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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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

SHOWING 1-10 OF 30 REFERENCES
Induction of Androgen Receptor by 1α,25-Dihydroxyvitamin D3 and 9-cis Retinoic Acid in LNCaP Human Prostate Cancer Cells.
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
Data demonstrate that androgens, mediated by the androgen receptor, stimulate the expression and activity of FAS and suggest that stimulation of Fas activity represents at least part of the mechanism by which androgens induce the accumulation of neutral lipids in LNCaP cells.
Selective activation of the fatty acid synthesis pathway in human prostate cancer
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.
Fatty acid synthesis: a potential selective target for antineoplastic therapy.
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.
Fatty acid synthase (FAS): a target for cytotoxic antimetabolites in HL60 promyelocytic leukemia cells.
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.
Overexpression of fatty acid synthase is an early and common event in the development of prostate cancer
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.
Pharmacological inhibitors of mammalian fatty acid synthase suppress DNA replication and induce apoptosis in tumor cell lines.
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.
Inhibition of fatty acid synthesis induces programmed cell death in human breast cancer cells.
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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