Evidence map›Paper›PMID 23094073›Full record

ArticlePloS one2012

WNT10A plays an oncogenic role in renal cell carcinoma by activating WNT/β-catenin pathway.

Ren-Jun Hsu, Jar-Yi Ho, Tai-Lung Cha, Dah-Shyong Yu, Chieh-Lin Wu, Wei-Ping Huang, Pauling Chu, Ying-Hsin Chen, Jiann-Torng Chen, Cheng-Ping Yu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Paracrine activation of WNT/β-catenin pathway in uterine leiomyoma stem cells promotes tumor growth.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Expression of WNT10A in papillary thyroid carcinoma and its effect on cell proliferation, invasion, and metastasis.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Article
  8. Unleashing Wnts: Wnt Ligands Fuel Cancer Spread.Journal of cancer biology · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

10 authors at 2 institutions in 1 country.

Ren-Jun HsuTri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Jar-Yi Ho
Tai-Lung Cha
Dah-Shyong Yu
Chieh-Lin Wu
Wei-Ping Huang
Pauling Chu
Ying-Hsin Chen
Jiann-Torng Chen
Cheng-Ping Yu
Tri-Service General Hospital · TWNational Defense Medical Center · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal cell carcinoma (RCC) is a malignancy with poor prognosis. WNT/β-catenin signaling dysregulation, especially β-catenin overactivation and WNT antagonist silencing, is associated with RCC carcinogenesis and progression. However, the role of WNT ligands in RCC has not yet been determined. We screened 19 WNT ligands from normal kidney and RCC cell lines and tissues and found that WNT10A was significantly increased in RCC cell lines and tissues as compared to that in normal controls. The clinical significance of increase in WNT10A was evaluated by performing an immunohistochemical association study in a 19-year follow-up cohort comprising 284 RCC and 267 benign renal disease (BRD) patients. The results of this study showed that WNT10A was dramatically upregulated in RCC tissues as compared to that in BRD tissues. This result suggests that WNT10A, nuclear β-catenin, and nuclear cyclin D1 act as independent risk factors for RCC carcinogenesis and progression, with accumulative risk effects. Molecular validation of cell line models with gain- or loss-of-function designs showed that forced WNT10A expression induced RCC cell proliferation and aggressiveness, including higher chemoresistance, cell migration, invasiveness, and cell transformation, due to the activation of β-catenin-dependent signaling. Conversely, WNT10A siRNA knockdown decreased cell proliferation and aggressiveness of RCC cells. In conclusion, we showed that WNT10A acts as an autocrine oncogene both in RCC carcinogenesis and progression by activating WNT/β-catenin signaling.

Indexed as

Gene Expression Regulation, NeoplasticAdultbeta CateninCarcinoma, Renal CellCell Line, TumorCell NucleusCell ProliferationCell Transformation, NeoplasticCyclin D1Disease ProgressionFemaleFollow-Up StudiesHumansKidneyKidney NeoplasmsMalebeta CateninCyclin D1RNA, Small InterferingWNT10A protein, humanWnt Proteins

Identifiers

PMID23094073
PMCPMC3477117
OpenAlexW2034029871

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.