ArticlePloS one2013
Loss of the keratin cytoskeleton is not sufficient to induce epithelial mesenchymal transition in a novel KRAS driven sporadic lung cancer mouse model.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 28 citations in OpenAlex.
- TAT-CRE inhalation enables tumor induction corresponding to adenoviral Cre-recombinase in a lung cancer mouse model.Communications biology · 2025Article
- Influence of CCancers · 2023Article
- Keratin 19 maintains E-cadherin localization at the cell surface and stabilizes cell-cell adhesion of MCF7 cells.Cell adhesion & migration · 2021Article
- The epithelial-mesenchymal transition and the cytoskeleton in bioengineered systems.Cell communication and signaling : CCS · 2021Review
- Notch1 Deficiency Induces Tumor Cell Accumulation Inside the Bronchiolar Lumen and Increases TAZ Expression in an AutochthonousPathology oncology research : POR · 2021Article
- Biological approaches for hypertrophic scars.International wound journal · 2020Review
- Multifaceted role of keratins in epithelial cell differentiation and transformation.Journal of biosciences · 2019Review
- Preclinical studies reveal that LSD1 inhibition results in tumor growth arrest in lung adenocarcinoma independently of driver mutations.Molecular oncology · 2018Article
- Loss of profilin 2 contributes to enhanced epithelial-mesenchymal transition and metastasis of colorectal cancer.International journal of oncology · 2018Article
- LIN28B enhanced tumorigenesis in an autochthonous KRASOncogene · 2018Article
- Association of epithelial-to-mesenchymal transition circulating tumor cells in non-small cell lung cancer (NSCLC) molecular subgroups.Journal of thoracic disease · 2017Article
- Keratin 13 expression reprograms bone and brain metastases of human prostate cancer cells.Oncotarget · 2016Article
- NOTCH, ASCL1, p53 and RB alterations define an alternative pathway driving neuroendocrine and small cell lung carcinomas.International journal of cancer · 2016Article
- Staurosporine and extracellular matrix proteins mediate the conversion of small cell lung carcinoma cells into a neuron-like phenotype.PloS one · 2014Article
- Downregulation of keratin 76 expression during oral carcinogenesis of human, hamster and mouse.PloS one · 2013Article
- Identification of Radil as a Ras binding partner and putative activator.The Journal of biological chemistryArticle
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-to-mesenchymal transition (EMT), the phenotypical change of cells from an epithelial to a mesenchymal type, is thought to be a key event in invasion and metastasis of adenocarcinomas. These changes involve loss of keratin expression as well as loss of cell polarity and adhesion. We here aimed to determine whether the loss of keratin expression itself drives increased invasion and metastasis in adenocarcinomas and whether keratin loss leads to the phenotypic changes associated with EMT. Therefore, we employed a recently described murine model in which conditional deletion of the Keratin cluster II by Cre-recombinase leads to the loss of the entire keratinmultiprotein family. These mice were crossed into a newly generated Cre-recombinase inducible KRAS-driven murine lung cancer model to examine the effect of keratin loss on morphology, invasion and metastasis as well as expression of EMT related genes in the resulting tumors. We here clearly show that loss of a functional keratin cytoskeleton did not significantly alter tumor morphology or biology in terms of invasion, metastasis, proliferation or tumor burden and did not lead to induction of EMT. Further, tumor cells did not induce synchronously expression of vimentin, which is often seen in EMT, to compensate for keratin loss. In summary, our data suggest that changes in cell shape and migration that underlie EMT are dependent on changes in signaling pathways that cause secondary changes in keratin expression and organization. Thus, we conclude that loss of the keratin cytoskeleton per se is not sufficient to causally drive EMT in this tumor model.
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