Evidence map›Paper›PMID 21604185›Full record

ArticleClinical & experimental metastasis2011

Fibroblast activation protein-α promotes tumor growth and invasion of breast cancer cells through non-enzymatic functions.

Yan Huang, Avis E Simms, Anna Mazur, Sophie Wang, Noel R León, Barry Jones, Nazneen Aziz, Thomas Kelly

Abstract read
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Article in Clinical & experimental metastasis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

61 citing papers in PubMed, 110 citations in OpenAlex.

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1 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

8 authors at 3 institutions in 1 country.

Yan HuangDepartment of Pathology, Winthrop P. Rockefeller Cancer Institute, Arkansas Cancer Research Center, University of Arkansas for Medical Sciences, Little Rock, AR 72205-7199, USA.
Avis E Simms
Anna Mazur
Sophie Wang
Noel R León
Barry Jones
Nazneen Aziz
Thomas Kelly
Winthrop Rockefeller Foundation · USCancer Research Center · USUniversity of Arkansas for Medical Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast activation protein-α (FAP) is a cell surface, serine protease of the post-prolyl peptidase family that is expressed in human breast cancer but not in normal tissues. Previously, we showed that FAP expression increased tumor growth rates in a mouse model of human breast cancer. Here the role of the proteolytic activities of FAP in promoting tumor growth, matrix degradation and invasion was investigated. Mammary fat pads of female SCID mice were inoculated with breast cancer cells that express FAP and the mice treated with normal saline or Val-boroPro (talabostat); Glu-boroPro (PT-630); or 1-[[(3-hydroxy-1-adamantyl)amino]acetyl]-2-cyano-(S)-pyrrolidine (LAF-237) that inhibit prolyl peptidases. Other mice were injected with breast cancer cells expressing a catalytically inactive mutant of FAP and did not receive inhibitor treatment. PT-630 and LAF-237 did not slow growth of tumors produced by any of the three cell lines expressing FAP. Talabostat slightly decreased the growth rates of the FAP-expressing tumors but because PT-630 and LAF-237 did not, the growth retardation was likely not related to the inhibition of FAP or the related post-prolyl peptidase dipeptidyl peptidase IV. Breast cancer cells expressing a catalytically inactive mutant of FAP (FAP(S624A)) also produced tumors that grew rapidly. In vitro studies revealed that cells expressing wild type FAP or FAP(S624A) degrade extracellular matrix (ECM) more extensively, accumulate higher levels of matrix metalloproteinase-9 (MMP-9) in conditioned medium, are more invasive in type I collagen gels, and have altered signaling compared to control transfectants that do not express FAP and form slow growing tumors. We conclude that the proteolytic activity of FAP participates in matrix degradation, but other functions of the protein stimulate increased tumor growth.

Indexed as

AnimalsAntigens, NeoplasmBiomarkers, TumorBreast NeoplasmsCell Line, TumorCell ProliferationDipeptidyl Peptidase 4EndopeptidasesFemaleFibroblast Activation Protein AlphaGelatinasesGene Expression Regulation, NeoplasticHumansMembrane ProteinsMiceMice, Inbred BALB CAntigens, NeoplasmBiomarkers, TumorDipeptidyl Peptidase 4EndopeptidasesFibroblast Activation Protein AlphaGelatinasesMembrane ProteinsSerine Endopeptidases

Identifiers

PMID21604185
OpenAlexW1975987306

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.