scholarly journals Fibroblast growth factor (Fgf) 21 is a novel target gene of the aryl hydrocarbon receptor (AhR)

2014 ◽  
Vol 278 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Xingguo Cheng ◽  
Saurabh G. Vispute ◽  
Jie Liu ◽  
Christine Cheng ◽  
Alexei Kharitonenkov ◽  
...  
Keyword(s):  
Growth Factor ◽  
Aryl Hydrocarbon Receptor ◽  
Fibroblast Growth Factor ◽  
Target Gene ◽  
Fibroblast Growth ◽  
Aryl Hydrocarbon ◽  
Novel Target

scholarly journals Inducible Loss of the Aryl Hydrocarbon Receptor Activates Perigonadal White Fat Respiration and Brown Fat Thermogenesis via Fibroblast Growth Factor 21

2019 ◽  
Vol 20 (4) ◽  
pp. 950 ◽  
Author(s):  
Nathaniel Girer ◽  
Dwayne Carter ◽  
Nisha Bhattarai ◽  
Mehnaz Mustafa ◽  
Larry Denner ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Growth Factor ◽  
Aryl Hydrocarbon Receptor ◽  
Fibroblast Growth Factor ◽  
Knockout Mouse ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Knockout Mouse Model ◽  
Aryl Hydrocarbon ◽  
Brown Adipose

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor highly expressed in hepatocytes. Researchers have employed global and liver-specific conditional Ahr knockout mouse models to characterize the physiological roles of the AHR; however, the gestational timing of AHR loss in these models can complicate efforts to distinguish the direct and indirect effects of post-gestational AHR deficiency. Utilizing a novel tamoxifen-inducible AHR knockout mouse model, we analyzed the effects of hepatocyte-targeted AHR loss in adult mice. The data demonstrate that AHR deficiency significantly reduces weight gain and adiposity, and increases multilocular lipid droplet formation within perigonadal white adipose tissue (gWAT). Protein and mRNA expression of fibroblast growth factor 21 (FGF21), an important hepatokine that activates thermogenesis in brown adipose tissue (BAT) and gWAT, significantly increases upon AHR loss and correlates with a significant increase of BAT and gWAT respiratory capacity. Confirming the role of FGF21 in mediating these effects, this phenotype is reversed in mice concomitantly lacking AHR and FGF21 expression. Chromatin immunoprecipitation analyses suggest that the AHR may constitutively suppress Fgf21 transcription through binding to a newly identified xenobiotic response element within the Fgf21 promoter. The data demonstrate an important AHR-FGF21 regulatory axis that influences adipose biology and may represent a “druggable” therapeutic target for obesity and its related metabolic disorders.

scholarly journals Hepatic Aryl Hydrocarbon Receptor Attenuates Fibroblast Growth Factor 21 Expression

2016 ◽  
Vol 291 (29) ◽  
pp. 15378-15387 ◽  
Author(s):  
Nathaniel G. Girer ◽  
Iain A. Murray ◽  
Curtis J. Omiecinski ◽  
Gary H. Perdew
Keyword(s):  
Growth Factor ◽  
Aryl Hydrocarbon Receptor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Aryl Hydrocarbon

scholarly journals Activation of aryl hydrocarbon receptor dissociates fatty liver from insulin resistance by inducing fibroblast growth factor 21

Hepatology ◽  
2015 ◽  
Vol 61 (6) ◽  
pp. 1908-1919 ◽  
Author(s):  
Peipei Lu ◽  
Jiong Yan ◽  
Ke Liu ◽  
Wojciech G. Garbacz ◽  
Pengcheng Wang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Growth Factor ◽  
Fatty Liver ◽  
Aryl Hydrocarbon Receptor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Aryl Hydrocarbon

scholarly journals Fibroblast Growth Factor Receptor 2: Expression, Roles, and Potential As a Novel Molecular Target for Colorectal Cancer

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Yoko Matsuda ◽  
Junji Ueda ◽  
Toshiyuki Ishiwata
Keyword(s):  
Colorectal Cancer ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cancer Progression ◽  
Fibroblast Growth Factor Receptor ◽  
Growth Factor Receptor ◽  
Fibroblast Growth ◽  
Type Iv ◽  
Well Differentiated ◽  
Novel Target

The fibroblast growth factor receptor (FGFR) family consists of four members, named FGFR1, 2, 3, and 4. All 4 FGFRs and their ligands, fibroblast growth factors (FGFs), are expressed in colorectal cancer (CRC). Recent studies have shown that FGFR2 plays important roles in cancer progression; therefore, it is of great interest as a novel target for cancers. Expression of FGFR2 regulates migration, invasion, and growth in CRC. Expression of the FGFR2 isoform FGFR2 IIIb was associated with well-differentiated histological types, and its specific ligand, FGF7, enhanced angiogenesis and adhesion to type-IV collagen via FGFR2 IIIb in CRC. FGFR2 IIIc is detected in CRC, but its roles have not been well elucidated. Interactions between FGFR2 IIIb and IIIc and FGFs may play important roles in CRC via autocrine and/or paracrine signaling. Several kinds of molecular-targeting agents against FGFR2 have been developed; however, it is not clear how a cancer treatment can most effectively inhibit FGFR2 IIIb or FGFR2 IIIc, or both isoforms. The aim of this paper is to summarize the roles of FGFR2 and its isoforms in CRC and clarify whether they are potent therapeutic targets for CRC.

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