Evidence map›Paper›PMID 26310932›Full record

ArticleCancer science2015

Retinoid X receptor α enhances human cholangiocarcinoma growth through simultaneous activation of Wnt/β-catenin and nuclear factor-κB pathways.

Gui-Li Huang, Wei Zhang, Hong-Yue Ren, Xue-Ying Shen, Qing-Xi Chen, Dong-Yan Shen

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Triorganotin compounds as emerging nuclear retinoid X receptor ligands and their implications in cancer.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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

6 authors at 2 institutions in 1 country.

Gui-Li HuangState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Wei ZhangDivision of Xiamen Diabetes Institute, The First Affiliated Hospital of Xiamen University, Xiamen, China.
Hong-Yue RenDivision of Biobank, The First Affiliated Hospital of Xiamen University, Xiamen, China.
Xue-Ying ShenState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Qing-Xi ChenState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Dong-Yan ShenDivision of Biobank, The First Affiliated Hospital of Xiamen University, Xiamen, China.
Xiamen University · CNFirst Affiliated Hospital of Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoid X receptor α (RXRα) plays important roles in the malignancy of several cancers such as human prostate tumor, breast cancer, and thyroid tumor. However, its exact functions and molecular mechanisms in cholangiocarcinoma (CCA), a chemoresistant carcinoma with poor prognosis, remain unclear. In this study we found that RXRα was frequently overexpressed in human CCA tissues and CCA cell lines. Downregulation of RXRα led to decreased expression of mitosis-promoting factors including cyclin D1and cyclin E, and the proliferating cell nuclear antigen, as well as increased expression of cell cycle inhibitor p21, resulting in inhibition of CCA cell proliferation. Furthermore, RXRα knockdown attenuated the expression of cyclin D1 through suppression of Wnt/β-catenin signaling. Retinoid X receptor α upregulated proliferating cell nuclear antigen expression through nuclear factor-κB (NF-κB) pathways, paralleled with downregulation of p21. Thus, the Wnt/β-catenin and NF-κB pathways account for the inhibition of CCA cell growth induced by RXRα downregulation. Retinoid X receptor α plays an important role in proliferation of CCA through simultaneous activation of Wnt/β-catenin and NF-κB pathways, indicating that RXRα might serve as a potential molecular target for CCA treatment.

Indexed as

AdultAgedAged, 80 and overbeta CateninBile Duct NeoplasmsBlotting, WesternCell Line, TumorCell ProliferationCell SurvivalCholangiocarcinomaFemaleFlow CytometryFluorescent Antibody TechniqueHumansImmunohistochemistryMalebeta CateninCTNNB1 protein, humanNF-kappa BRetinoid X Receptor alphaWnt ProteinsCholangiocarcinomaNF-κBproliferationretinoid X receptor αβ-catenin

Identifiers

PMID26310932
PMCPMC4714697
OpenAlexW1981803982

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.