Genes that mediate breast cancer metastasis to lung
Open accessAbstract
By means of in vivo selection, transcriptomic analysis, functional verification and clinical validation, here we identify a set of genes that marks and mediates breast cancer metastasis to the lungs. Some of these genes serve dual functions, providing growth advantages both in the primary tumour and in the lung microenvironment. Others contribute to aggressive growth selectively in the lung. Many encode extracellular proteins and are of previously unknown relevance to cancer metastasis.
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CXCL1 expression is associated with lung relapse in breast tumors, including tumors not exposed to prior chemotherapy, and increases aggressiveness of circulating breast tumor cells.
“CXCL1 emerged among a set of genes whose expression is associated with lung relapse in breast tumors, including tumors that had not been exposed to prior chemotherapy (Minn et al., 2007; Minn et al., 2005), and as a gene that increases the aggressiveness of circulating breast tumor cells (Kim et al., 2009).”
From A CXCL1 Paracrine Network Links Cancer Chemoresistance and Metastasis (2012) · cites this paper as Minn et al., 2005
Fascin, part of a lung metastasis gene signature, does not show the same trend upon chemotherapy treatment as S100A8/9, confirming specificity of the association of S100A8/9 with chemotherapy resistance.
“In contrast, Fascin that is part of a lung metastasis gene signature (Minn et al., 2005) did not show the same trend upon chemotherapy treatment as S100A8/9 (Figure S5E), further confirming the specificity of the association of S100A8/9 with chemotherapy resistance.”
From A CXCL1 Paracrine Network Links Cancer Chemoresistance and Metastasis (2012) · cites this paper as Minn et al., 2005
MDA-MB-231-LM2 (LM2) is an ideal xenograft model for studying tumor growth and lung metastasis.
“which is an ideal xenograft model for studying tumor growth and lung metastasis47.”
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Positively selected enhancer elements endow osteosarcoma cells with metastatic competence
Morrow, J. J., Bayles, I., Funnell, A. P. W., Miller, T. E., Saiakhova, A., Lizardo, M. M., Bartels, C. F., Kapteijn, M. Y., Hung, S., Mendoza, A., et al. (2018) · Nature Medicine · doi:10.1038/nm.4475 · Cited by 161 · see citing works
Intermittent hypoxia induces a metastatic phenotype in breast cancer
Chen, A., Sceneay, J., Gödde, N., Kinwel, T., Ham, S., Thompson, E. W., Humbert, P. O., & Möller, A. (2018) · Oncogene · doi:10.1038/s41388-018-0259-3 · Cited by 133 · see citing works
Monnier, Y., Farmer, P., Bieler, G., Imaizumi, N., Sengstag, T., Alghisi, G. C., Stehle, J.-C., Ciarloni, L., Andrejevic-Blant, S., Moeckli, R., et al. (2008) · Cancer Research · doi:10.1158/0008-5472.can-08-0841 · Cited by 123 · see citing works
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Altered propionate metabolism contributes to tumour progression and aggressiveness
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MRTF potentiates TEAD‐YAP transcriptional activity causing metastasis
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Amyloid-β precursor protein promotes cell proliferation and motility of advanced breast cancer
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Yamaguchi, N., Weinberg, E. M., Nguyen, A., Liberti, M. V., Goodarzi, H., Janjigian, Y. Y., Paty, P. B., Saltz, L. B., Kingham, T. P., Loo, J. M., et al. (2019) · eLife · doi:10.7554/elife.52135 · Cited by 91 · see citing works
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Tumor heterogeneity in VHL drives metastasis in clear cell renal cell carcinoma
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A novel Cas family member, HEPL, regulates FAK and cell spreading
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ATM regulation of IL-8 links oxidative stress to cancer cell migration and invasion
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“Analysis of breast cancer patient gene expression data Publically available breast cancer patient gene expression data from GEO was pooled (GSE2603, GSE2034, GSE5327, and GSE12276) as previously described (Minn et al., 2005; Barrett et al., 2007; Morales et al., 2014).”
MethodIn vitro models of the metastatic cascade: from local invasion to extravasation
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Antitumorigenic effects of cannabinoids beyond apoptosis.
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The CCL2-CCR2 astrocyte-cancer cell axis in tumor extravasation at the brain
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The co‐chaperone p23 promotes prostate cancer motility and metastasis
Querol Cano, L., Lavery, D. N., Sin, S., Spanjaard, E., Brooke, G. N., Tilman, J. D., Abroaf, A., Gaughan, L., Robson, C. N., Heer, R., et al. (2015) · Molecular Oncology · doi:10.1016/j.molonc.2014.08.014 · Cited by 33 · see citing works
“KYNU, CTSD and PMP22 are known to be up-regulated in advanced metastatic cancers and correlate with poor prognosis whereas LAMB1 encodes a laminin-1 protein shown to have reduced expression in breast cancer (Minn et al., 2005; Pruitt et al., 2012; Simpson et al., 2010; Tong et al., 2010).”
BackgroundTransplantable Mouse Tumor Models of Breast Cancer Metastasis
Chakrabarti, R., & Kang, Y. (2015) · Methods in Molecular Biology · doi:10.1007/978-1-4939-2297-0_18 · Cited by 20 · see citing works
- Authors
- Minn, A. J., Gupta, G. P., Siegel, P. M., Bos, P. D., Shu, W., Giri, D. D., Viale, A., Olshen, A. B., Gerald, W. L., & Massagué, J.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Massagué, Joan
- ORCID
- Venue
- Nature
- Published
- 2005-07-28
- Volume
- 436
- Issue
- 7050
- Pages
- 518-524
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC1283098
- OpenAlex
- W2082833890
- Cited by
- 2,922
- References
- 35
- Citations by year
- 2026: 33 · 2025: 80 · 2024: 99 · 2023: 185 · 2022: 89 · 2021: 148 · 2020: 128 · 2019: 151 · 2018: 122 · 2017: 152 · 2016: 175 · 2015: 175 · 2014: 162 · 2013: 159 · 2012: 184
- FWCI
- 57.37
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Cancer Institute (P01CA094060)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Keywords
- breast cancer, lung metastasis, metastasis-associated genes, gene expression signatures, tumor microenvironment, extracellular proteins, prognostic factors, therapeutic target, in vivo selection
- MeSH terms
- Breast Neoplasms, Humans, Lung Neoplasms, Neoplasm Metastasis, RNA, Neoplasm, Transcription, Genetic, Reproducibility of Results, Gene Expression Regulation, Neoplastic, Gene Expression Profiling, Cell Line, Tumor
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