The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Polarity and proliferation are controlled by distinct signaling pathways downstream of PI3-kinase in breast epithelial tumor cells
Open accessAbstract
Loss of tissue polarity and increased proliferation are the characteristic alterations of the breast tumor phenotype. To investigate these processes, we used a three-dimensional (3D) culture system in which malignant human breast cells can be reverted to a normal phenotype by exposure to inhibitors of phosphatidylinositol 3-kinase (PI3K). Using this assay, we find that Akt and Rac1 act as downstream effectors of PI3K and function as control points of cellular proliferation and tissue polarity, respectively. Our results also demonstrate that the PI3K signaling pathway is an integral component of the overall signaling network induced by growth in 3D, as reversion affected by inhibition of PI3K signaling also down-modulates the endogenous levels of β1 integrin and epidermal growth factor receptor, the upstream modulators of PI3K, and up-regulates PTEN, the antagonist of PI3K. These findings reveal key events of the PI3K pathway that play distinct roles to maintain tissue polarity and that when disrupted are instrumental in the malignant phenotype.
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Cites
Taking Cell-Matrix Adhesions to the Third Dimension
Cukierman, E., Pankov, R., Stevens, D. R., & Yamada, K. M. (2001) · Science · doi:10.1126/science.1064829 · Cited by 3,027
Weaver, V. M., Petersen, O. W., Wang, F., Larabell, C. A., Briand, P., Damsky, C., & Bissell, M. J. (1997) · The Journal of Cell Biology · doi:10.1083/jcb.137.1.231 · Cited by 1,483
Self-citationHippocampal Neuronal Polarity Specified by Spatially Localized mPar3/mPar6 and PI 3-Kinase Activity
Shi, S.-H., Jan, L. Y., & Jan, Y.-N. (2003) · Cell · doi:10.1016/s0092-8674(02)01249-7 · Cited by 600
Conditional loss of PTEN leads to precocious development and neoplasia in the mammary gland
Li, G., Robinson, G. W., Lesche, R., Martinez-Diaz, H., Jiang, Z., Rozengurt, N., Wagner, K.-U., Wu, D.-C., Lane, T. F., Liu, X., et al. (2002) · Development · doi:10.1242/dev.129.17.4159 · Cited by 272
Cited by
Tensional homeostasis and the malignant phenotype
Paszek, M. J., Zahir, N., Johnson, K. R., Lakins, J. N., Rozenberg, G. I., Gefen, A., Reinhart-King, C. A., Margulies, S. S., Dembo, M., Boettiger, D., et al. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.08.010 · Cited by 3,941
Modeling Tissue Morphogenesis and Cancer in 3D
Yamada, K. M., & Cukierman, E. (2007) · Cell · doi:10.1016/j.cell.2007.08.006 · Cited by 1,751
Three-dimensional culture models of normal and malignant breast epithelial cells
Lee, G. Y., Kenny, P. A., Lee, E. H., & Bissell, M. J. (2007) · Nature Methods · doi:10.1038/nmeth1015 · Cited by 1,336
Self-citationModelling glandular epithelial cancers in three-dimensional cultures
Debnath, J., & Brugge, J. S. (2005) · Nature Reviews Cancer · doi:10.1038/nrc1695 · Cited by 1,015
Chaudhuri, O., Koshy, S. T., Branco da Cunha, C., Shin, J.-W., Verbeke, C. S., Allison, K. H., & Mooney, D. J. (2014) · Nature Materials · doi:10.1038/nmat4009 · Cited by 820
Metadata
- Authors
- Liu, H., Radisky, D. C., Wang, F., & Bissell, M. J.
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2004-02-09
- Volume
- 164
- Issue
- 4
- Pages
- 603-612
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W2086336448
- Cited by
- 222
- References
- 4
- FWCI
- 7.43
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Liu, H., Radisky, D. C., Wang, F., & Bissell, M. J. (2004). Polarity and proliferation are controlled by distinct signaling pathways downstream of PI3-kinase in breast epithelial tumor cells. The Journal of Cell Biology. https://doi.org/10.1083/jcb.200306090
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
