Evidence map›Paper›PMID 29357008›Full record

ReviewJournal of cell communication and signaling2018

Matricellular CCN6 (WISP3) protein: a tumor suppressor for mammary metaplastic carcinomas.

Mai N Tran, Celina G Kleer

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of cell communication and signaling, 2018. 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
0.9field-weighted citation impact, top 26% 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, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Molecular Consequences ofInternational journal of molecular sciences · 2025
    Article
  4. Article
  5. Matricellular proteins: Potential biomarkers in head and neck cancer.Journal of cell communication and signaling · 2024
    Review
  6. CCN proteins: opportunities for clinical studies-a personal perspective.Journal of cell communication and signaling · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. The CCN axis in cancer development and progression.Journal of cell communication and signaling · 2021
    Review
  12. Review
  13. Review
  14. Review
  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

2 authors at 1 institution in 1 country.

Mai N TranDepartment of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Celina G KleerDepartment of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI, 48109, USA. kleer@umich.edu.
University of Michigan–Ann Arbor · US

Funding

Role of CCN6 (WISP3) in the Progression and Metastasis of Breast Cancer.R01CA125577 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Celina G Kleer · 2008 to 2026
$5.5M
National Cancer Institute R01 CA125577NCI NIH HHS R01 CA125577
6 · The paper itself

Abstract

Located at 6q22-23, Ccn6 (WISP3) encodes for a matrix-associated protein of the CCN family, characterized by regulatory, rather than structural, roles in development and cancer. CCN6, the least studied member of the CCN family, shares the conserved multimodular structure of CCN proteins, as well as their tissue and cell-type specific functions. In the breast, CCN6 is a critical regulator of epithelial-to-mesenchymal transitions (EMT) and tumor initiating cells. Studies using human breast cancer tissue samples demonstrated that CCN6 messenger RNA and protein are expressed in normal breast epithelia but reduced or lost in aggressive breast cancer phenotypes, especially inflammatory breast cancer and metaplastic carcinomas. Metaplastic carcinomas are mesenchymal-like triple negative breast carcinomas, enriched for markers of EMT and stemness. RNAseq analyses of the TCGA Breast Cancer cohort show reduced CCN6 expression in approximately 50% of metaplastic carcinomas compared to normal breast. Our group identified frameshift mutations of Ccn6 in a subset of human metaplastic breast carcinoma. Importantly, conditional, mammary epithelial-cell specific ccn6 (wisp3) knockout mice develop invasive high-grade mammary carcinomas that recapitulate human spindle cell metaplastic carcinomas, demonstrating a tumor suppressor function for ccn6. Our studies on CCN6 functions in metaplastic carcinoma highlight the potential of CCN6 as a novel therapeutic approach for this specific type of breast cancer.

Indexed as

Breast cancerCCN6EMTEpithelial to mesenchymalKnockout mouseMetaplasticMMTV-creSpindle cellStem cellsWISP3

Identifiers

PMID29357008
PMCPMC5842205
OpenAlexW2788982151

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.