The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Mesenchymal Cancer Cell-Stroma Crosstalk Promotes Niche Activation, Epithelial Reversion, and Metastatic Colonization
Open accessAbstract
During metastatic colonization, tumor cells must establish a favorable microenvironment or niche that will sustain their growth. However, both the temporal and molecular details of this process remain poorly understood. Here, we found that metastatic initiating cells (MICs) exhibit a high capacity for lung fibroblast activation as a result of Thrombospondin 2 (THBS2) expression. Importantly, inhibiting the mesenchymal phenotype of MICs by blocking the epithelial-to-mesenchymal transition (EMT)-associated kinase AXL reduces THBS2 secretion, niche-activating ability, and, consequently, metastatic competence. Subsequently, disseminated metastatic cells revert to an AXL-negative, more epithelial phenotype to proliferate and decrease the phosphorylation levels of TGF-β-dependent SMAD2-3 in favor of BMP/SMAD1-5 signaling. Remarkably, newly activated fibroblasts promote this transition. In summary, our data reveal a crosstalk between cancer cells and their microenvironment whereby the EMT status initially triggers and then is regulated by niche activation during metastatic colonization.
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Cites
Massagué, J. (2008) · Cell · doi:10.1016/j.cell.2008.07.001 · Cited by 3,907
Snail, Zeb and bHLH factors in tumour progression: An alliance against the epithelial phenotype?
Peinado, H., Olmeda, D., & Cano, A. (2007) · Nature reviews. Cancer · doi:10.1038/nrc2131 · Cited by 3,121 · cited 2×
“The process is initiated by the activation of the EMT core transcription factors (TFs) Snail, Zeb, and Twist1 (Peinado et al., 2007), which drive epithelial cancer cells to switch off the expression of epithelial markers such as the adherens junction protein E-Cadherin and activate the expression of mesenchymalmarkers…”
BackgroundCCL2 recruits inflammatory monocytes to facilitate breast-tumour metastasis
Qian, B.-Z., Li, J., Zhang, H., Kitamura, T., Zhang, J., Campion, L. R., Kaiser, E. A., Snyder, L. A., & Pollard, J. W. (2011) · Nature · doi:10.1038/nature10138 · Cited by 2,874
A restricted cell population propagates glioblastoma growth after chemotherapy
Chen, J., Li, Y., Yu, T.-S., McKay, R. M., Burns, D. K., Kernie, S. G., & Parada, L. F. (2012) · Nature · doi:10.1038/nature11287 · Cited by 2,354
Gaggioli, C., Hooper, S., Hidalgo-Carcedo, C., Grosse, R., Marshall, J. F., Harrington, K., & Sahai, E. (2007) · Nature Cell Biology · doi:10.1038/ncb1658 · Cited by 1,589 · cited 1×
“In line with previous studies (Gaggioli et al., 2007; Yu et al., 2014), carcinoma cells in a non-invasive epithelial state (non-MICs) activated both single and collective cell invasion modalities.”
ResultCalvo, F., Ege, N., Grande-Garcia, A., Hooper, S., Jenkins, R. P., Chaudhry, S. I., Harrington, K., Williamson, P., Moeendarbary, E., Charras, G., et al. (2013) · Nature Cell Biology · doi:10.1038/ncb2756 · Cited by 1,478
Self-citationBreast cancer cells produce tenascin C as a metastatic niche component to colonize the lungs
Oskarsson, T., Acharyya, S., Zhang, X. H.-F., Vanharanta, S., Tavazoie, S. F., Morris, P. G., Downey, R. J., Manova-Todorova, K., Brogi, E., & Massagué, J. (2011) · Nature Medicine · doi:10.1038/nm.2379 · Cited by 869
Gjerdrum, C., Tiron, C., Høiby, T., Stefansson, I., Haugen, H., Sandal, T., Collett, K., Li, S., McCormack, E., Gjertsen, B. T., et al. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0909333107 · Cited by 594
Cited by
Nieto, M. A., Huang, R. Y.-J., Jackson, R. A., & Thiery, J. P. (2016) · Cell · doi:10.1016/j.cell.2016.06.028 · Cited by 4,492
The biology and function of fibroblasts in cancer
Kalluri, R. (2016) · Nature Reviews Cancer · doi:10.1038/nrc.2016.73 · Cited by 4,366
Inflammation and cancer: triggers, mechanisms, and consequences
Greten, F. R., & Grivennikov, S. I. (2019) · Immunity · doi:10.1016/j.immuni.2019.06.025 · Cited by 3,806
EMT, CSCs, and drug resistance: the mechanistic link and clinical implications
Shibue, T., & Weinberg, R. A. (2017) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2017.44 · Cited by 2,539
Epithelial Mesenchymal Transition in Tumor Metastasis
Mittal, V. (2018) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-020117-043854 · Cited by 1,528
Metadata
- Authors
- del Pozo Martin, Y., Park, D., Ramachandran, A., Ombrato, L., Calvo, F., Chakravarty, P., Spencer-Dene, B., Derzsi, S., Hill, C. S., Sahai, E., & Malanchi, I.
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2015-12
- Volume
- 13
- Issue
- 11
- Pages
- 2456-2469
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W2186103292
- Cited by
- 248
- References
- 8
- FWCI
- 10.01
- Type
- journal article
- Language
- en
- Open access
- gold
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- The paper
- del Pozo Martin, Y., Park, D., Ramachandran, A., Ombrato, L., Calvo, F., Chakravarty, P., Spencer-Dene, B., Derzsi, S., Hill, C. S., Sahai, E., & Malanchi, I. (2015). Mesenchymal Cancer Cell-Stroma Crosstalk Promotes Niche Activation, Epithelial Reversion, and Metastatic Colonization. Cell Reports. https://doi.org/10.1016/j.celrep.2015.11.025
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