Role of the Transforming Growth Factor-β in regulating hepatocellular carcinoma oxidative metabolism
Transforming Growth Factor beta (TGF-β) induces tumor cell migration and invasion. However, its role in inducing metabolic reprogramming is poorly understood. Here we analyzed the metabolic profile of hepatocellular carcinoma (HCC) cells that show differences in TGF-β expression. Oxygen consumption...
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| Published in | Scientific reports Vol. 7; no. 1; pp. 12486 - 15 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
02.10.2017
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2045-2322 2045-2322 |
| DOI | 10.1038/s41598-017-12837-y |
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| Abstract | Transforming Growth Factor beta (TGF-β) induces tumor cell migration and invasion. However, its role in inducing metabolic reprogramming is poorly understood. Here we analyzed the metabolic profile of hepatocellular carcinoma (HCC) cells that show differences in TGF-β expression. Oxygen consumption rate (OCR), extracellular acidification rate (ECAR), metabolomics and transcriptomics were performed. Results indicated that the switch from an epithelial to a mesenchymal/migratory phenotype in HCC cells is characterized by reduced mitochondrial respiration, without significant differences in glycolytic activity. Concomitantly, enhanced glutamine anaplerosis and biosynthetic use of TCA metabolites were proved through analysis of metabolite levels, as well as metabolic fluxes from U-13C6-Glucose and U-13C5-Glutamine. This correlated with increase in glutaminase 1 (
GLS1
) expression, whose inhibition reduced cell migration. Experiments where TGF-β function was activated with extracellular TGF-β1 or inhibited through TGF-β receptor I silencing showed that TGF-β induces a switch from oxidative metabolism, coincident with a decrease in OCR and the upregulation of glutamine transporter Solute Carrier Family 7 Member 5 (
SLC7A5
) and
GLS1
. TGF-β also regulated the expression of key genes involved in the flux of glycolytic intermediates and fatty acid metabolism. Together, these results indicate that autocrine activation of the TGF-β pathway regulates oxidative metabolism in HCC cells. |
|---|---|
| AbstractList | Transforming Growth Factor beta (TGF-β) induces tumor cell migration and invasion. However, its role in inducing metabolic reprogramming is poorly understood. Here we analyzed the metabolic profile of hepatocellular carcinoma (HCC) cells that show differences in TGF-β expression. Oxygen consumption rate (OCR), extracellular acidification rate (ECAR), metabolomics and transcriptomics were performed. Results indicated that the switch from an epithelial to a mesenchymal/migratory phenotype in HCC cells is characterized by reduced mitochondrial respiration, without significant differences in glycolytic activity. Concomitantly, enhanced glutamine anaplerosis and biosynthetic use of TCA metabolites were proved through analysis of metabolite levels, as well as metabolic fluxes from U-13C6-Glucose and U-13C5-Glutamine. This correlated with increase in glutaminase 1 (GLS1) expression, whose inhibition reduced cell migration. Experiments where TGF-β function was activated with extracellular TGF-β1 or inhibited through TGF-β receptor I silencing showed that TGF-β induces a switch from oxidative metabolism, coincident with a decrease in OCR and the upregulation of glutamine transporter Solute Carrier Family 7 Member 5 (SLC7A5) and GLS1. TGF-β also regulated the expression of key genes involved in the flux of glycolytic intermediates and fatty acid metabolism. Together, these results indicate that autocrine activation of the TGF-β pathway regulates oxidative metabolism in HCC cells. Transforming Growth Factor beta (TGF-β) induces tumor cell migration and invasion. However, its role in inducing metabolic reprogramming is poorly understood. Here we analyzed the metabolic profile of hepatocellular carcinoma (HCC) cells that show differences in TGF-β expression. Oxygen consumption rate (OCR), extracellular acidification rate (ECAR), metabolomics and transcriptomics were performed. Results indicated that the switch from an epithelial to a mesenchymal/migratory phenotype in HCC cells is characterized by reduced mitochondrial respiration, without significant differences in glycolytic activity. Concomitantly, enhanced glutamine anaplerosis and biosynthetic use of TCA metabolites were proved through analysis of metabolite levels, as well as metabolic fluxes from U-13C6-Glucose and U-13C5-Glutamine. This correlated with increase in glutaminase 1 ( GLS1 ) expression, whose inhibition reduced cell migration. Experiments where TGF-β function was activated with extracellular TGF-β1 or inhibited through TGF-β receptor I silencing showed that TGF-β induces a switch from oxidative metabolism, coincident with a decrease in OCR and the upregulation of glutamine transporter Solute Carrier Family 7 Member 5 ( SLC7A5 ) and GLS1 . TGF-β also regulated the expression of key genes involved in the flux of glycolytic intermediates and fatty acid metabolism. Together, these results indicate that autocrine activation of the TGF-β pathway regulates oxidative metabolism in HCC cells. Transforming Growth Factor beta (TGF-β) induces tumor cell migration and invasion. However, its role in inducing metabolic reprogramming is poorly understood. Here we analyzed the metabolic profile of hepatocellular carcinoma (HCC) cells that show differences in TGF-β expression. Oxygen consumption rate (OCR), extracellular acidification rate (ECAR), metabolomics and transcriptomics were performed. Results indicated that the switch from an epithelial to a mesenchymal/migratory phenotype in HCC cells is characterized by reduced mitochondrial respiration, without significant differences in glycolytic activity. Concomitantly, enhanced glutamine anaplerosis and biosynthetic use of TCA metabolites were proved through analysis of metabolite levels, as well as metabolic fluxes from U-13C6-Glucose and U-13C5-Glutamine. This correlated with increase in glutaminase 1 (GLS1) expression, whose inhibition reduced cell migration. Experiments where TGF-β function was activated with extracellular TGF-β1 or inhibited through TGF-β receptor I silencing showed that TGF-β induces a switch from oxidative metabolism, coincident with a decrease in OCR and the upregulation of glutamine transporter Solute Carrier Family 7 Member 5 (SLC7A5) and GLS1. TGF-β also regulated the expression of key genes involved in the flux of glycolytic intermediates and fatty acid metabolism. Together, these results indicate that autocrine activation of the TGF-β pathway regulates oxidative metabolism in HCC cells.Transforming Growth Factor beta (TGF-β) induces tumor cell migration and invasion. However, its role in inducing metabolic reprogramming is poorly understood. Here we analyzed the metabolic profile of hepatocellular carcinoma (HCC) cells that show differences in TGF-β expression. Oxygen consumption rate (OCR), extracellular acidification rate (ECAR), metabolomics and transcriptomics were performed. Results indicated that the switch from an epithelial to a mesenchymal/migratory phenotype in HCC cells is characterized by reduced mitochondrial respiration, without significant differences in glycolytic activity. Concomitantly, enhanced glutamine anaplerosis and biosynthetic use of TCA metabolites were proved through analysis of metabolite levels, as well as metabolic fluxes from U-13C6-Glucose and U-13C5-Glutamine. This correlated with increase in glutaminase 1 (GLS1) expression, whose inhibition reduced cell migration. Experiments where TGF-β function was activated with extracellular TGF-β1 or inhibited through TGF-β receptor I silencing showed that TGF-β induces a switch from oxidative metabolism, coincident with a decrease in OCR and the upregulation of glutamine transporter Solute Carrier Family 7 Member 5 (SLC7A5) and GLS1. TGF-β also regulated the expression of key genes involved in the flux of glycolytic intermediates and fatty acid metabolism. Together, these results indicate that autocrine activation of the TGF-β pathway regulates oxidative metabolism in HCC cells. Transforming Growth Factor beta (TGF-β) induces tumor cell migration and invasion. However, its role in inducing metabolic reprogramming is poorly understood. Here we analyzed the metabolic profle of hepatocellular carcinoma (HCC) cells that show diferences in TGF-β expression. Oxygen consumption rate (OCR), extracellular acidifcation rate (ECAR), metabolomics and transcriptomics were performed. Results indicated that the switch from an epithelial to a mesenchymal/migratory phenotype in HCC cells is characterized by reduced mitochondrial respiration, without signifcant diferences in glycolytic activity. Concomitantly, enhanced glutamine anaplerosis and biosynthetic use of TCA metabolites were proved through analysis of metabolite levels, as well as metabolic fuxes from U-13C6-Glucose and U-13C5-Glutamine. This correlated with increase in glutaminase 1 (GLS1) expression, whose inhibition reduced cell migration. Experiments where TGF-β function was activated with extracellular TGF-β1 or inhibited through TGF-β receptor I silencing showed that TGF-β induces a switch from oxidative metabolism, coincident with a decrease in OCR and the upregulation of glutamine transporter Solute Carrier Family 7 Member 5 (SLC7A5) and GLS1. TGF-β also regulated the expression of key genes involved in the fux of glycolytic intermediates and fatty acid metabolism. Together, these results indicate that autocrine activation of the TGF-β pathway regulates oxidative metabolism in HCC cells. |
| ArticleNumber | 12486 |
| Author | Hyroššová, Petra Fabregat, Isabel Zorzano, Antonio Peñuelas-Haro, Irene Hernández-Alvarez, María-Isabel Junza, Alexandra Giannelli, Gianluigi Yanes, Oscar Perales, José Carlos Malfettone, Andrea Bertran, Esther Soukupova, Jitka Capellades, Jordi |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28970582$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1111/febs.13665 10.1002/ijc.29097 10.1158/0008-5472.CAN-16-1559 10.18632/oncotarget.3196 10.1016/j.jhep.2013.05.030 10.1038/srep41089 10.1016/j.canlet.2016.10.012 10.1016/j.canlet.2017.01.037 10.1111/eci.12596 10.1158/0008-5472.CAN-13-0308 10.1097/MD.0000000000001583 10.1002/hep.26597 10.1038/srep41241 10.1002/pmic.200800609 10.1038/onc.2015.447 10.1371/journal.pone.0115036 10.18632/oncotarget.2749 10.1152/ajpgi.00160.2014 10.1111/bpa.12299 10.1002/iub.1216 10.15252/embr.201643300 10.1093/cercor/bhu281 10.1016/j.tibs.2015.12.001 10.1111/j.1742-4658.2012.08748.x 10.1158/1078-0432.CCR-11-2322 10.4155/fmc.13.130 10.1038/srep14752 10.1016/j.cmet.2015.12.006 10.1038/nrclinonc.2015.103 10.18632/oncotarget.8632 |
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| References | Liberti, Locasale (CR4) 2016; 41 Zielinski (CR21) 2017; 7 Bertran (CR12) 2013; 58 Hu (CR23) 2014; 307 Huang (CR9) 2013; 73 Beyoğlu, Idle (CR6) 2013; 59 Sheng (CR26) 2012; 279 Yu (CR20) 2015; 6 Miao, Sheng, Sun, Liu, Huang (CR25) 2013; 65 Fabregat (CR1) 2016; 283 Allain, Angenard, Clément, Coulouarn (CR7) 2016; 76 Valvona, Fillmore, Nunn, Pilkington (CR24) 2016; 26 Lukey, Wilson, Cerione (CR16) 2013; 5 Zhang (CR18) 2016; 5 Chen, Zhou, Yu, Liu, Huang (CR27) 2015; 94 Dayton, Jacks, Heiden (CR28) 2016; 17 Kuo (CR19) 2016; 383 Wong (CR29) 2014; 9 Lachenmayer (CR11) 2012; 18 CR5 Giannelli (CR2) 2016; 46 CR8 Malfettone (CR14) 2017; 392 Jin, Alesi, Kang (CR17) 2016; 35 Liu (CR30) 2015; 6 Xie (CR15) 2017; 7 Fernando (CR13) 2015; 136 Álvarez, Hyroššová, Perales, Alcántara (CR31) 2016; 26 Chafey (CR10) 2009; 9 Nath, Li, Roberts, Chan (CR22) 2015; 5 Pavlova, Thomson (CR3) 2016; 23 Q Xie (12837_CR15) 2017; 7 C Allain (12837_CR7) 2016; 76 I Fabregat (12837_CR1) 2016; 283 C Zhang (12837_CR18) 2016; 5 C Wong (12837_CR29) 2014; 9 N Pavlova (12837_CR3) 2016; 23 D Beyoğlu (12837_CR6) 2013; 59 A Lachenmayer (12837_CR11) 2012; 18 D Yu (12837_CR20) 2015; 6 S Sheng (12837_CR26) 2012; 279 12837_CR5 E Bertran (12837_CR12) 2013; 58 L Jin (12837_CR17) 2016; 35 T Kuo (12837_CR19) 2016; 383 T Dayton (12837_CR28) 2016; 17 R Chen (12837_CR27) 2015; 94 Q Huang (12837_CR9) 2013; 73 12837_CR8 Z Álvarez (12837_CR31) 2016; 26 A Malfettone (12837_CR14) 2017; 392 G Giannelli (12837_CR2) 2016; 46 A Nath (12837_CR22) 2015; 5 M Lukey (12837_CR16) 2013; 5 J Fernando (12837_CR13) 2015; 136 C Valvona (12837_CR24) 2016; 26 P Miao (12837_CR25) 2013; 65 D Zielinski (12837_CR21) 2017; 7 W Liu (12837_CR30) 2015; 6 M Liberti (12837_CR4) 2016; 41 H Hu (12837_CR23) 2014; 307 P Chafey (12837_CR10) 2009; 9 |
| References_xml | – volume: 283 start-page: 2219 issue: 12 year: 2016 end-page: 2232 ident: CR1 article-title: TGF-β signalling and liver disease publication-title: FEBS J. doi: 10.1111/febs.13665 – volume: 136 start-page: E161 issue: 4 year: 2015 end-page: 172 ident: CR13 article-title: A mesenchymal-like phenotype and expression of CD44 predict lack of apoptotic response to sorafenib in liver tumor cells publication-title: Int J Cancer doi: 10.1002/ijc.29097 – volume: 76 start-page: 6374 issue: 21 year: 2016 end-page: 6381 ident: CR7 article-title: Integrative Genomic Analysis Identifies the Core Transcriptional Hallmarks of Human Hepatocellular Carcinoma publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-16-1559 – volume: 6 start-page: 7619 issue: 10 year: 2015 end-page: 7631 ident: CR20 article-title: Kidney-type glutaminase (GLS1) is a biomarker for pathologic diagnosis and prognosis of hepatocellular carcinoma publication-title: Oncotarget doi: 10.18632/oncotarget.3196 – volume: 59 start-page: 842 year: 2013 end-page: 858 ident: CR6 article-title: The metabolic window into hepatobiliary disease publication-title: J Hepatol doi: 10.1016/j.jhep.2013.05.030 – volume: 7 year: 2017 ident: CR15 article-title: Multi-omics analyses reveal metabolic alterations regulated by hepatitis B virus core protein in hepatocellular carcinoma cells publication-title: Sci Rep doi: 10.1038/srep41089 – volume: 383 start-page: 282 issue: 2 year: 2016 end-page: 294 ident: CR19 article-title: Glutaminase 2 stabilizes Dicer to repress Snail and metastasis in hepatocellular carcinoma cells publication-title: Cancer Lett doi: 10.1016/j.canlet.2016.10.012 – volume: 392 start-page: 39 year: 2017 end-page: 50 ident: CR14 article-title: Transforming growth factor-β-induced plasticity causes a migratory stemness phenotype in hepatocellular carcinoma publication-title: Cancer Lett doi: 10.1016/j.canlet.2017.01.037 – volume: 46 start-page: 349 issue: 6 year: 2016 end-page: 361 ident: CR2 article-title: The rationale for targeting TGF-β in chronic liver diseases publication-title: Eur J Clin Invest doi: 10.1111/eci.12596 – volume: 5 year: 2016 ident: CR18 article-title: Glutaminase 2 is a novel negative regulator of small GTPase Rac1 and mediates p53 function in suppressing metastasis publication-title: Elife – volume: 73 start-page: 4992 issue: 16 year: 2013 end-page: 5002 ident: CR9 article-title: Metabolic characterization of hepatocellular carcinoma using nontargeted tissue metabolomics publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-13-0308 – volume: 94 issue: 39 year: 2015 ident: CR27 article-title: Low Expression of LDHB Correlates With Unfavorable Survival in Hepatocellular Carcinoma: Strobe-Compliant Article publication-title: Medicine (Baltimore) doi: 10.1097/MD.0000000000001583 – volume: 58 start-page: 2032 issue: 6 year: 2013 end-page: 2044 ident: CR12 article-title: Overactivation of the TGF-β pathway confers a mesenchymal-like phenotype and CXCR4-dependent migratory properties to liver tumor cells publication-title: Hepatology doi: 10.1002/hep.26597 – volume: 7 year: 2017 ident: CR21 article-title: System biology analysis of drivers underlying hallmarks of cancer cell metabolism publication-title: Sci Rep doi: 10.1038/srep41241 – ident: CR8 – volume: 9 start-page: 3889 issue: 15 year: 2009 end-page: 3900 ident: CR10 article-title: Proteomic analysis of beta-catenin activation in mouse liver by DIGE analysis identifies glucose metabolism as a new target of the Wnt pathway publication-title: Proteomics doi: 10.1002/pmic.200800609 – volume: 35 start-page: 3619 issue: 28 year: 2016 end-page: 3625 ident: CR17 article-title: Glutaminolysis as a target for cancer therapy publication-title: Oncogene doi: 10.1038/onc.2015.447 – volume: 9 issue: 12 year: 2014 ident: CR29 article-title: Switching of pyruvate kinase isoform L to M2 promotes metabolic reprogramming in hepatocarcinogenesis publication-title: PLoS One doi: 10.1371/journal.pone.0115036 – volume: 6 start-page: 846 issue: 2 year: 2015 end-page: 861 ident: CR30 article-title: PKM2 promotes metastasis by recruiting myeloid-derived suppressor cells and indicates poor prognosis for hepatocellular carcinoma publication-title: Oncotarget doi: 10.18632/oncotarget.2749 – volume: 307 start-page: G611 issue: 6 year: 2014 end-page: 622 ident: CR23 article-title: Changes in glucose-6-phosphate dehydrogenase expression results in altered behavior of HBV-associated liver cancer cells publication-title: Am J Physiol Gastrointest Liver Physiol. doi: 10.1152/ajpgi.00160.2014 – volume: 26 start-page: 3 issue: 1 year: 2016 end-page: 17 ident: CR24 article-title: The Regulation and Function of Lactate Dehydrogenase A: Therapeutic Potential in Brain Tumor publication-title: Brain Pathol doi: 10.1111/bpa.12299 – volume: 65 start-page: 904 issue: 11 year: 2013 end-page: 910 ident: CR25 article-title: Lactate dehydrogenase A in cancer: a promising target for diagnosis and therapy publication-title: IUBMB Life doi: 10.1002/iub.1216 – volume: 17 start-page: 1721 issue: 12 year: 2016 end-page: 1730 ident: CR28 article-title: PKM2, cancer metabolism, and the road ahead publication-title: EMBO Rep. doi: 10.15252/embr.201643300 – volume: 26 start-page: 1046 issue: 3 year: 2016 end-page: 1058 ident: CR31 article-title: Neuronal Progenitor Maintenance Requires Lactate Metabolism and PEPCK-M-Directed Cataplerosis publication-title: Cereb Cortex doi: 10.1093/cercor/bhu281 – volume: 41 start-page: 211 issue: 3 year: 2016 end-page: 218 ident: CR4 article-title: The Warburg Effect: How Does it Benefit Cancer Cells? publication-title: Trends Biochem Sci doi: 10.1016/j.tibs.2015.12.001 – volume: 279 start-page: 3898 issue: 20 year: 2012 end-page: 3910 ident: CR26 article-title: Knockdown of lactate dehydrogenase A suppresses tumor growth and metastasis of human hepatocellular carcinoma publication-title: FEBS J. doi: 10.1111/j.1742-4658.2012.08748.x – ident: CR5 – volume: 18 start-page: 4997 issue: 18 year: 2012 end-page: 5007 ident: CR11 article-title: Wnt-pathway activation in two molecular classes of hepatocellular carcinoma and experimental modulation by sorafenib publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-11-2322 – volume: 5 start-page: 1685 issue: 14 year: 2013 end-page: 1700 ident: CR16 article-title: Therapeutic strategies impacting cancer cell glutamine metabolism publication-title: Future Med Chem doi: 10.4155/fmc.13.130 – volume: 5 year: 2015 ident: CR22 article-title: Elevated free fatty acid uptake via CD36 promotes epithelial-mesenchymal transition in hepatocellular carcinoma publication-title: Sci Rep doi: 10.1038/srep14752 – volume: 23 start-page: 27 issue: 1 year: 2016 end-page: 47 ident: CR3 article-title: The emerging hallmarks of cancer metabolism publication-title: Cell Metab doi: 10.1016/j.cmet.2015.12.006 – volume: 136 start-page: E161 issue: 4 year: 2015 ident: 12837_CR13 publication-title: Int J Cancer doi: 10.1002/ijc.29097 – volume: 7 year: 2017 ident: 12837_CR15 publication-title: Sci Rep doi: 10.1038/srep41089 – volume: 23 start-page: 27 issue: 1 year: 2016 ident: 12837_CR3 publication-title: Cell Metab doi: 10.1016/j.cmet.2015.12.006 – ident: 12837_CR5 doi: 10.1038/nrclinonc.2015.103 – volume: 94 issue: 39 year: 2015 ident: 12837_CR27 publication-title: Medicine (Baltimore) doi: 10.1097/MD.0000000000001583 – volume: 73 start-page: 4992 issue: 16 year: 2013 ident: 12837_CR9 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-13-0308 – volume: 41 start-page: 211 issue: 3 year: 2016 ident: 12837_CR4 publication-title: Trends Biochem Sci doi: 10.1016/j.tibs.2015.12.001 – volume: 9 issue: 12 year: 2014 ident: 12837_CR29 publication-title: PLoS One doi: 10.1371/journal.pone.0115036 – volume: 5 year: 2015 ident: 12837_CR22 publication-title: Sci Rep doi: 10.1038/srep14752 – volume: 76 start-page: 6374 issue: 21 year: 2016 ident: 12837_CR7 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-16-1559 – volume: 392 start-page: 39 year: 2017 ident: 12837_CR14 publication-title: Cancer Lett doi: 10.1016/j.canlet.2017.01.037 – volume: 26 start-page: 1046 issue: 3 year: 2016 ident: 12837_CR31 publication-title: Cereb Cortex doi: 10.1093/cercor/bhu281 – volume: 283 start-page: 2219 issue: 12 year: 2016 ident: 12837_CR1 publication-title: FEBS J. doi: 10.1111/febs.13665 – volume: 17 start-page: 1721 issue: 12 year: 2016 ident: 12837_CR28 publication-title: EMBO Rep. doi: 10.15252/embr.201643300 – volume: 35 start-page: 3619 issue: 28 year: 2016 ident: 12837_CR17 publication-title: Oncogene doi: 10.1038/onc.2015.447 – volume: 9 start-page: 3889 issue: 15 year: 2009 ident: 12837_CR10 publication-title: Proteomics doi: 10.1002/pmic.200800609 – volume: 18 start-page: 4997 issue: 18 year: 2012 ident: 12837_CR11 publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-11-2322 – volume: 26 start-page: 3 issue: 1 year: 2016 ident: 12837_CR24 publication-title: Brain Pathol doi: 10.1111/bpa.12299 – volume: 279 start-page: 3898 issue: 20 year: 2012 ident: 12837_CR26 publication-title: FEBS J. doi: 10.1111/j.1742-4658.2012.08748.x – volume: 7 year: 2017 ident: 12837_CR21 publication-title: Sci Rep doi: 10.1038/srep41241 – volume: 46 start-page: 349 issue: 6 year: 2016 ident: 12837_CR2 publication-title: Eur J Clin Invest doi: 10.1111/eci.12596 – volume: 65 start-page: 904 issue: 11 year: 2013 ident: 12837_CR25 publication-title: IUBMB Life doi: 10.1002/iub.1216 – volume: 6 start-page: 846 issue: 2 year: 2015 ident: 12837_CR30 publication-title: Oncotarget doi: 10.18632/oncotarget.2749 – volume: 5 year: 2016 ident: 12837_CR18 publication-title: Elife – volume: 6 start-page: 7619 issue: 10 year: 2015 ident: 12837_CR20 publication-title: Oncotarget doi: 10.18632/oncotarget.3196 – volume: 5 start-page: 1685 issue: 14 year: 2013 ident: 12837_CR16 publication-title: Future Med Chem doi: 10.4155/fmc.13.130 – volume: 383 start-page: 282 issue: 2 year: 2016 ident: 12837_CR19 publication-title: Cancer Lett doi: 10.1016/j.canlet.2016.10.012 – ident: 12837_CR8 doi: 10.18632/oncotarget.8632 – volume: 59 start-page: 842 year: 2013 ident: 12837_CR6 publication-title: J Hepatol doi: 10.1016/j.jhep.2013.05.030 – volume: 307 start-page: G611 issue: 6 year: 2014 ident: 12837_CR23 publication-title: Am J Physiol Gastrointest Liver Physiol. doi: 10.1152/ajpgi.00160.2014 – volume: 58 start-page: 2032 issue: 6 year: 2013 ident: 12837_CR12 publication-title: Hepatology doi: 10.1002/hep.26597 |
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