Evidence map›Paper›PMID 25499541›Full record

ArticleJournal of experimental & clinical cancer research : CR2014

Wnt3a expression is associated with epithelial-mesenchymal transition and promotes colon cancer progression.

Lisha Qi, Baocun Sun, Zhiyong Liu, Runfen Cheng, Yixian Li, Xiulan Zhao

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

81 citing papers in PubMed, 122 citations in OpenAlex.

  1. Article
  2. WNT3a induces external anal sphincter fibrosis and dysfunction in rabbits.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Evolutionary conservation and cancer implications of the WNT signaling pathway.Medical oncology (Northwood, London, England) · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Wnt3a is a promising target in colorectal cancer.Medical oncology (Northwood, London, England) · 2023
    Review
  19. Review
  20. Article

21 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

6 authors at 2 institutions in 1 country.

Lisha QiDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China. qilisha2005@163.com.
Baocun SunDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China. sunbaocun2014@163.com.
Zhiyong LiuDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China. liuzhiyong@tjmuch.com.
Runfen ChengDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China. chengrunfen@163.com.
Yixian LiDepartment of Pathology, Tianjin Medical University, Tianjin, 300070, China. liyixian89@163.com.
Xiulan ZhaoDepartment of Pathology, Tianjin Medical University, Tianjin, 300070, China. zhaoxiulan2014@163.com.
Tianjin Medical University Cancer Institute and Hospital · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionEpithelial-mesenchymal transition (EMT) contributes to the progression and metastasis of cancer cells and is associated with a more invasive phenotype of cancer. The Wnt/β-catenin signaling pathway is one of the major pathways involved in EMT regulation. Many studies provide evidence that β-catenin, the key regulator of the canonical Wnt signaling pathway, is important in regulating EMT in cancer. However, the roles of Wnt3a, the representative canonical Wnt ligand, in EMT and colon cancer progression have not yet been fully explored.

methodsThe expression levels of Wnt3a and EMT-associated proteins (E-cadherin, vimentin, and β-catenin) were assessed by immunohistochemistry in human colon cancer tissues to evaluate the clinicopathological significance of Wnt3a, as well as the correlation between Wnt3a and EMT. We then upregulated Wnt3a expression in HCT116 colon cancer cells, established a nude mouse xenograft model, detected the expression of EMT and Wnt/β-catenin signaling-associated proteins, and observed invasion and clone-initiating abilities.

resultsIn 203 human colon cancer tissue samples, Wnt3a protein overexpression was related to colon cancer histological differentiation (P = 0.004), clinical stage (P = 0.008), presence of metastasis and recurrence (P = 0.036), and survival time (P = 0.007) of colon cancer patients. Wnt3a expression was notably concomitant with EMT immunohistochemical features, such as reduced expression of the epithelial marker E-cadherin (P = 0.012), increased expression of the mesenchymal marker vimentin (P = 0.002), and cytoplasmic distribution of β-catenin (P = 0.021). Results of in vitro and in vivo experiments showed that Wnt3a overexpression could alter cell morphology, regulate EMT-associated protein expression, and enhance clone-initiation and invasion. Dkk1 (antagonist of Wnt/β-catenin signaling) could also partially reverse the expression of EMT-associated proteins in Wnt3a-overexpressing cells.

conclusionsWnt3a expression was associated with EMT and promoted colon cancer progression. The EMT-inducing effect was partially due to the stimulative effect of Wnt3a on the Wnt/β-catenin pathway.

Indexed as

Epithelial-Mesenchymal TransitionWnt Signaling PathwayAdultAnimalsAntigens, CDbeta CateninCadherinsColonic NeoplasmsDisease ProgressionFemaleHCT116 CellsHumansKaplan-Meier EstimateMaleMice, NudeMiddle AgedAntigens, CDbeta CateninCadherinsCDH1 protein, humanCTNNB1 protein, humanVimentinWnt3A ProteinWNT3A protein, human

Identifiers

PMID25499541
PMCPMC4269867
OpenAlexW2133208956

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.