Signaling Pathways of the Neuroendocrine-Immune Network

Author(s):  
Thomas L. Roszman ◽  
William H. Brooks
PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7718 ◽  
Author(s):  
Bangbei Wan ◽  
Yuan Huang ◽  
Bo Liu ◽  
Likui Lu ◽  
Cai Lv

BackgroundAurora kinase B (AURKB) is an important carcinogenic factor in various tumors, while its role in clear cell renal cell carcinoma (ccRCC) still remains unclear. This study aimed to investigate its prognostic value and mechanism of action in ccRCC.MethodsGene expression profiles and clinical data of ccRCC patients were downloaded from The Cancer Genome Atlas database. R software was utilized to analyze the expression and prognostic role ofAURKBin ccRCC. Gene set enrichment analysis (GSEA) was used to analyzeAURKBrelated signaling pathways in ccRCC.ResultsAURKBwas expressed at higher levels in ccRCC tissues than normal kidney tissues. IncreasedAURKBexpression in ccRCC correlated with high histological grade, pathological stage, T stage, N stage and distant metastasis (M stage). Kaplan-Meier survival analysis suggested that highAURKBexpression patients had a worse prognosis than patients with lowAURKBexpression levels. Multivariate Cox analysis showed thatAURKBexpression is a prognostic factor of ccRCC. GSEA indicated that genes involved in autoimmune thyroid disease, intestinal immune network for IgA production, antigen processing and presentation, cytokine-cytokine receptor interaction, asthma, etc., were differentially enriched in theAURKBhigh expression phenotype.ConclusionsAURKBis a promising biomarker for predicting prognosis of ccRCC patients and a potential therapeutic target. In addition,AURKBmight regulate progression of ccRCC through modulating intestinal immune network for IgA production and cytokine-cytokine receptor interaction, etc. signaling pathways. However, more research is necessary to validate the findings.


2020 ◽  
Vol 134 (5) ◽  
pp. 473-512 ◽  
Author(s):  
Ryan P. Ceddia ◽  
Sheila Collins

Abstract With the ever-increasing burden of obesity and Type 2 diabetes, it is generally acknowledged that there remains a need for developing new therapeutics. One potential mechanism to combat obesity is to raise energy expenditure via increasing the amount of uncoupled respiration from the mitochondria-rich brown and beige adipocytes. With the recent appreciation of thermogenic adipocytes in humans, much effort is being made to elucidate the signaling pathways that regulate the browning of adipose tissue. In this review, we focus on the ligand–receptor signaling pathways that influence the cyclic nucleotides, cAMP and cGMP, in adipocytes. We chose to focus on G-protein–coupled receptor (GPCR), guanylyl cyclase and phosphodiesterase regulation of adipocytes because they are the targets of a large proportion of all currently available therapeutics. Furthermore, there is a large overlap in their signaling pathways, as signaling events that raise cAMP or cGMP generally increase adipocyte lipolysis and cause changes that are commonly referred to as browning: increasing mitochondrial biogenesis, uncoupling protein 1 (UCP1) expression and respiration.


Planta Medica ◽  
2014 ◽  
Vol 80 (10) ◽  
Author(s):  
P Balachandran ◽  
FH Sarkar ◽  
DS Pasco

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