ArticleThe Journal of cell biology1991
Multilayering and loss of apical polarity in MDCK cells transformed with viral K-ras.
Article in The Journal of cell biology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 93 citations in OpenAlex.
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- SOS1 and Ras regulate epithelial tight junction formation in the human airway through EMP1.EMBO reports · 2015Article
- Cyr61 promotes epithelial-mesenchymal transition and tumor metastasis of osteosarcoma by Raf-1/MEK/ERK/Elk-1/TWIST-1 signaling pathway.Molecular cancer · 2014Article
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- Heterogeneity of the tumorigenic phenotype expressed by Madin-Darby canine kidney cells.Comparative medicine · 2011Article
- Claudin family of proteins and cancer: an overview.Journal of oncology · 2010Article
- Polarity proteins regulate mammalian cell-cell junctions and cancer pathogenesis.Current opinion in cell biology · 2009Review
- Characterization of the interface between normal and transformed epithelial cells.Nature cell biology · 2009Article
- Ras mutation impairs epithelial barrier function to a wide range of nonelectrolytes.Molecular biology of the cell · 2005Article
- NZO-3 expression causes global changes to actin cytoskeleton in Madin-Darby canine kidney cells: linking a tight junction protein to Rho GTPases.Molecular biology of the cell · 2003Article
- Mechanisms in epithelial plasticity and metastasis: insights from 3D cultures and expression profiling.Journal of mammary gland biology and neoplasia · 2002Review
- Ras and TGF[beta] cooperatively regulate epithelial cell plasticity and metastasis: dissection of Ras signaling pathways.The Journal of cell biology · 2002Article
- ErbB2, but not ErbB1, reinitiates proliferation and induces luminal repopulation in epithelial acini.Nature cell biology · 2001Article
- Induced expression of Rnd3 is associated with transformation of polarized epithelial cells by the Raf-MEK-extracellular signal-regulated kinase pathway.Molecular and cellular biology · 2000Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The effects of viral Kirsten ras oncogene expression on the polarized phenotype of MDCK cells were investigated. Stable transformed MDCK cell lines expressing the v-K-ras oncogene were generated via infection with a helper-independent retroviral vector construct. When grown on plastic substrata, transformed cells formed continuous monolayers with epithelial-like morphology. However, on permeable filter supports where normal cells form highly polarized monolayers, transformed MDCK cells detached from the substratum and developed multilayers. Morphological analysis of the multilayers revealed that oncogene expression perturbed the polarized organization of MDCK cells such that the transformed cells lacked an apical--basal axis around which the cytoplasm is normally organized. Evidence for selective disruption of apical membrane polarity was provided by immunolocalization of membrane proteins; a normally apical 114-kD protein was randomly distributed on the cell surface in the transformed cell line, whereas normally basolateral proteins remained exclusively localized to areas of cell contact and did not appear on the free cell surface. The discrete distribution of the tight junction-associated ZO-1 protein as well as transepithelial resistance and flux measurements suggested that tight junctions were also assembled. These findings indicate that v-K-ras transformation alters cell-substratum and cell-cell interactions in MDCK cells. Furthermore, v-K-ras expression perturbs apical polarization but does not interfere with the development of a basolateral domain, suggesting that apical and basolateral polarity in epithelial cells may be regulated independently.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.