Evidence map›Paper›PMID 27698922›Full record

ArticleJournal of Cancer2016

Potential Function of Exogenous Vimentin on the Activation of Wnt Signaling Pathway in Cancer Cells.

Arun Satelli, Jiemiao Hu, Xueqing Xia, Shulin Li

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Extracellular vimentin amplifies inflammation: Perspectives for immune injury and therapeutics for periodontitis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
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  6. Circulating Vimentin Over-Expression in Patients with Oral Sub Mucosal Fibrosis and Oral Squamous Cell Carcinoma.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2022
    Article
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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 1 institution in 1 country.

Arun SatelliDepartment of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Jiemiao HuDepartment of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Xueqing XiaDepartment of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Shulin LiDepartment of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas;; The University of Texas Graduate School of Biomedical Sciences, Houston, Texas.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Gene-Product Auto-Targeting to Tumor VesselsR01CA120895 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LI, SHULIN · 2007 to 2025
$4.8M
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA120895
6 · The paper itself

Abstract

Cancer cell signaling, growth, morphology, proliferation and tumorigenic potential are largely depending on the signaling molecules present naturally in the tumor microenvironment and the identification of key molecules that drive the tumor progression is critical for the development of new modalities for the prevention of tumor progression. High concentrations of vimentin in the blood of cancer patients have been reported, however the function of blood circulating vimentin remains unknown. Here, we investigated the functional role of exogenously supplemented vimentin on colon cancer cells and examined the Wnt Signaling activation and cancer cell invasion. Vimentin when supplemented to the cancer cells remained bound to the surface of the cancer cells. Furthermore, bound vimentin activates Wnt signaling pathway as detectable by increased β-catenin accumulation in the nucleus with concomitant activation of β-catenin-dependent transcription of Wnt signaling downstream targets. Functionally, there was an increase in the rate of cellular invasion in these cancer cells upon binding with vimentin. Our results thus suggest that free vimentin in the tumor microenvironment acts as a positive regulator of the β-catenin signaling pathway, thus providing a basis for cancer invasive properties.

Indexed as

EMTinvasionVimentinWnt Signalingβ-catenin.

Identifiers

PMID27698922
PMCPMC5039366
OpenAlexW2513954847

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.