Evidence map›Paper›PMID 35260882›Full record

ArticleCancer research2022

Chemotherapy-Induced Collagen IV Drives Cancer Cell Motility through Activation of Src and Focal Adhesion Kinase.

Jackson P Fatherree, Justinne R Guarin, Rachel A McGinn, Stephen P Naber, Madeleine J Oudin

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
9.8field-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

46 citing papers in PubMed, 72 citations in OpenAlex.

  1. Biomimetic Scaffold-Based 3D Models for Decoding Cancer Biology and Advancing Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  8. The Duality of Collagens in Metastases of Solid Tumors.International journal of molecular sciences · 2025
    Review
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  11. Sequential drug release system: Targeting the tumor ECM for enhanced chemotherapy efficacy.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

5 authors at 2 institutions in 1 country.

Jackson P FatherreeDepartment of Biomedical Engineering, Tufts School of Engineering, Tufts University, Medford, Massachusetts.ORCID 0000-0003-0316-0643
Justinne R GuarinDepartment of Biomedical Engineering, Tufts School of Engineering, Tufts University, Medford, Massachusetts.ORCID 0000-0002-4373-9679
Rachel A McGinnDepartment of Biomedical Engineering, Tufts School of Engineering, Tufts University, Medford, Massachusetts.ORCID 0000-0002-2340-3318
Stephen P NaberDepartment of Pathology and Laboratory Medicine, Tufts Medical Center, Boston, Massachusetts.
Madeleine J OudinDepartment of Biomedical Engineering, Tufts School of Engineering, Tufts University, Medford, Massachusetts.ORCID 0000-0001-6988-4260
Tufts University · USTufts Medical Center · US

Funding

Investigating the role of the extracellular matrix in metastasis and chemo-resistanceR00CA207866 · NCI · TUFTS UNIVERSITY MEDFORD · PI OUDIN, MADELEINE JULIE · 2018 to 2020
$696k
NCI NIH HHS R00 CA207866
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is the most aggressive and deadly subtype of breast cancer, accounting for 30,000 cases annually in the United States. While there are several clinical trials ongoing to identify new agents to treat TNBC, the majority of patients with TNBC are treated with anthracycline- or taxane-based chemotherapies in the neoadjuvant setting, followed by surgical resection and adjuvant chemotherapy. While many patients respond well to this approach, as many as 25% will suffer local or metastatic recurrence within 5 years. Understanding the mechanisms that drive recurrence after chemotherapy treatment is critical to improving survival for patients with TNBC. It is well established that the extracellular matrix (ECM), which provides structure and support to tissues, is a major driver of tumor growth, local invasion, and dissemination of cancer cells to distant metastatic sites. In the present study, we show that decellularized ECM (dECM) obtained from chemotherapy-treated mice increases motility of treatment-naïve breast cancer cells compared with vehicle-treated dECM. Tandem-mass-tag proteomics revealed that anthracycline- and taxane-based chemotherapies induce drug-specific changes in tumor ECM composition. The basement membrane protein collagen IV was significantly upregulated in the ECM of chemotherapy-treated mice and patients treated with neoadjuvant chemotherapy. Collagen IV drove invasion via activation of Src and focal adhesion kinase signaling downstream of integrin α1 and α2, and inhibition of collagen IV-driven signaling decreased motility in chemotherapy-treated dECM. These studies provide a novel mechanism by which chemotherapy may induce metastasis via its effects on ECM composition. SIGNIFICANCE: Cytotoxic chemotherapy induces significant changes in the composition of tumor ECM, inducing a more invasive and aggressive phenotype in residual tumor cells following chemotherapy.

Indexed as

Antineoplastic AgentsTriple Negative Breast NeoplasmsAnimalsAnthracyclinesCell MovementCollagen Type IVFocal Adhesion Protein-Tyrosine KinasesHumansMiceTaxoidsAnthracyclinesAntineoplastic AgentsCollagen Type IVFocal Adhesion Protein-Tyrosine KinasesTaxoids

Identifiers

PMID35260882
PMCPMC9381104
OpenAlexW4220765294

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.