scholarly journals Biological Behavior and Lipid Metabolism of Colon Cancer Cells are Regulated by a Combination of Sterol Regulatory Element-Binding Protein 1 and ATP Citrate Lyase

2021 ◽  
Vol Volume 14 ◽  
pp. 1531-1542
Author(s):  
Zhendong Qiu ◽  
Wenhong Deng ◽  
Yupu Hong ◽  
Liang Zhao ◽  
Man Li ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Lipid Metabolism ◽  
Cancer Cells ◽  
Regulatory Element ◽  
Biological Behavior ◽  
Colon Cancer Cells ◽  
Atp Citrate Lyase ◽  
Citrate Lyase ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

scholarly journals Tissue-Specific Effects of Central Leptin on the Expression of Genes Involved in Lipid Metabolism in Liver and White Adipose Tissue

Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 5604-5610 ◽  
Author(s):  
Nilda Gallardo ◽  
Elena Bonzón-Kulichenko ◽  
Teresa Fernández-Agulló ◽  
Eduardo Moltó ◽  
Sergio Gómez-Alonso ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
White Adipose Tissue ◽  
Binding Protein ◽  
Regulatory Element ◽  
Epididymal Adipose Tissue ◽  
Key Enzymes ◽  
Specific Effects ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

Leptin reduces adiposity and exerts antisteatotic effects on nonadipose tissues. However, the mechanisms underlying leptin effects on lipid metabolism in liver and white adipose tissue have not been fully clarified. Here, we have studied the effects of central leptin administration on key enzymes and transcription factors involved in lipid metabolism in liver and epididymal adipose tissue. Intracerebroventricular leptin infusion for 7 d did not change leptin plasma levels but decreased triacylglyceride content in liver, epididymal adipose tissue, and plasma. In both tissues this treatment markedly decreased the expression of key enzymes of the de novo fatty acid (FA) synthesis such as acetyl-coenzyme A-carboxylase, FA synthase, and stearoyl-coenzyme A desaturase-1, in parallel with a reduction in mRNA expression of sterol regulatory element binding protein-1c in liver and carbohydrate regulatory element binding protein in adipose tissue. In addition, leptin also decreased phosphoenol-pyruvate carboxykinase-C expression in adipose tissue, an enzyme involved in glyceroneogenesis in this tissue. Central leptin administration down-regulates delta-6-desaturase expression in liver and adipose tissue, in parallel with the decrease of the expression of sterol regulatory element binding protein-1c in liver and peroxisome proliferator activated receptor α in adipose tissue. Finally, leptin treatment, by regulating adipose triglyceride lipase/hormone sensitive lipase/diacylglycerol transferase 1 expression, also established a new partitioning in the FA-triacylglyceride cycling in adipose tissue, increasing lipolysis and probably the FA efflux from this tissue, and favoring in parallel the FA uptake and oxidation in the liver. These results suggest that leptin, acting at central level, exerts tissue-specific effects in limiting fat tissue mass and lipid accumulation in nonadipose tissues, preventing the development of obesity and type 2 diabetes.

Influence of butyrate on lipid metabolism, survival, and differentiation of colon cancer cells

1991 ◽  
Vol 16 (2) ◽  
pp. 125-133 ◽  
Author(s):  
Atif B. Awad ◽  
Peter J. Horvath ◽  
Martha S. Andersen
Keyword(s):  
Colon Cancer ◽  
Lipid Metabolism ◽  
Cancer Cells ◽  
Colon Cancer Cells

scholarly journals Primary cilium suppression by SREBP1c involves distortion of vesicular trafficking by PLA2G3

2015 ◽  
Vol 26 (12) ◽  
pp. 2321-2332 ◽  
Author(s):  
Hannah Laura Gijs ◽  
Nicolas Willemarck ◽  
Frank Vanderhoydonc ◽  
Niamat Ali Khan ◽  
Jonas Dehairs ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Primary Cilium ◽  
Regulatory Element ◽  
Vesicular Trafficking ◽  
Group Iii ◽  
Cellular Models ◽  
Endosomal Recycling ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Underlying Mechanisms

Distortion of primary cilium formation is increasingly recognized as a key event in many human pathologies. One of the underlying mechanisms involves aberrant activation of the lipogenic transcription factor sterol regulatory element–binding protein 1c (SREBP1c), as observed in cancer cells. To gain more insight into the molecular pathways by which SREBP1c suppresses primary ciliogenesis, we searched for overlap between known ciliogenesis regulators and targets of SREBP1. One of the candidate genes that was consistently up-regulated in cellular models of SREBP1c-induced cilium repression was phospholipase A2 group III (PLA2G3), a phospholipase that hydrolyzes the sn-2 position of glycerophospholipids. Use of RNA interference and a chemical inhibitor of PLA2G3 rescued SREBP1c-induced cilium repression. Cilium repression by SREBP1c and PLA2G3 involved alterations in endosomal recycling and vesicular transport toward the cilium, as revealed by aberrant transferrin and Rab11 localization, and was largely mediated by an increase in lysophosphatidylcholine and lysophosphatidylethanolamine levels. Together these findings indicate that aberrant activation of SREBP1c suppresses primary ciliogenesis by PLA2G3-mediated distortion of vesicular trafficking and suggest that PLA2G3 is a novel potential target to normalize ciliogenesis in SREBP1c-overexpressing cells, including cancer cells.

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