S100A8/A9 activate key genes and pathways in colon tumor progression
Open accessAbstract
The tumor microenvironment plays an important role in modulating tumor progression. Earlier, we showed that S100A8/A9 proteins secreted by myeloid-derived suppressor cells (MDSC) present within tumors and metastatic sites promote an autocrine pathway for accumulation of MDSC. In a mouse model of colitis-associated colon cancer, we also showed that S100A8/A9-positive cells accumulate in all regions of dysplasia and adenoma. Here we present evidence that S100A8/A9 interact with RAGE and carboxylated glycans on colon tumor cells and promote activation of MAPK and NF-κB signaling pathways. Comparison of gene expression profiles of S100A8/A9-activated colon tumor cells versus unactivated cells led us to identify a small cohort of genes upregulated in activated cells, including Cxcl1, Ccl5 and Ccl7, Slc39a10, Lcn2, Zc3h12a, Enpp2, and other genes, whose products promote leukocyte recruitment, angiogenesis, tumor migration, wound healing, and formation of premetastatic niches in distal metastatic organs. Consistent with this observation, in murine colon tumor models we found that chemokines were upregulated in tumors, and elevated in sera of tumor-bearing wild-type mice. Mice lacking S100A9 showed significantly reduced tumor incidence, growth and metastasis, reduced chemokine levels, and reduced infiltration of CD11b+Gr1+ cells within tumors and premetastatic organs. Studies using bone marrow chimeric mice revealed that S100A8/A9 expression on myeloid cells is essential for development of colon tumors. Our results thus reveal a novel role for myeloid-derived S100A8/A9 in activating specific downstream genes associated with tumorigenesis and in promoting tumor growth and metastasis. Mol Cancer Res; 9(2); 133–48. ©2011 AACR.
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The relevance of targeting the CXCL1/2-S100A8/9 axis may extend beyond breast cancer.
“Moreover, the important role of CXCR2 in pancreatic adenocarcinoma models (Ijichi et al., 2011) and of S100A8/9 in colorectal cancer (Ichikawa et al., 2011) suggest that the relevance of targeting the CXCL1/2–S100A8/9 axis may extend beyond breast cancer.”
From A CXCL1 Paracrine Network Links Cancer Chemoresistance and Metastasis (2012) · cites this paper as Ichikawa et al., 2011
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- Authors
- Ichikawa, M., Williams, R., Wang, L., Vogl, T., & Srikrishna, G.
- Affiliations
- Sanford Burnham Prebys Medical Discovery Institute (US)
- Corresponding author
- Srikrishna, Geetha
- Venue
- Molecular Cancer Research
- Published
- 2011-02-01
- Volume
- 9
- Issue
- 2
- Pages
- 133-148
- ISSN
- 1541-7786 (ISSN-L)
- 1557-3125
- PMC
- PMC3078037
- OpenAlex
- W2125021772
- Cited by
- 346
- References
- 80
- Citations by year
- 2026: 16 · 2025: 9 · 2024: 17 · 2023: 13 · 2022: 24 · 2021: 38 · 2020: 23 · 2019: 19 · 2018: 20 · 2017: 16 · 2016: 27 · 2015: 34 · 2014: 24 · 2013: 33 · 2012: 28
- FWCI
- 11.70
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R21CA127780)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › S100 Proteins and Annexins
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Keywords
- S100A8/A9, colon cancer, tumor microenvironment, myeloid-derived suppressor cells, RAGE, MAPK signaling, NF-κB signaling, chemokines, CXCL1, RANTES, CCL7, neutrophil gelatinase-associated lipocalin, ZC3H12A, autotaxin, pre-metastatic niche, metastasis, tumor growth, tumor progression, colitis-associated colorectal cancer, leukocyte recruitment, angiogenesis, tumor cell migration, bone marrow chimeric mice
- MeSH terms
- Receptor for Advanced Glycation End Products, Animals, Bone Marrow Cells, Colonic Neoplasms, Disease Models, Animal, Humans, Neoplasm Metastasis, Polysaccharides, Precancerous Conditions, Protein Binding, Receptors, Immunologic, Signal Transduction, Gene Expression Regulation, Neoplastic, NF-kappa B, Disease Progression, Chemokines, Mitogen-Activated Protein Kinases, MAP Kinase Signaling System, Calgranulin A, Calgranulin B, Cell Line, Tumor, Cell Proliferation, Mice, Genes, Neoplasm, Tumor Microenvironment
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.
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