Evidence map›Paper›PMID 27613407›Full record

ArticleJournal of cell communication and signaling2016

A potential role for CCN2/CTGF in aggressive colorectal cancer.

Inge Ubink, Elisha R Verhaar, Onno Kranenburg, Roel Goldschmeding

Open access · hybridAbstract read
In one paragraph

Article in Journal of cell communication and signaling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 33 citations in OpenAlex.

  1. THAP7-AS1 orchestrates IGF2BP3-mAmerican journal of cancer research · 2026
    Article
  2. Article
  3. Article
  4. Integrating plasma proteome with genome reveals novel protein biomarkers in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The CCN axis in cancer development and progression.Journal of cell communication and signaling · 2021
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Caffeine and its main targets of colorectal cancer.World journal of gastrointestinal oncology · 2020
    Review
  16. The Microenvironment of Tongue Cancer.Advances in experimental medicine and biology · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. The Role of SATB1 in Tumour Progression and Metastasis.International journal of molecular sciences · 2019
    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

4 authors at 2 institutions in 2 countries.

Inge UbinkCancer Center, University Medical Center Utrecht, Heidelberglaan 100, 3584CX, Utrecht, The Netherlands.
Elisha R VerhaarDepartment of Pathology, University Medical Center Utrecht, Heidelberglaan 100, 3584CX, Utrecht, The Netherlands.
Onno KranenburgCancer Center, University Medical Center Utrecht, Heidelberglaan 100, 3584CX, Utrecht, The Netherlands.
Roel GoldschmedingDepartment of Pathology, University Medical Center Utrecht, Heidelberglaan 100, 3584CX, Utrecht, The Netherlands. r.goldschmeding@umcutrecht.nl.ORCID http://orcid.org/0000-0002-5471-1153
Heidelberg University · DEUtrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CCN2, also known as connective tissue growth factor (CTGF) is a transcriptional target of TGF-β signaling. Unlike its original name ("CTGF") suggested, CCN2 is not an actual growth factor but a matricellular protein that plays an important role in fibrosis, inflammation and connective tissue remodeling in a variety of diseases, including cancer. In pancreatic ductal adenocarcinoma, CCN2 signaling induces stromal infiltration and facilitates a strong tumor-stromal interaction. In many types of cancer, CCN2 overexpression has been associated with poor outcome. CMS4 (Consensus Molecular Subtype 4) is a recently identified aggressive colorectal cancer subtype, that is characterized by up-regulation of genes involved in epithelial-to-mesenchymal transition, TGF-β signaling, angiogenesis, complement activation, and extracellular matrix remodeling. In addition, a high influx of stromal fibroblasts contributes to the mesenchymal-like gene expression profile of this subtype. Furthermore, compared with the other three CMS groups, CMS4 tumors have the worst prognosis. Based on these observations, we postulated that CCN2 might contribute to colorectal cancer progression, especially in the CMS4 subtype. This review discusses the available literature on the role of CCN2 in colorectal cancer, with a focus on the 'fibrotic subtype' CMS4.

Indexed as

CCN2Colorectal cancerConnective tissue growth factorFibrosis

Identifiers

PMID27613407
PMCPMC5055504
OpenAlexW2518234399

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.