ArticleMolecular biology of the cell2002
Inhibition of anchorage-independent growth of transformed NIH3T3 cells by epithelial protein lost in neoplasm (EPLIN) requires localization of EPLIN to actin cytoskeleton.
Article in Molecular biology of the cell, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 51 citations in OpenAlex.
- Article
- Differential effects of KRAS G-domain and hypervariable region mutants on cancer phenotypes.Scientific reports · 2025Article
- Exploring the Enigma: The Role of the Epithelial Protein Lost in Neoplasm in Normal Physiology and Cancer Pathogenesis.International journal of molecular sciences · 2024Review
- EPLIN-β is a novel substrate of ornithine decarboxylase antizyme 1 and mediates cellular migration.Journal of cell science · 2023Article
- Characterization of LIMA1 and its emerging roles and potential therapeutic prospects in cancers.Frontiers in oncology · 2023Review
- Where all the Roads Meet? A Crossover Perspective on Host Factors Regulating SARS-CoV-2 infection.Journal of molecular biology · 2022Review
- Epithelial Protein Lost in Neoplasm, EPLIN, the Cellular and Molecular Prospects in Cancers.Biomolecules · 2021Review
- Article
- Epithelial protein lost in neoplasm (EPLIN) and prostate cancer: lessons learned from the ARCaP model.American journal of clinical and experimental urology · 2021Review
- LUZP1 Controls Cell Division, Migration and Invasion Through Regulation of the Actin Cytoskeleton.Frontiers in cell and developmental biology · 2021Article
- Radiosensitization by Kinase Inhibition Revealed by Phosphoproteomic Analysis of Pancreatic Cancer Cells.Molecular & cellular proteomics : MCP · 2020Article
- Epithelial protein lost in neoplasm (EPLIN): Beyond a tumor suppressor.Genes & diseases · 2017Review
- EPLIN: a fundamental actin regulator in cancer metastasis?Cancer metastasis reviews · 2015Review
- Combined comparative genomic hybridization and transcriptomic analyses of ovarian granulosa cell tumors point to novel candidate driver genes.BMC cancer · 2015Article
- Zinc finger protein 185 is a liver metastasis-associated factor in colon cancer patients.Molecular and clinical oncology · 2014Article
- Epidermal growth factor promotes protein degradation of epithelial protein lost in neoplasm (EPLIN), a putative metastasis suppressor, during epithelial-mesenchymal transition.The Journal of biological chemistry · 2013Article
- Epithelial protein lost in neoplasm (EPLIN) interacts with α-catenin and actin filaments in endothelial cells and stabilizes vascular capillary network in vitro.The Journal of biological chemistry · 2012Article
- The EWS/FLI Oncogene Drives Changes in Cellular Morphology, Adhesion, and Migration in Ewing Sarcoma.Genes & cancer · 2012Article
- Article
- Novel interactors and a role for supervillin in early cytokinesis.Cytoskeleton (Hoboken, N.J.) · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Epithelial protein lost in neoplasm (EPLIN) is a cytoskeleton-associated protein characterized by the presence of a single centrally located lin-11, isl-1, and mec-3 (LIM) domain. We have reported previously that EPLIN is down-regulated in transformed cells. In this study, we have investigated whether ectopic expression of EPLIN affects transformation. In untransformed NIH3T3 cells, retroviral-mediated transduction of EPLIN did not alter the cell morphology or growth. NIH3T3 cells expressing EPLIN, however, failed to form colonies when transformed by the activated Cdc42 or the chimeric nuclear oncogene EWS/Fli-1. This suppression of anchorage-independent growth was not universal because EPLIN failed to inhibit the colony formation of Ras-transformed cells. Interestingly, the localization of EPLIN to the actin cytoskeleton was maintained in the EWS/Fli-1- or Cdc42-transformed cells, but not in Ras-transformed cells where it was distributed heterogeneously in the cytoplasm. Using truncated EPLIN constructs, we demonstrated that the NH(2)-terminal region of EPLIN is necessary for both the localization of EPLIN to the actin cytoskeleton and suppression of anchorage-independent growth of EWS/Fli-1-transformed cells. The LIM domain or the COOH-terminal region of EPLIN could be deleted without affecting its cytoskeletal localization or ability to suppress anchorage-dependent growth. Our study indicates EPLIN may function in growth control by associating with and regulating the actin cytoskeleton.
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