scholarly journals Lipid Metabolism in Development and Progression of Hepatocellular Carcinoma

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1419 ◽  
Author(s):  
Moris Sangineto ◽  
Rosanna Villani ◽  
Francesco Cavallone ◽  
Antonino Romano ◽  
Domenico Loizzi ◽  
...  

Metabolic reprogramming is critically involved in the development and progression of cancer. In particular, lipid metabolism has been investigated as a source of energy, micro-environmental adaptation, and cell signalling in neoplastic cells. However, the specific role of lipid metabolism dysregulation in hepatocellular carcinoma (HCC) has not been widely described yet. Alterations in fatty acid synthesis, β-oxidation, and cellular lipidic composition contribute to initiation and progression of HCC. The aim of this review is to elucidate the mechanisms by which lipid metabolism is involved in hepatocarcinogenesis and tumour adaptation to different conditions, focusing on the transcriptional aberrations with new insights in lipidomics and lipid zonation. This will help detect new putative therapeutic approaches in the second most frequent cause of cancer-related death.

1967 ◽  
Vol 242 (18) ◽  
pp. 4013-4022 ◽  
Author(s):  
Arthur F. Whereat ◽  
Franklin E. Hull ◽  
Margaret W. Orishimo ◽  
Joseph L. Rabinowitz

2015 ◽  
Vol 125 (3) ◽  
pp. 407-422 ◽  
Author(s):  
Nastassia Shtaida ◽  
Inna Khozin-Goldberg ◽  
Sammy Boussiba

2014 ◽  
Vol 80 (9) ◽  
pp. 2672-2678 ◽  
Author(s):  
G. Hao ◽  
H. Chen ◽  
L. Wang ◽  
Z. Gu ◽  
Y. Song ◽  
...  

1996 ◽  
Vol 271 (3) ◽  
pp. E521-E528 ◽  
Author(s):  
K. Nonogaki ◽  
X. M. Pan ◽  
A. H. Moser ◽  
J. Shigenaga ◽  
I. Staprans ◽  
...  

We determined the effects of leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF) on lipid metabolism in intact rats. Administration of LIF and CNTF increased serum triglycerides in a dose-dependent manner with peak values at 2 h. The effects of LIF and CNTF on serum cholesterol were very small, and serum glucose was unaffected. Both LIF and CNTF stimulated hepatic triglyceride secretion, hepatic de novo fatty acid synthesis, and lipolysis. Pretreatment with phenylisopropyl adenosine, which inhibits lipolysis, partially inhibited LIF- and CNTF-induced hypertriglyceridemia. Interleukin-4, which inhibits cytokine-induced hepatic fatty acid synthesis, also partially inhibited LIF- and CNTF-induced hypertriglyceridemia. These results indicate that both lipolysis and de novo fatty acid synthesis play a role in providing fatty acids for the increase in hepatic triglyceride secretion. Neither indomethacin nor adrenergic receptor antagonists affected the hypertriglyceridemia. The combination of LIF plus CNTF showed no additive effects consistent with the action of both cytokines through the gp130 transduction system. Thus LIF and CNTF have similar effects on lipid metabolism; they join a growing list of cytokines that stimulate hepatic triglyceride secretion and may mediate the changes in lipid metabolism that accompany the acute phase response.


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