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Metformin regulates breast cancer stem cello ntogeny by transcriptional regulation of the epithelial-mesenchymal transition (EMT) status
Open accessAbstract
The sole overexpression of pivotal regulators of the embryonic Epithelial-Mesenchymal Transition (EMT) genetic program ("EMT status") may be sufficient to efficiently drive the ontogeny of the breast cancer stem cell molecular signature independently of changes in EMT functioning ("EMT phenotype"). Using basal-like breast cancer models naturally enriched in either CD44(pos)CD24(low/neg) or CD44(pos)CD24(pos) tumor-initiating cell populations we herein illustrate that non-cytotoxic concentrations of the anti-diabetic drug metformin efficiently impedes the ontogeny of generating the stem cell phenotype by transcriptionally repressing the stem cell property EMT. Metformin treatment dynamically regulated the CD44(pos)CD24(neg/low) breast cancer stem cell immunophenotype, transcriptionally reprogrammed cells through decreased expression of key drivers of the EMT machinery including the transcription factors ZEB1, TWIST1 and SNAI2 (Slug) and the pleiotrophic cytokines TGFβs, and lastly impeded the propensity of breast cancer stem cells to form multicellular "microtumors" in non-adherent and non-differentiating conditions (i.e., "mammospheres"). These findings, altogether, provide strong motivation for the continued molecular understanding and clinical development of metformin as a non-toxic therapeutic aimed to interdict the breast cancer stem cell phenotype by targeting EMT, a molecular process that is central to the ontogenesis of the breast cancer stem cell molecular signature.
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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
Rac1b and reactive oxygen species mediate MMP-3-induced EMT and genomic instability
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Auffinger, B., Tobias, A. L., Han, Y., Lee, G., Guo, D., Dey, M., Lesniak, M. S., & Ahmed, A. U. (2014) · Cell Death & Differentiation · doi:10.1038/cdd.2014.31 · Cited by 349
Martinez-Outschoorn, U. E., Prisco, M., Ertel, A., Tsirigos, A., Lin, Z., Pavlides, S., Wang, C., Flomenberg, N., Knudsen, E. S., Howell, A., et al. (2011) · Cell Cycle · doi:10.4161/cc.10.8.15330 · Cited by 338
McCubrey, J. A., Steelman, L. S., Chappell, W. H., Abrams, S. L., Franklin, R. A., Montalto, G., Cervello, M., Libra, M., Candido, S., Malaponte, G., et al. (2012) · Oncotarget · doi:10.18632/oncotarget.659 · Cited by 314
Metadata
- Authors
- Vazquez-Martin, A., Oliveras-Ferraros, C., Cufí, S., Del Barco, S., Martin-Castillo, B., & Menendez, J. A.
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2010-09-15
- Volume
- 9
- Issue
- 18
- Pages
- 3831-3838
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- OpenAlex
- W2043376395
- Cited by
- 205
- References
- 2
- FWCI
- 9.54
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Vazquez-Martin, A., Oliveras-Ferraros, C., Cufí, S., Del Barco, S., Martin-Castillo, B., & Menendez, J. A. (2010). Metformin regulates breast cancer stem cello ntogeny by transcriptional regulation of the epithelial-mesenchymal transition (EMT) status. Cell Cycle. https://doi.org/10.4161/cc.9.18.13131
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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