{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang YD"],"funding":["NCI NIH HHS","PHS HHS"],"pagination":["322-31"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4318883"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["29(2)"],"pubmed_abstract":["The farnesoid X receptor (FXR) is a key metabolic and homeostatic regulator in the liver. In the present work, we identify a novel role of FXR in antagonizing c-Jun N-terminal kinase (JNK) signaling pathway in liver carcinogenesis by activating superoxide dismutase 3 (SOD3) transcription. Compared with wild-type mouse liver, FXR(-/-) mouse liver showed elevated JNK phosphorylation. JNK1 deletion suppressed the increase of diethylnitrosamine-induced tumor number in FXR(-/-) mice. These results suggest that JNK1 plays a key role in chemical-induced liver carcinogenesis in FXR(-/-) mice. We found that ligand-activated FXR was able to alleviate H₂O₂or tetradecanoylphorbol acetate-induced JNK phosphorylation in human hepatoblastoma (HepG2) cells or mouse primary hepatocytes. FXR ligand decrease"],"journal":["Molecular endocrinology (Baltimore, Md.)"],"pubmed_title":["Farnesoid X receptor antagonizes JNK signaling pathway in liver carcinogenesis by activating SOD3."],"pmcid":["PMC4318883"],"funding_grant_id":["R01-139158","R01 CA139158","P30 CA033572"],"pubmed_authors":["Li Y","Yuan F","Chen WD","Li C","Long X","Qi H","Huang W","Wang YD","Guo C","Wang X","Kong J","Shen H"],"additional_accession":[]},"is_claimable":false,"name":"Farnesoid X receptor antagonizes JNK signaling pathway in liver carcinogenesis by activating SOD3.","description":"The farnesoid X receptor (FXR) is a key metabolic and homeostatic regulator in the liver. In the present work, we identify a novel role of FXR in antagonizing c-Jun N-terminal kinase (JNK) signaling pathway in liver carcinogenesis by activating superoxide dismutase 3 (SOD3) transcription. Compared with wild-type mouse liver, FXR(-/-) mouse liver showed elevated JNK phosphorylation. JNK1 deletion suppressed the increase of diethylnitrosamine-induced tumor number in FXR(-/-) mice. These results suggest that JNK1 plays a key role in chemical-induced liver carcinogenesis in FXR(-/-) mice. We found that ligand-activated FXR was able to alleviate H₂O₂or tetradecanoylphorbol acetate-induced JNK phosphorylation in human hepatoblastoma (HepG2) cells or mouse primary hepatocytes. FXR ligand decrease","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Feb","modification":"2025-04-20T02:51:18.762Z","creation":"2019-03-27T01:44:43Z"},"accession":"S-EPMC4318883","cross_references":{"pubmed":["25496033"],"doi":["10.1210/me.2014-1225"]}}