ArticleScientific reports2017
Plectin is a novel regulator for apical extrusion of RasV12-transformed cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Mechanics of cell sheets: plectin as an integrator of cytoskeletal networks.Open biology · 2025Review
- Exploring the Enigma: The Role of the Epithelial Protein Lost in Neoplasm in Normal Physiology and Cancer Pathogenesis.International journal of molecular sciences · 2024Review
- Role of plectin and its interacting molecules in cancer.Medical oncology (Northwood, London, England) · 2023Review
- TCN1 Deficiency Inhibits the Malignancy of Colorectal Cancer Cells by Regulating the ITGB4 Pathway.Gut and liver · 2023Article
- Pleiotropic effects of cell competition between normal and transformed cells in mammalian cancers.Journal of cancer research and clinical oncology · 2023Review
- Characterization of LIMA1 and its emerging roles and potential therapeutic prospects in cancers.Frontiers in oncology · 2023Review
- A novel peptidomimetic therapeutic for selective suppression of lung cancer stem cells over non-stem cancer cells.Bioorganic chemistry · 2021Article
- Review
- Epithelial Protein Lost in Neoplasm, EPLIN, the Cellular and Molecular Prospects in Cancers.Biomolecules · 2021Review
- Article
- Neuroepithelial cell competition triggers loss of cellular juvenescence.Scientific reports · 2020Article
- Article
- Symmetry Breaking and Epithelial Cell Extrusion.Cells · 2020Review
- Unbiased peptoid combinatorial cell screen identifies plectin protein as a potential biomarker for lung cancer stem cells.Scientific reports · 2019Article
- Actin dynamics and the Bmp pathway drive apical extrusion of proepicardial cells.Development (Cambridge, England) · 2019Article
- Normal epithelial cells trigger EphA2-dependent RasV12 cell repulsion at the single cell level.Small GTPases · 2019Article
- The paxillin-plectin-EPLIN complex promotes apical elimination of RasV12-transformed cells by modulating HDAC6-regulated tubulin acetylation.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several lines of evidence have revealed that newly emerging transformed cells are often eliminated from the epithelium, though the underlying molecular mechanisms of this cancer preventive phenomenon still remain elusive. In this study, using mammalian cell culture systems we have identified plectin, a versatile cytoskeletal linker protein, as a novel regulator for apical extrusion of RasV12-transformed cells. Plectin is accumulated in RasV12 cells when they are surrounded by normal epithelial cells. Similarly, cytoskeletal proteins tubulin, keratin, and Epithelial Protein Lost In Neoplasm (EPLIN) are also accumulated in the transformed cells surrounded by normal cells. Knockdown or functional disruption of one of these molecules diminishes the accumulation of the others, indicating that the accumulation process of the individual protein mutually depends on each other. Furthermore, plectin-knockdown attenuates caveolin-1 (Cav-1) enrichment and PKA activity in RasV12 cells and profoundly suppresses the apical extrusion. These results indicate that the plectin-microtubules-EPLIN complex positively regulates apical elimination of RasV12-transformed cells from the epithelium in a coordinated fashion. Further development of this study would open a new avenue for cancer preventive medicine.
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