Evidence map›Paper›PMID 21424122›Full record

ArticleInternational journal of oncology2011

Nuclear receptor CAR-regulated expression of the FAM84A gene during the development of mouse liver tumors.

Hiroki Kamino, Yuichi Yamazaki, Kosuke Saito, Daichi Takizawa, Satoru Kakizaki, Rick Moore, Masahiko Negishi

Open access · bronzeAbstract read
In one paragraph

Article in International journal of oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Targeting of the mNature communications · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Clinical Relevance of the Constitutive Androstane Receptor.Drug metabolism and disposition: the biological fate of chemicals · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. The Roles of Xenobiotic Receptors: Beyond Chemical Disposition.Drug metabolism and disposition: the biological fate of chemicals · 2018
    Review
  11. Article
  12. Article
  13. Review
  14. Review
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

7 authors at 1 institution in 1 country.

Hiroki KaminoLaboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Yuichi Yamazaki
Kosuke Saito
Daichi Takizawa
Satoru Kakizaki
Rick Moore
Masahiko Negishi
National Institutes of Health · US

Funding

Mechanisms and biological consequences of the nuclear receptor CAR activationZIAES080040 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI NEGISHI, MASAHIKO · 2009 to 2020
$35.3M
Pharmacogenetics Of Microsomal Steroid HydroxylasesZ01ES080040 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI NEGISHI, MASAHIKO · 1985 to 2008
$5.7M
Intramural NIH HHS Z01 ES080040NIEHS NIH HHS Z01ES1005-01
6 · The paper itself

Abstract

The nuclear xenobiotic receptor CAR is a phenobarbital (PB)-activated transcription factor. Using a mouse model of two-step liver tumorigenesis, in which tumor growth was initiated by diethyl nitrosamine (DEN) and promoted by chronic treatment with PB, we previously demonstrated that tumors developed only in the presence of CAR. Here, we have identified the FAM84A (family with sequence similarity 84, member A) gene as a CAR-regulated gene that is over-expressed during development of phenobarbital-promoted mouse liver tumors. FAM84A mRNA was induced in the liver of DEN/PB-treated mice prior to the development of liver tumors and this induction continued in the non-tumor as well as tumor tissues of a tumor-bearing liver. Western blotting demonstated that FAM84A protein expression increased in mouse liver after PB treatment; however, the FAM84A protein in liver and liver tumors was not phosphorylated at the serine 38 residue, which has been reported to correlate with morphological changes in cells. Immunohistochemistry analysis revealed the cytoplasmic localization of FAM84A protein and its expression during tumor development in normal tissues (especially in hepatocytes around the central vein), eosinophilic foci, adenomas and carcinomas. HepG2 cell-based reporter assays indicated that CAR activated the FAM84A promoter. Exogenous over-expression of FAM84A in HepG2 cells resulted in increased cell migration. The physiological function of FAM84A remains unknown, but our results suggest that FAM84A is up-regulated by CAR during the development of liver tumors, and may play an important role in the progression of liver cancer by increasing cell migration.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCell Line, TumorCell MovementConstitutive Androstane ReceptorDisease Models, AnimalFemaleGABA ModulatorsHep G2 CellsHumansLiverLiver Neoplasms, ExperimentalMaleMiceMice, Inbred C3HMice, Inbred C57BLConstitutive Androstane ReceptorGABA ModulatorsNeoplasm ProteinsPhenobarbitalReceptors, Cytoplasmic and Nuclear

Identifiers

PMID21424122
PMCPMC3176583
OpenAlexW1990797384

What OpenQuestion holds

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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.