Evidence map›Paper›PMID 22474109›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2012

Hepatocarcinogenesis in FXR-/- mice mimics human HCC progression that operates through HNF1α regulation of FXR expression.

Nian Liu, Zhipeng Meng, Guiyu Lou, Weiping Zhou, Xiaoqiong Wang, Yunfeng Zhang, Lisheng Zhang, Xiyong Liu, Yun Yen, Lily Lai and 4 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

65 citing papers in PubMed, 108 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Pleiotropic roles of FXR in liver and colorectal cancers.Molecular and cellular endocrinology · 2022
    Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review

5 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

14 authors at 6 institutions in 2 countries.

Nian LiuDivision of Gene Regulation and Drug Discovery, Beckman Research Institute, City of Hope National Medical Center, Duarte, California 91010, USA.
Zhipeng Meng
Guiyu Lou
Weiping Zhou
Xiaoqiong Wang
Yunfeng Zhang
Lisheng Zhang
Xiyong Liu
Yun Yen
Lily Lai
Barry M Forman
Zhonggao Xu
Rongzhen Xu
Wendong Huang
City Of Hope National Medical Center · USSecond Affiliated Hospital of Zhejiang University · CNArmy Medical University · CNSecond Affiliated Hospital of Jilin University · CNSecond Military Medical University · CNZhejiang University · CN

Funding

MiRNAs in hepatocellular carcinoma development and treatmentR01CA139158 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI HUANG, WENDONG, YU, HUA E · 2011 to 2021
$3.7M
NCI NIH HHS R01 CA139158NCI NIH HHS R01CA139158
6 · The paper itself

Abstract

Farnesoid X receptor (FXR) (nuclear receptor subfamily 1, group H, member 4) is a member of nuclear hormone receptor superfamily, which plays essential roles in metabolism of bile acids, lipid, and glucose. We previously showed spontaneously hepatocarcinogenesis in aged FXR(-/-) mice, but its relevance to human hepatocellular carcinoma (HCC) is unclear. Here, we report a systematical analysis of hepatocarcinogenesis in FXR(-/-) mice and FXR expression in human liver cancer. In this study, liver tissues obtained from FXR(-/-) and wild-type mice at different ages were compared by microarray gene profiling, histological staining, chemical analysis, and quantitative real-time PCR. Primary hepatic stellate cells and primary hepatocytes isolated from FXR(-/-) and wild-type mice were also analyzed and compared. The results showed that the altered genes in FXR(-/-) livers were mainly related to metabolism, inflammation, and fibrosis, which suggest that hepatocarcinogenesis in FXR(-/-) mice recapitulated the progression of human liver cancer. Indeed, FXR expression in human HCC was down-regulated compared with normal liver tissues. Furthermore, the proinflammatory cytokines, which were up-regulated in human HCC microenvironment, decreased FXR expression by inhibiting the transactivity of hepatic nuclear factor 1α on FXR gene promoter. Our study thereby demonstrates that the down-regulation of FXR has an important role in human hepatocarcinogenesis and FXR(-/-) mice provide a unique animal model for HCC study.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCarcinoma, HepatocellularCells, CulturedCytokinesDisease ProgressionFemaleGene Expression ProfilingHepatocyte Nuclear Factor 1-alphaHep G2 CellsHumansLiverLiver NeoplasmsMaleMiceMice, Inbred C57BLCytokinesHepatocyte Nuclear Factor 1-alphaNeoplasm ProteinsReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearRecombinant ProteinsRNA, Messenger

Identifiers

PMID22474109
PMCPMC3355555
OpenAlexW2011600366

What OpenQuestion holds

Textmetadata
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.