ArticleThe Journal of cell biology2003
Tenascin-C signaling through induction of 14-3-3 tau.
Article in The Journal of cell biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 51 citations in OpenAlex.
- Review
- 14-3-3τ drives estrogen receptor loss via ERα36 induction and GATA3 inhibition in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Matricellular protein tenascin C: Implications in glioma progression, gliomagenesis, and treatment.Frontiers in oncology · 2022Review
- Radioimmunotherapy (RIT) in Brain Tumors.Nuclear medicine and molecular imaging · 2019Review
- YWHAE promotes proliferation, metastasis, and chemoresistance in breast cancer cells.The Kaohsiung journal of medical sciences · 2019Article
- Article
- Tenascin-C Is Associated with Cored Amyloid-β Plaques in Alzheimer Disease and Pathology Burdened Cognitively Normal Elderly.Journal of neuropathology and experimental neurology · 2016Article
- 14-3-3τ promotes breast cancer invasion and metastasis by inhibiting RhoGDIα.Molecular and cellular biology · 2014Article
- Collagen type I and decorin expression in tenocytes depend on the cell isolation method.BMC musculoskeletal disorders · 2012Article
- Rsk-mediated phosphorylation and 14-3-3ɛ binding of Apaf-1 suppresses cytochrome c-induced apoptosis.The EMBO journal · 2012Article
- How do tenascins influence the birth and life of a malignant cell?Journal of cellular and molecular medicine · 2012Review
- Tenascins and the importance of adhesion modulation.Cold Spring Harbor perspectives in biology · 2011Review
- Tenascin C induces epithelial-mesenchymal transition-like change accompanied by SRC activation and focal adhesion kinase phosphorylation in human breast cancer cells.The American journal of pathology · 2011Article
- Article
- 14-3-3ζ Overexpression and abnormal β-catenin expression are associated with poor differentiation and progression in stage I non-small cell lung cancer.Clinical and experimental medicine · 2010Article
- 14-3-3Tau regulates Beclin 1 and is required for autophagy.PloS one · 2010Article
- 14-3-3Tau regulates ubiquitin-independent proteasomal degradation of p21, a novel mechanism of p21 downregulation in breast cancer.Molecular and cellular biology · 2010Article
- The role of tenascin-C in tissue injury and tumorigenesis.Journal of cell communication and signaling · 2009Article
- Human 14-3-3 gamma protein results in abnormal cell proliferation in the developing eye of Drosophila melanogaster.Cell division · 2008Article
- Down-regulation of 14-3-3zeta suppresses anchorage-independent growth of lung cancer cells through anoikis activation.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We searched by a cDNA subtraction screen for differentially expressed transcripts in MCF-7 mammary carcinoma cells grown on tenascin-C versus fibronectin. On tenascin-C, cells had irregular shapes with many processes, whereas on fibronectin they were flat with a cobble stone-like appearance. We found elevated levels of 14-3-3 tau transcripts and protein in cells grown on tenascin-C. To investigate the consequences of an increased level of this phospho-serine/threonine-binding adaptor protein, we transfected MCF-7 cells with a construct encoding full-length 14-3-3 tau protein and selected clones with the highest expression levels. The morphology of these cells on tenascin-C was flat, resembling that of cells on fibronectin. This was reflected by a similar pattern of F-actin staining on either substratum. Furthermore, the growth rate on tenascin-C was increased compared with the parental cells. After transient transfection of HT1080 fibrosarcoma and T98G glioblastoma cells with 14-3-3 tau, only the 14-3-3 tau-expressing cells were able to adhere and survive on tenascin-C, whereas all cells adhered well on fibronectin. Therefore, we postulate that tenascin-C promotes the growth of tumor cells by causing an increase in the expression of 14-3-3 tau, which in turn has a positive effect on tumor cell adhesion and growth.
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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 Socratic graph.