Evidence map›Paper›PMID 31988451›Full record

ArticleOncogene2020

FAK signaling in cancer-associated fibroblasts promotes breast cancer cell migration and metastasis by exosomal miRNAs-mediated intercellular communication.

Hsin-Jung Wu, Mingang Hao, Syn Kok Yeo, Jun-Lin Guan

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
9.3field-weighted citation impact, top 1% 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

106 citing papers in PubMed, 174 citations in OpenAlex.

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  8. PDPNCell communication and signaling : CCS · 2025
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46 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

4 authors at 2 institutions in 1 country.

Hsin-Jung Wu *Department of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Mingang Hao *Department of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Syn Kok YeoDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.ORCID http://orcid.org/0000-0002-4333-2510
Jun-Lin GuanDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA. guanjl@uc.edu.
University of Cincinnati Medical Center · USUniversity of Cincinnati · US

Funding

Mechanisms of progression of vascular malformation to lymphangiosarcomaR01HL073394 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUAN, JUN-LIN · 2003 to 2025
$8.4M
Regulation of Neural Stem Cells and Neurogenesis by Autophagy GenesR01NS094144 · NINDS · UNIVERSITY OF CINCINNATI · PI GUAN, JUN-LIN · 2015 to 2024
$3.6M
Mechanisms of FIP200 regulation of breast cancer through its autophagy and non-autophagy functionsR01CA211066 · NCI · UNIVERSITY OF CINCINNATI · PI JUN-LIN GUAN · 2017 to 2026
$3.4M
Genetic Analysis of FAK kinase and scaffold functions in breast cancerR01CA163493 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUAN, JUN-LIN · 2012 to 2016
$1.6M
NCI NIH HHS R01 CA163493NCI NIH HHS R01 CA211066NHLBI NIH HHS R01 HL073394NINDS NIH HHS R01 NS094144
6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAFs) are activated fibroblasts that constitute the major components of tumor microenvironment (TME) and play crucial roles in tumor development and metastasis. Here, we generated fibroblast-specific inducible focal adhesion kinase (FAK) knockout (cKO) mice in a breast cancer model to study potential role and mechanisms of FAK signaling in CAF to promote breast cancer metastasis in vivo. While not affecting primary tumor development and growth, FAK deletion significantly suppressed breast cancer metastasis in vivo. Analyses of CAFs derived from cKO mice as well as human CAFs showed that FAK is required for their activity to promote mammary tumor cell migration. We further showed that FAK ablation in CAFs decreased exosome functions to promote tumor cell migration and other activities, which could contribute to the reduced metastasis observed in cKO mice. Lastly, profiling of miRs from CAF exosomes showed alterations of several exosomal miRs in FAK-null CAFs, and further analysis suggested that miR-16 and miR-148a enriched in exosomes from FAK-null CAFs contribute to the reduced tumor cell activities and metastasis. Together, these results identify a new role for FAK signaling in CAFs that regulate their intercellular communication with tumor cells to promote breast cancer metastasis.

Indexed as

Cell MovementNeoplasm MetastasisAnimalsBreast NeoplasmsCancer-Associated FibroblastsCell CommunicationCell Line, TumorExosomesFemaleFocal Adhesion Kinase 1HumansMiceMice, KnockoutMicroRNAsNeoplastic Cells, CirculatingSignal TransductionFocal Adhesion Kinase 1MicroRNAsPTK2 protein, humanPtk2 protein, mouse

Identifiers

PMID31988451
PMCPMC7310603
OpenAlexW3003958110

What OpenQuestion holds

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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.