cancer cells. In this review, we assess how changes to bile acid biosynthesis, bile acid flux and local bile acid concentration modulate the behavior of different cancers. Here, we present in-depth the involvement of bile acids in oesophageal, gastric, hepatocellular, pancreatic, colorectal, breast, prostate, ovarian cancer. Previous studies often used bile acids in supraphysiological concentration, sometimes in concentrations 1000 times higher than the highest reported tissue or serum concentrations likely eliciting unspecific effects, a practice that we advocate against in this review. Furthermore, we show that, although bile acids were classically considered as pro-carcinogenic agents (e.g. oesophageal cancer), the dogma that switch, as lower concentrations of bile acids that correspond to their serum or tissue reference concentration possess anticancer activity in a subset of cancers. Differences in the response of cancers to bile acids lie in the differential expression of bile acid receptors between cancers (e.g. FXR vs. TGR5). UDCA, a bile acid that is sold as a generic medication against cholestasis or biliary surge, and its conjugates were identified with almost purely anticancer features suggesting a possibility for drug repurposing. Taken together, bile acids were considered as tumor inducers or tumor promoter molecules; nevertheless, in certain cancers, like breast cancer, bile acids in their reference concentrations may act as tumor suppressors suggesting a Janus-faced nature of bile acids in carcinogenesis.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Science

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

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Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We find it hard to spot revenue streams.

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Keywords {🔍}

pubmed, google, scholar, article, cas, bile, acid, cancer, receptor, bas, cells, acids, central, cell, expression, human, liver, wang, activation, nuclear, protein, signaling, kim, fxr, receptors, tgr, breast, zhang, factor, growth, carcinoma, pxr, apoptosis, res, pathway, role, colon, mol, chen, intestinal, effects, gastric, deoxycholic, ovarian, table, kinase, concentrations, ursodeoxycholic, cholesterol, farnesoid,

Topics {✒️}

promotes epithelial-mesenchymal transition induce epithelial–mesenchymal transition nuclear factor κappa-light-chain-enhancer epithelial–mesenchymal transition uplc-mrm-ms-validated method chrm3 muscarinic receptor-3 chrm2 muscarinic receptor-2 c-jun n-terminal kinase negative jnk/c-jun/ap-1 pathway mesenchymal transition organic anion-transporting polypeptide fak-dependent c-jun activation phorbol-ester-type tumor promoters positive egfr/pkc/ras/erk/creb bone marrow-derived monocyte/macrophage bile acid-responsive element fxr/nf-κb signalling pathway nf-kappab-mediated xiap expression wnt/β-catenin signaling pathway bile acid biosynthesis atp-dependent cassette transporter pi3k/akt/ikappab/nf-kappab lxr-dependent gene expression uridine 5′-diphosphate-glucuronosyltransferase 2b4 muscarinic acetylcholine receptor muscarinic receptor signaling p38-mapk-p53-nfκb pathway [212 receptor/bile acid receptor intestine-specific vdr-deficient mice bile acid-induced proliferation m3 muscarinic receptors induce oxidative stress article download pdf activate muscarinic receptors increases oxidative stress protein-coupled receptor responsive inducing oxidative stress bile acid-induced activation full access lithocholic acid-induced hepatotoxicity regulating oxidative stress exert anti-inflammatory responses 3b-hydroxy-5-cholenoic acid c-myc-dependent fashion [179 bile acid-stimulated expression human hepatocellular carcinoma protein-coupled receptor superfamily c24 n-acyl bond wnt/β-catenin pathway endoplasmic reticulum stress

Questions {❓}

  • Lagergren J, Ye W, Ekbom A (2001) Intestinal cancer after cholecystectomy: is bile involved in carcinogenesis?
  • Li J, Li B, Jiang Q, Zhang Y, Liu A, Wang H, Zhang J, Qin Q, Hong Z, Li BA (2018) Do genetic polymorphisms of the vitamin D receptor contribute to breast/ovarian cancer?
  • Ochsenkuhn T, Marsteller I, Hay U, Diebold J, Paumgartner G, Goke B, Sackmann M (2003) Does ursodeoxycholic acid change the proliferation of the colorectal mucosa?
  • Stieger B (2003) Biliary cholesterol secretion: more lessons from plants?
  • Thomas RM, Jobin C (2015) The microbiome and cancer: is the “oncobiome” mirage real?

Schema {🗺️}

WebPage:
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         headline:The role of bile acids in carcinogenesis
         description:Bile acids are soluble derivatives of cholesterol produced in the liver that subsequently undergo bacterial transformation yielding a diverse array of metabolites. The bulk of bile acid synthesis takes place in the liver yielding primary bile acids; however, other tissues have also the capacity to generate bile acids (e.g. ovaries). Hepatic bile acids are then transported to bile and are subsequently released into the intestines. In the large intestine, a fraction of primary bile acids is converted to secondary bile acids by gut bacteria. The majority of the intestinal bile acids undergo reuptake and return to the liver. A small fraction of secondary and primary bile acids remains in the circulation and exert receptor-mediated and pure chemical effects (e.g. acidic bile in oesophageal cancer) on cancer cells. In this review, we assess how changes to bile acid biosynthesis, bile acid flux and local bile acid concentration modulate the behavior of different cancers. Here, we present in-depth the involvement of bile acids in oesophageal, gastric, hepatocellular, pancreatic, colorectal, breast, prostate, ovarian cancer. Previous studies often used bile acids in supraphysiological concentration, sometimes in concentrations 1000 times higher than the highest reported tissue or serum concentrations likely eliciting unspecific effects, a practice that we advocate against in this review. Furthermore, we show that, although bile acids were classically considered as pro-carcinogenic agents (e.g. oesophageal cancer), the dogma that switch, as lower concentrations of bile acids that correspond to their serum or tissue reference concentration possess anticancer activity in a subset of cancers. Differences in the response of cancers to bile acids lie in the differential expression of bile acid receptors between cancers (e.g. FXR vs. TGR5). UDCA, a bile acid that is sold as a generic medication against cholestasis or biliary surge, and its conjugates were identified with almost purely anticancer features suggesting a possibility for drug repurposing. Taken together, bile acids were considered as tumor inducers or tumor promoter molecules; nevertheless, in certain cancers, like breast cancer, bile acids in their reference concentrations may act as tumor suppressors suggesting a Janus-faced nature of bile acids in carcinogenesis.
         datePublished:2022-04-16T00:00:00Z
         dateModified:2022-04-16T00:00:00Z
         pageStart:1
         pageEnd:39
         license:http://creativecommons.org/licenses/by/4.0/
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            Bile acid
            Primary bile acid
            Secondary bile acid
            Bile acid biosynthesis
            Bile acid receptors
            Bile acid transporters
            Microbiome
            CA
            CDCA
            DCA
            LCA
            UDCA
            Carcinogenesis
            TGR5
            S1PR2
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            Muscarinic receptor CHRM3
            FXR
            PXR
            CAR
            VDR
            LXR
            SHP
            Oesophageal carcinoma
            Gastric cancer
            Hepatocellular carcinoma
            Pancreatic adenocarcinoma
            Colorectal carcinoma
            Breast cancer
            Prostate cancer
            Ovarian cancer
            Epithelial–mesenchymal transition
            Oxidative stress
            Warburg metabolism
            Cell Biology
            Biomedicine
            general
            Life Sciences
            Biochemistry
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      headline:The role of bile acids in carcinogenesis
      description:Bile acids are soluble derivatives of cholesterol produced in the liver that subsequently undergo bacterial transformation yielding a diverse array of metabolites. The bulk of bile acid synthesis takes place in the liver yielding primary bile acids; however, other tissues have also the capacity to generate bile acids (e.g. ovaries). Hepatic bile acids are then transported to bile and are subsequently released into the intestines. In the large intestine, a fraction of primary bile acids is converted to secondary bile acids by gut bacteria. The majority of the intestinal bile acids undergo reuptake and return to the liver. A small fraction of secondary and primary bile acids remains in the circulation and exert receptor-mediated and pure chemical effects (e.g. acidic bile in oesophageal cancer) on cancer cells. In this review, we assess how changes to bile acid biosynthesis, bile acid flux and local bile acid concentration modulate the behavior of different cancers. Here, we present in-depth the involvement of bile acids in oesophageal, gastric, hepatocellular, pancreatic, colorectal, breast, prostate, ovarian cancer. Previous studies often used bile acids in supraphysiological concentration, sometimes in concentrations 1000 times higher than the highest reported tissue or serum concentrations likely eliciting unspecific effects, a practice that we advocate against in this review. Furthermore, we show that, although bile acids were classically considered as pro-carcinogenic agents (e.g. oesophageal cancer), the dogma that switch, as lower concentrations of bile acids that correspond to their serum or tissue reference concentration possess anticancer activity in a subset of cancers. Differences in the response of cancers to bile acids lie in the differential expression of bile acid receptors between cancers (e.g. FXR vs. TGR5). UDCA, a bile acid that is sold as a generic medication against cholestasis or biliary surge, and its conjugates were identified with almost purely anticancer features suggesting a possibility for drug repurposing. Taken together, bile acids were considered as tumor inducers or tumor promoter molecules; nevertheless, in certain cancers, like breast cancer, bile acids in their reference concentrations may act as tumor suppressors suggesting a Janus-faced nature of bile acids in carcinogenesis.
      datePublished:2022-04-16T00:00:00Z
      dateModified:2022-04-16T00:00:00Z
      pageStart:1
      pageEnd:39
      license:http://creativecommons.org/licenses/by/4.0/
      sameAs:https://doi.org/10.1007/s00018-022-04278-2
      keywords:
         Bile acid
         Primary bile acid
         Secondary bile acid
         Bile acid biosynthesis
         Bile acid receptors
         Bile acid transporters
         Microbiome
         CA
         CDCA
         DCA
         LCA
         UDCA
         Carcinogenesis
         TGR5
         S1PR2
         Muscarinic receptor CHRM2
         Muscarinic receptor CHRM3
         FXR
         PXR
         CAR
         VDR
         LXR
         SHP
         Oesophageal carcinoma
         Gastric cancer
         Hepatocellular carcinoma
         Pancreatic adenocarcinoma
         Colorectal carcinoma
         Breast cancer
         Prostate cancer
         Ovarian cancer
         Epithelial–mesenchymal transition
         Oxidative stress
         Warburg metabolism
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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         name:Springer International Publishing
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            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Tadeja Režen
            affiliation:
                  name:University of Ljubljana
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                  name:University of Ljubljana
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                     name:Centre for Functional Genomics and Bio-Chips, Institute of Biochemistry and Molecular Genetics, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
                     type:PostalAddress
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            type:Person
            name:Tünde Kovács
            affiliation:
                  name:University of Debrecen
                  address:
                     name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
                     type:PostalAddress
                  type:Organization
                  name:MTA-DE Lendület Laboratory of Cellular Metabolism
                  address:
                     name:MTA-DE Lendület Laboratory of Cellular Metabolism, Debrecen, Hungary
                     type:PostalAddress
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            name:Patrik Kovács
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                     name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
                     type:PostalAddress
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            type:Person
            name:Adrienn Sipos
            affiliation:
                  name:University of Debrecen
                  address:
                     name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
                     type:PostalAddress
                  type:Organization
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            name:Péter Bai
            affiliation:
                  name:University of Debrecen
                  address:
                     name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
                     type:PostalAddress
                  type:Organization
                  name:MTA-DE Lendület Laboratory of Cellular Metabolism
                  address:
                     name:MTA-DE Lendület Laboratory of Cellular Metabolism, Debrecen, Hungary
                     type:PostalAddress
                  type:Organization
                  name:University of Debrecen
                  address:
                     name:Research Center for Molecular Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Edit Mikó
            url:http://orcid.org/0000-0001-7584-445X
            affiliation:
                  name:University of Debrecen
                  address:
                     name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
                     type:PostalAddress
                  type:Organization
                  name:MTA-DE Lendület Laboratory of Cellular Metabolism
                  address:
                     name:MTA-DE Lendület Laboratory of Cellular Metabolism, Debrecen, Hungary
                     type:PostalAddress
                  type:Organization
            email:[email protected]
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         name:MTA-DE Lendület Laboratory of Cellular Metabolism, Debrecen, Hungary
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      name:Tünde Kovács
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            name:MTA-DE Lendület Laboratory of Cellular Metabolism
            address:
               name:MTA-DE Lendület Laboratory of Cellular Metabolism, Debrecen, Hungary
               type:PostalAddress
            type:Organization
      name:Patrik Kovács
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            name:University of Debrecen
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               name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
               type:PostalAddress
            type:Organization
      name:Adrienn Sipos
      affiliation:
            name:University of Debrecen
            address:
               name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
               type:PostalAddress
            type:Organization
      name:Péter Bai
      affiliation:
            name:University of Debrecen
            address:
               name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
               type:PostalAddress
            type:Organization
            name:MTA-DE Lendület Laboratory of Cellular Metabolism
            address:
               name:MTA-DE Lendület Laboratory of Cellular Metabolism, Debrecen, Hungary
               type:PostalAddress
            type:Organization
            name:University of Debrecen
            address:
               name:Research Center for Molecular Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary
               type:PostalAddress
            type:Organization
      name:Edit Mikó
      url:http://orcid.org/0000-0001-7584-445X
      affiliation:
            name:University of Debrecen
            address:
               name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
               type:PostalAddress
            type:Organization
            name:MTA-DE Lendület Laboratory of Cellular Metabolism
            address:
               name:MTA-DE Lendület Laboratory of Cellular Metabolism, Debrecen, Hungary
               type:PostalAddress
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      email:[email protected]
PostalAddress:
      name:Centre for Functional Genomics and Bio-Chips, Institute of Biochemistry and Molecular Genetics, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
      name:Centre for Functional Genomics and Bio-Chips, Institute of Biochemistry and Molecular Genetics, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
      name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
      name:MTA-DE Lendület Laboratory of Cellular Metabolism, Debrecen, Hungary
      name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
      name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
      name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
      name:MTA-DE Lendület Laboratory of Cellular Metabolism, Debrecen, Hungary
      name:Research Center for Molecular Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary
      name:Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary
      name:MTA-DE Lendület Laboratory of Cellular Metabolism, Debrecen, Hungary

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