Vitamin D3 inhibits fatty acid synthase expression by stimulating the expression of long‐chain fatty‐acid‐CoA ligase 3 in prostate cancer cells

  title={Vitamin D3 inhibits fatty acid synthase expression by stimulating the expression of long‐chain fatty‐acid‐CoA ligase 3 in prostate cancer cells},
  author={Shengjun Qiao and Pentti Tuohimaa},
  journal={FEBS Letters},
Expression and vitamin D3 regulation of long-chain fatty-acid-CoA ligase 3 in human prostate cancer cells.
Vitamin D regulation of energy metabolism in cancer
Mechanisms involved in energy metabolism regulation are an emerging area in which vitamin D may inhibit multiple stages of cancer progression, as well as oxidative stress protection, as it is closely associated with energy metabolism.
Remodeling of phospholipid composition in colon cancer cells by 1α,25(OH)2D3 and its analogs
Therapeutic and toxicologic evaluation of anti-lipogenic agents in cancer cells compared with non-neoplastic cells.
DNA fragmentation analysis suggests that FASN inhibitors induced apoptotic DNA damage in retinoblastoma cells, suggesting that FasN inhibition can be an effective strategy in ret inoblastomas therapy.
Soluble fatty acid synthase relates to bone biomarkers in prepubertal children
Circulating soluble FASN relates to both adipose tissue and bone biomarkers in prepubertal children, with associations that are dependent on Vit D concentrations, which suggest that FASn may participate in the crosstalk between fat and bone metabolism.
Cerulenin-mediated apoptosis is involved in adenine metabolic pathway.
The lipogenesis pathway as a cancer target.
  • H. Abramson
  • Biology, Chemistry
    Journal of medicinal chemistry
  • 2011
The objectives of this Perspective are to provide an overview of the lipogenic process, primarily as it relates to these three enzymes, examine the relationship of lipogenesis to tumor biology, and outline the opportunities and prospects for targeting the process in the search for new anticancer drugs.
Chemopreventive Effects of Dietary Selenium and Soy Isoflavones in a Mouse Model of Prostate Cancer
This study identifies a previously unknown effect of isoflavones in the upregulation of FOXO expression and confirms previous studies of is oflavones’anticancer effects.
Global liver proteome analysis using iTRAQ labeling quantitative proteomic technology to reveal biomarkers in mice exposed to perfluorooctane sulfonate (PFOS).
Insight is provided into the molecular mechanism and biomarkers for PFOS-induced effects of liver proteome characterization in mice exposed to perfluorooctane sulfonate.


Selective activation of the fatty acid synthesis pathway in human prostate cancer
It is reported that in prostate cancer fatty acid synthase expression is up‐regulated at the mRNA level together with other enzymes of the same metabolic pathway, pointing to selective activation of the fatty acid synthesis pathway and suggesting a shift in the balance of lipogenic gene expression in a subgroup of prostate cancers.
RNA interference-mediated silencing of the fatty acid synthase gene attenuates growth and induces morphological changes and apoptosis of LNCaP prostate cancer cells.
Silencing of the FASE gene by RNAi significantly inhibited LNCaP cell growth and ultimately resulted in induction of apoptosis, indicating that RNAi opens new avenues toward the study of the role of FASE overexpression in tumor cells and provides an interesting and selective alternative in the development of antineoplastic therapy.
Overexpression of fatty acid synthase is an early and common event in the development of prostate cancer
Findings indicate that increased FAS expression is one of the earliest and most common events in the development of prostate cancer, suggesting that FAS may be used as a general prostate cancer marker and that antineoplastic therapy based on FAS inhibition may be an option for chemoprevention or curative treatment for nearly all prostate cancers.
Regulation of fatty acid synthesis in isolated hepatocytes. Evidence for a physiological role for long chain fatty acyl coenzyme A and citrate.
  • A. Goodridge
  • Biology, Computer Science
    The Journal of biological chemistry
  • 1973
Abstract In isolated hepatocytes prepared from unfed neonatal chicks, stimulation of fatty acid synthesis by fructose or dihydroxyacetone required acetate or octanoate in the medium, suggesting that
Role of long-chain fatty acyl-CoA esters in the regulation of metabolism and in cell signalling.
The intracellular concentration of free unbound acyl-CoA esters is tightly controlled by feedback inhibition of the acyl-CoA synthetase and is buffered by specific acyl-CoA binding proteins.
Mechanism responsible for 5-(tetradecyloxy)-2-furoic acid inhibition of hepatic lipogenesis.
It is proposed that many of the metabolic effects of TOFA can be explained by TOFyl- coA inhibition of acetyl-CoA carboxylase, which stimulates fatty acid oxidation and ketogenesis by relieving the inhibition on carnltine acyltransferase I.