ArticleMolecular biology of the cell2009
Loss of E-cadherin-mediated cell-cell contacts activates a novel mechanism for up-regulation of the proto-oncogene c-Jun.
Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Network Analysis for the Discovery of Common Oncogenic Biomarkers in Liver Cancer Experimental Models.Biomedicines · 2023Article
- MiR-1284 suppresses gastric cancer progression by targeting EIF4A1.OncoTargets and therapy · 2019Article
- Effects of Prisma® Skin dermal regeneration device containing glycosaminoglycans on human keratinocytes and fibroblasts.Cell adhesion & migration · 2018Article
- Cadherin complexes recruit mRNAs and RISC to regulate epithelial cell signaling.The Journal of cell biology · 2017Article
- A central role for cadherin signaling in cancer.Experimental cell research · 2017Review
- MicroRNA 10b promotes abnormal expression of the proto-oncogene c-Jun in metastatic breast cancer cells.Oncotarget · 2016Article
- Cap-Independent Translational Control of Carcinogenesis.Frontiers in oncology · 2016Review
- Regulation of protein translation and c-Jun expression by prostate tumor overexpressed 1.Oncogene · 2014Article
- Article
- Aberrant expression of c-Jun in glioblastoma by internal ribosome entry site (IRES)-mediated translational activation.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- raw Functions through JNK signaling and cadherin-based adhesion to regulate Drosophila gonad morphogenesis.Developmental biology · 2012Article
- Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of E-cadherin-mediated cell-cell contacts can elicit a signaling pathway that leads to acquisition of an invasive phenotype. Here, we show that at the receiving end of this pathway is the proto-oncogene c-Jun, a member of the activator protein-1 family of transcription factors that play a key role in stimulation of cell proliferation and tumor promotion. Cell separation or abrogation of E-cadherin-mediated cell-cell contacts both cause a dramatic increase in accumulation of the c-Jun protein. Unlike growth factors that enhance the expression of c-Jun by activating the transcription of the c-jun gene, the cell contact-dependent increase in c-Jun accumulation is not accompanied by a corresponding increase in c-Jun mRNA or c-Jun protein stability but rather in the translatability of the c-Jun transcript. Consistently, the increase in c-Jun accumulation is not dependent on activation of the mitogen-activated protein kinase or beta-catenin pathways but is mediated by signals triggered by the restructured cytoskeleton. Depolymerization of the cytoskeleton can mimic the effect of cell separation and cause a dramatic increase in c-Jun accumulation, whereas Taxol inhibits the cell contact-dependent increase. This novel mechanism of c-Jun regulation seems to underlie the robust overexpression of c-Jun in tumor cells of patients with colon carcinoma.
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