Oxidative stress promotes myofibroblast differentiation and tumour spreading
Open accessAbstract
JunD regulates genes involved in antioxidant defence. We took advantage of the chronic oxidative stress resulting from junD deletion to examine the role of reactive oxygen species (ROS) in tumour development. In a model of mammary carcinogenesis, junD inactivation increased tumour incidence and revealed an associated reactive stroma. junD-inactivation in the stroma was sufficient to shorten tumour-free survival rate and enhance metastatic spread. ROS promoted conversion of fibroblasts into highly migrating myofibroblasts through accumulation of the hypoxia-inducible factor (HIF)-1alpha transcription factor and the CXCL12 chemokine. Accordingly, treatment with an antioxidant reduced the levels of HIF and CXCL12 and numerous myofibroblast features. CXCL12 accumulated in the stroma of HER2-human breast adenocarcinomas. Moreover, HER2 tumours exhibited a high proportion of myofibroblasts, which was significantly correlated to nodal metastases. Interestingly, this subset of tumours exhibited a significant nuclear exclusion of JunD and revealed an associated oxido-reduction signature, further demonstrating the relevance of our findings in human cancers. Collectively, our data uncover a new mechanism by which oxidative stress increases the migratory properties of stromal fibroblasts, which in turn potentiate tumour dissemination.
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CAFs and ROS engage in two-way cross-talk: fibroblasts are targeted by ROS, particularly H2O2, which converts them into active CAFs through upregulation of HIF1α, and CAFs are critical for the increase in ROS levels observed in cancer.
“CAFs and ROS engage in two-way cross-talk: on the one hand, fibroblasts are targeted by ROS, particularly H2O2, which is able to convert them into active CAFs through the upregulation of HIF1α; on the other hand, CAFs are critical for the increase in ROS levels observed in cancer50,51.”
From ROS in cancer therapy: the bright side of the moon (2020) · cites this paper as [51]
The Discussion and the model in Results (page not provided) support ROS-driven HIF-1α accumulation and conversion of fibroblasts into myofibroblasts; the model also says H2O2 can diffuse to surrounding fibroblasts. They do not establish the other half of the claimed two-way cross-talk—that CAFs are critical to increasing ROS levels in cancer. Instead, the model describes oxidative stress as arising within fibroblasts or from tumour cells. (LLM, conf=0.87)
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Antitumor activity of phenethyl isothiocyanate in HER2-positive breast cancer models
Gupta, P., & Srivastava, S. (2012) · BMC Medicine · doi:10.1186/1741-7015-10-80 · Cited by 93 · see citing works
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Guzik, T. J., & Cosentino, F. (2017) · Antioxidants and Redox Signaling · doi:10.1089/ars.2017.7299 · Cited by 93 · see citing works
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CXCR4 inhibitors could benefit to HER2 but not to triple-negative breast cancer patients
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- Authors
- Toullec, A., Gerald, D., Despouy, G., Bourachot, B., Cardon, M., Lefort, S., Richardson, M., Rigaill, G., Parrini, M., Lucchesi, C., Bellanger, D., Stern, M., Dubois, T., Sastre‐Garau, X., Delattre, O., Vincent‐Salomon, A., & Mechta‐Grigoriou, F.
- Affiliations
- Inserm (FR)
- Institut Curie (FR)
- Corresponding author
- Mechta‐Grigoriou, Fatima
- ORCID
- Venue
- EMBO Molecular Medicine
- Published
- 2010-06-01
- Volume
- 2
- Issue
- 6
- Pages
- 211-230
- ISSN
- 1757-4676 (ISSN-L)
- 1757-4684
- PMC
- PMC3377319
- OpenAlex
- W2107028932
- Cited by
- 339
- References
- 91
- Citations by year
- 2026: 16 · 2025: 15 · 2024: 27 · 2023: 38 · 2022: 33 · 2021: 30 · 2020: 23 · 2019: 12 · 2018: 11 · 2017: 17 · 2016: 14 · 2015: 13 · 2014: 19 · 2013: 22 · 2012: 22
- FWCI
- 11.24
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- EMBO Molecular Medicine (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by-nc)
- Funders
- Institut National de la Santé et de la Recherche Médicale
- Institut Curie
- Fondation de France
- Agence Nationale de la Recherche
- French National Institut of Cancer
- Association pour la Recherche contre le Cancer
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- oxidative stress, JunD, myofibroblast differentiation, tumour metastasis, reactive oxygen species, mammary carcinogenesis, stromal fibroblasts, HIF-1α, CXCL12, HER2-positive breast cancer, antioxidant therapy, tumor microenvironment, hypoxia
- MeSH terms
- Animals, Breast Neoplasms, Cell Differentiation, Cell Line, Female, Fibroblasts, Histocytochemistry, Humans, Immunohistochemistry, Locomotion, Microscopy, Microscopy, Fluorescence, Models, Biological, Neoplasm Metastasis, Proto-Oncogene Proteins, Mammary Neoplasms, Animal, Incidence, Survival Analysis, Proto-Oncogene Proteins c-jun, Reactive Oxygen Species, Mice, Knockout, Oxidative Stress, Mice, Hypoxia-Inducible Factor 1, alpha Subunit, Chemokine CXCL12
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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