Evidence map›Paper›PMID 32256977›Full record

ArticleOncotarget2020

Cancer associated fibroblasts confer shear resistance to circulating tumor cells during prostate cancer metastatic progression.

Nerymar Ortiz-Otero, Andrea B Clinch, Jacob Hope, Wenjun Wang, Cynthia A Reinhart-King, Michael R King

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 85 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Nerymar Ortiz-OteroMeinig School of Biomedical Engineering, Cornell University, Ithaca, NY 14850, USA.
Andrea B ClinchDepartment of Biomedical Engineering, Vanderbilt University, Nashville, TN 37202, USA.
Jacob HopeDepartment of Biomedical Engineering, Vanderbilt University, Nashville, TN 37202, USA.
Wenjun WangDepartment of Biomedical Engineering, Vanderbilt University, Nashville, TN 37202, USA.
Cynthia A Reinhart-KingDepartment of Biomedical Engineering, Vanderbilt University, Nashville, TN 37202, USA.
Michael R KingDepartment of Biomedical Engineering, Vanderbilt University, Nashville, TN 37202, USA.
Vanderbilt University · USCornell University · US

Funding

Super Natural Killer Cells That Target Metastases in the Tumor-Draining Lymph NodesR01CA203991 · NCI · VANDERBILT UNIVERSITY · PI KING, MICHAEL R. · 2017 to 2021
$1.9M
NCI NIH HHS R01 CA203991
6 · The paper itself

Abstract

Previous studies have demonstrated that CTCs do not travel in the bloodstream alone, but rather are accompanied by clusters of stromal cells such as cancer associated fibroblasts (CAFs). Our laboratory has confirmed the presence of CAFs in the peripheral blood of prostate cancer (PC) patients. The observation that CAFs disseminate with CTCs prompts the examination of the role of CAFs in CTC survival under physiological shear stress during the dissemination process using a clinically relevant, three-dimensional (3D) co-culture model. In this study, we found that "reactive CAFs" induce shear resistance to prostate tumor cells via intercellular contact and soluble derived factors. In addition, these reactive CAFs conserve the proliferative capability of tumor cells in the presence of high magnitude fluid shear stress (FSS). This reactive CAF phenotype emerges from normal fibroblasts (NF), which take on the CAF phenotype when co-cultured with tumor cells. The reactive CAFs showed higher expression of α-smooth muscle actin (α-SMA) and fibroblast activation protein (FAP) compared to differentiated CAFs, when co-cultured with PC cells at the same experimental conditions. Together, we found that the activation mechanism of NF to CAF comprises different stages that progress from a reactive to quiescent cellular state in which these two states are differentiated by the fluctuation of intensity in CAF markers. Here we determined that a reactive state of CAFs proved to be important for supporting tumor cell survival and proliferation. These findings suggest the use of CAFs as a marker for cancer progression and a potential target for novel cancer therapeutics to treat metastatic disease.

Indexed as

cancer associated fibroblastscirculating tumor cellscollective migrationcytoprotectionmetastasis

Identifiers

PMID32256977
PMCPMC7105166
OpenAlexW3013825685

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.