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Corrigendum Open Access | 10.1172/JCI165107

Stromal oncostatin M cytokine promotes breast cancer progression by reprogramming the tumor microenvironment

Angela M. Araujo, Andrea Abaurrea, Peio Azcoaga, Joanna I. López-Velazco, Sara Manzano, Javier Rodriguez, Ricardo Rezola, Leire Egia-Mendikute, Fátima Valdés-Mora, Juana M. Flores, Liam Jenkins, Laura Pulido, Iñaki Osorio-Querejeta, Patricia Fernández-Nogueira, Nicola Ferrari, Cristina Viera, Natalia Martín-Martín, Alexandar Tzankov, Serenella Eppenberger-Castori, Isabel Alvarez-Lopez, Ander Urruticoechea, Paloma Bragado, Nicholas Coleman, Asís Palazón, Arkaitz Carracedo, David Gallego-Ortega, Fernando Calvo, Clare M. Isacke, María M. Caffarel, and Charles H. Lawrie

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Published September 28, 2022 - More info

Published in Volume 132, Issue 19 on October 3, 2022
J Clin Invest. 2022;132(19):e165107. https://doi.org/10.1172/JCI165107.
© 2022 Araujo et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Published September 28, 2022 - Version history
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Stromal oncostatin M cytokine promotes breast cancer progression by reprogramming the tumor microenvironment
Angela M. Araujo, … , María M. Caffarel, Charles H. Lawrie
Angela M. Araujo, … , María M. Caffarel, Charles H. Lawrie
Research Article Inflammation Oncology

Stromal oncostatin M cytokine promotes breast cancer progression by reprogramming the tumor microenvironment

Abstract

The tumor microenvironment (TME) is reprogrammed by cancer cells and participates in all stages of tumor progression. The contribution of stromal cells to the reprogramming of the TME is not well understood. Here, we provide evidence of the role of the cytokine oncostatin M (OSM) as central node for multicellular interactions between immune and nonimmune stromal cells and the epithelial cancer cell compartment. OSM receptor (OSMR) deletion in a multistage breast cancer model halted tumor progression. We ascribed causality to the stromal function of the OSM axis by demonstrating reduced tumor burden of syngeneic tumors implanted in mice lacking OSMR. Single-cell and bioinformatic analysis of murine and human breast tumors revealed that OSM expression was restricted to myeloid cells, whereas OSMR was detected predominantly in fibroblasts and, to a lower extent, cancer cells. Myeloid-derived OSM reprogrammed fibroblasts to a more contractile and tumorigenic phenotype and elicited the secretion of VEGF and proinflammatory chemokines CXCL1 and CXCL16, leading to increased myeloid cell recruitment. Collectively, our data support the notion that the stromal OSM/OSMR axis reprograms the immune and nonimmune microenvironment and plays a key role in breast cancer progression.

Authors

Angela M. Araujo, Andrea Abaurrea, Peio Azcoaga, Joanna I. López-Velazco, Sara Manzano, Javier Rodriguez, Ricardo Rezola, Leire Egia-Mendikute, Fátima Valdés-Mora, Juana M. Flores, Liam Jenkins, Laura Pulido, Iñaki Osorio-Querejeta, Patricia Fernández-Nogueira, Nicola Ferrari, Cristina Viera, Natalia Martín-Martín, Alexandar Tzankov, Serenella Eppenberger-Castori, Isabel Alvarez-Lopez, Ander Urruticoechea, Paloma Bragado, Nicholas Coleman, Asís Palazón, Arkaitz Carracedo, David Gallego-Ortega, Fernando Calvo, Clare M. Isacke, María M. Caffarel, Charles H. Lawrie

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Original citation: J Clin Invest. 2022;132(7):e148667. https://doi.org/10.1172/JCI148667

Citation for this corrigendum: J Clin Invest. 2022;132(19):e165107. https://doi.org/10.1172/JCI165107

The authors recently became aware that, following the recent update of Cancertool (http://genomics.cicbiogune.es/CANCERTOOL/index.html), the two panels included in Supplemental Figure 3B needed to be modified. These panels included data downloaded from Cancertool reporting the prognostic potential of OSM in two independent breast cancer patient datasets, namely METABRIC (PMID 22522925) and Wang et al. (PMID 15721472). Based on the results from the updated Cancertool data, we cannot conclude that OSM is shown to exhibit prognostic potential in the Wang dataset. In addition, the analysis of the METABRIC dataset presented in Supplemental Figure 3B pertains to overall survival, but data were inadvertently reported as showing disease-free survival. The corrected panels are shown below. Corrected sentences referring to Supplemental Figure 3B data in Results and Methods are also shown below. The online supplemental file has been updated.

Results

We also observed that increased OSM mRNA levels associated with decreased overall survival in the METABRIC (19) breast cancer dataset (Supplemental Figure 3B). Of note, the prognostic analysis of OSM in the Wang (20) dataset did not reveal a significant association with disease-free survival (Supplemental Figure 3B).

Methods

Gene expression analyses of clinical datasets and bioinformatics analyses. Overall survival (OS) and disease-free survival (DFS) data for breast cancer patients based on OSM mRNA expression in the METABRIC (19) and Wang (20) datasets were analyzed and represented using the CANCERTOOL interface (59) in combination with cBioPortal (www.cbioportal.org).

The authors regret the errors.

Footnotes

See the related article at Stromal Oncostatin M cytokine promotes breast cancer progression by reprogramming the tumour microenvironment.

Version history
  • Version 1 (September 28, 2022): Electronic publication
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