Evidence map›Paper›PMID 35042959›Full record

ArticleOncogene2022

STAT3 induces breast cancer growth via ANGPTL4, MMP13 and STC1 secretion by cancer associated fibroblasts.

Lidia Avalle, Laura Raggi, Emanuele Monteleone, Aurora Savino, Daniele Viavattene, Luisa Statello, Andrea Camperi, Simona Aversano Stabile, Vincenzo Salemme, Niccolò De Marzo and 9 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
18.4field-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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026
    Review
  5. Multi-omics exploration of hypoxia in gastric cancer.World journal of surgical oncology · 2026
    Article
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12 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

19 authors at 5 institutions in 3 countries.

Lidia Avalle *Department of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy. lidia.avalle@unito.it.ORCID http://orcid.org/0000-0002-5060-633X
Laura Raggi *Department of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy.ORCID http://orcid.org/0000-0003-0809-9909
Emanuele Monteleone *Department of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy.ORCID http://orcid.org/0000-0001-7440-900X
Aurora Savino *Department of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy.ORCID http://orcid.org/0000-0002-0783-7191
Daniele ViavatteneDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy.ORCID http://orcid.org/0000-0002-6216-3986
Luisa StatelloDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy.ORCID http://orcid.org/0000-0001-8261-4214
Andrea CamperiDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy.
Simona Aversano StabileDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy.
Vincenzo SalemmeDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy.
Niccolò De MarzoDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy.
Francesca MarinoDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy.
Chiara GuglielmiDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy.
Andrea LobascioDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy.ORCID http://orcid.org/0000-0003-0065-5931
Cristina ZaniniBioAir SPA Scientific Department, Via Nizza, 52, 10126, Torino, Italy.ORCID http://orcid.org/0000-0002-6554-2113
Marco ForniBioAir SPA Scientific Department, Via Nizza, 52, 10126, Torino, Italy.
Danny IncarnatoDepartment of Life Sciences and Systems Biology, University of Torino, Via Nizza 52, 10126, Torino, Italy.ORCID http://orcid.org/0000-0003-3944-2327
Paola DefilippiDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy.ORCID http://orcid.org/0000-0001-6427-4906
Salvatore OlivieroDepartment of Life Sciences and Systems Biology, University of Torino, Via Nizza 52, 10126, Torino, Italy.ORCID http://orcid.org/0000-0002-3405-765X
Valeria PoliDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126, Torino, Italy. valeria.poli@unito.it.ORCID http://orcid.org/0000-0002-3739-3966
University of Turin · ITAzienda Ospedaliera Universitaria Pisana · ITThe San Raffaele Telethon Institute for Gene Therapy · ITUniversity of Groningen · NLVita-Salute San Raffaele University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the tumor microenvironment, Cancer Associated Fibroblasts (CAFs) become activated by cancer cells and increase their secretory activity to produce soluble factors that contribute to tumor cells proliferation, invasion and dissemination to distant organs. The pro-tumorigenic transcription factor STAT3 and its canonical inducer, the pro-inflammatory cytokine IL-6, act conjunctly in a positive feedback loop that maintains high levels of IL-6 secretion and STAT3 activation in both tumor and stromal cells. Here, we demonstrate that STAT3 is essential for the pro-tumorigenic functions of murine breast cancer CAFs both in vitro and in vivo, and identify a STAT3 signature significantly enriched for genes encoding for secreted proteins. Among these, ANGPTL4, MMP13 and STC-1 were functionally validated as STAT3-dependent mediators of CAF pro-tumorigenic functions by different approaches. Both in vitro and in vivo CAFs activities were moreover impaired by MMP13 inhibition, supporting the feasibility of a therapeutic approach based on inhibiting STAT3-induced CAF-secreted proteins. The clinical potential of such an approach is supported by the observation that an equivalent CAF-STAT3 signature in humans is expressed at high levels in breast cancer stromal cells and characterizes patients with a shorter disease specific survival, including those with basal-like disease.

Indexed as

Breast NeoplasmsCancer-Associated FibroblastsAngiopoietin-Like Protein 4AnimalsCell Line, TumorFemaleFibroblastsGlycoproteinsHumansInterleukin-6Matrix Metalloproteinase 13MiceSignal TransductionSTAT3 Transcription FactorTumor MicroenvironmentAngiopoietin-Like Protein 4Angptl4 protein, mouseGlycoproteinsInterleukin-6Matrix Metalloproteinase 13Mmp13 protein, mouseSTAT3 protein, humanSTAT3 Transcription Factorteleocalcin

Identifiers

PMID35042959
OpenAlexW4205638247

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.