Evidence map›Paper›PMID 19520495›Full record

ReviewCancer letters2010

Molecular mechanisms involved in farnesol-induced apoptosis.

Joung Hyuck Joo, Anton M Jetten

Open access · greenAbstract readReview
In one paragraph

Review in Cancer letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
6.0field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

70 citing papers in PubMed, 193 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
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  7. Review
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  9. Physiological adventures inMicrobiology and molecular biology reviews : MMBR · 2024
    Review
  10. Article
  11. Article
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  15. Article
  16. Biological effects ofFrontiers in cellular and infection microbiology · 2023
    Article
  17. Review
  18. Article
  19. Article
  20. Article

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Joung Hyuck JooCell Biology Section, LRB, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, United States.
Anton M Jetten
National Institutes of Health · US

Funding

Nuclear receptors: action, functions, and roles in diseaseZIAES101586 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI JETTEN, ANTON M · 2009 to 2025
$13.5M
Nuclear receptors--Action, functions, &roles in diseaseZ01ES101586 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI JETTEN, ANTON M · 2003 to 2008
$3.2M
Intramural NIH HHS Z01 ES101586
6 · The paper itself

Abstract

The isoprenoid alcohol farnesol is an effective inducer of cell cycle arrest and apoptosis in a variety of carcinoma cell types. In addition, farnesol has been reported to inhibit tumorigenesis in several animal models suggesting that it functions as a chemopreventative and anti-tumor agent in vivo. A number of different biochemical and cellular processes have been implicated in the growth-inhibitory and apoptosis-inducing effects of farnesol. These include regulation of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase and CTP:phosphocholine cytidylyltransferase alpha (CCTalpha), rate-limiting enzymes in the mevalonate pathway and phosphatidylcholine biosynthesis, respectively, and the generation of reactive oxygen species. In some cell types the action of farnesol is mediated through nuclear receptors, including activation of farnesoid X receptor (FXR) and peroxisome proliferator-activated receptors (PPARs). Recent studies have revealed that induction of endoplasmic reticulum (ER) stress and the subsequent activation of the unfolded protein response (UPR) play a critical role in the induction of apoptosis by farnesol in lung carcinoma cells. This induction was found to be dependent on the activation of the MEK1/2-ERK1/2 pathway. In addition, farnesol induces activation of the NF-kappaB signaling pathway and a number of NF-kappaB target genes. Optimal activation of NF-kappaB was reported to depend on the phosphorylation of p65/RelA by the MEK1/2-MSK1 signaling pathway. In a number of cells farnesol-induced apoptosis was found to be linked to activation of the apoptosome. This review provides an overview of the biochemical and cellular processes regulated by farnesol in relationship to its growth-inhibitory, apoptosis-promoting, and anti-tumor effects.

Indexed as

ApoptosisSignal TransductionAnimalsAntineoplastic AgentsApoptosomesCell ProliferationCytidine Diphosphate CholineEndoplasmic ReticulumFarnesolHumansHydroxymethylglutaryl CoA ReductasesMitogen-Activated Protein KinasesNeoplasmsNF-kappa BOxidative StressPPAR gammaAntineoplastic AgentsApoptosomesCytidine Diphosphate CholineFarnesolHydroxymethylglutaryl CoA ReductasesMitogen-Activated Protein KinasesNF-kappa BPPAR gammaReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearThyroid Hormone Receptors beta

Identifiers

PMID19520495
PMCPMC2815016
OpenAlexW1970835750

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.