Inhibition of fatty acid synthase expression by 1α,25-dihydroxyvitamin D3 in prostate cancer cells

@article{Qiao2003InhibitionOF,
  title={Inhibition of fatty acid synthase expression by 1$\alpha$,25-dihydroxyvitamin D3 in prostate cancer cells},
  author={Shengjun Qiao and Pasi T. Pennanen and Nadja Nazarova and Yan-Ru Lou and Pentti Tuohimaa},
  journal={The Journal of Steroid Biochemistry and Molecular Biology},
  year={2003},
  volume={85},
  pages={1-8}
}
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28 Citations
Background Citations
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28 Citations

The impact of 1,25(OH)2D3 and its structural analogs on gene expression in cancer cells--a microarray approach.
TLDR
Upon comparison of the lists of genes regulated by 1,25(OH)2D3 in the different microarray studies, only a small set of individual genes were commonly regulated, among which are included 24-hydroxylase, growth arrest and DNA-damage-inducible protein, cathelicidin antimicrobial peptide and multiple cyclins.
Expression and vitamin D3 regulation of long-chain fatty-acid-CoA ligase 3 in human prostate cancer cells.
The role of long-chain fatty-acid-CoA ligase 3 in vitamin D3 and androgen control of prostate cancer LNCaP cell growth.
Regulation of cholesterol 25-hydroxylase expression by vitamin D3 metabolites in human prostate stromal cells.
Vitamin D, Lipid Metabolism and Prostate Cancer
TLDR
The data suggest that ch25h could be a vitamin D3 target gene and may partly mediate anti-proliferative action ofitamin D3 in human primary prostate stromal cells.
Remodeling of phospholipid composition in colon cancer cells by 1α,25(OH)2D3 and its analogs
Vitamin D3 inhibits fatty acid synthase expression by stimulating the expression of long‐chain fatty‐acid‐CoA ligase 3 in prostate cancer cells
Vitamin D regulation of energy metabolism in cancer
TLDR
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.
The role of Vitamin D3 metabolism in prostate cancer
Vitamin D and prostate cancer.
TLDR
Further research into the mechanisms of vitamin D action in prostate and identification of suitable analogs for use in vivo may lead to its use in the treatment or prevention of prostate cancer.
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References

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TLDR
The results demonstrate that growth inhibition of LNCaP cells by 1,25-(OH)2D3 and 9-cis RA is mediated by an AR-dependent mechanism and preceded by the induction of AR gene expression, which may have clinical implications in the treatment of prostate cancer.
1α,25-Dihydroxyvitamin D3 Inhibits Prostate Cancer Cell Growth by Androgen-Dependent and Androgen-Independent Mechanisms.
TLDR
1,25-(OH)2D3 causes significant growth inhibition in both MDA cell lines, greater (for 2b cells) or lesser ( for 2a cells) than that in the LNCaP cell line.
Androgens stimulate fatty acid synthase in the human prostate cancer cell line LNCaP.
TLDR
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TLDR
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.
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TLDR
Tumor cell lines with elevated fatty acid synthase showed commensurate increases in incorporation of [U-14C]acetate into acylglycerols demonstrating that fatty acids synthase increases occur in the context of overall increases in endogenous fatty acid synthesis.
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TLDR
It is demonstrated that malignant cells can retain dependence on endogenous fatty acid synthesis and sensitivity to FAS inhibitor in the presence of physiological fatty acid levels and thus support the notion that FAS inhibitors may be useful in treating cancer in vivo.
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TLDR
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.
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TLDR
The data suggest a direct linkage at a regulatory level, between fatty acid synthesis and DNA synthesis in proliferating tumor cells, as part of a larger effort to understand the immediate downstream effect of FAS inhibition that leads to apoptosis.
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TLDR
Cerulenin treatment of human breast cancer cells inhibits fatty acid synthesis within 6 h after exposure, that loss of clonogenic capacity occurs within the same interval, and that DNA fragmentation and morphological changes characteristic of apoptosis ensue.
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