ArticleThe Journal of cell biology2003
FAK induces expression of Prx1 to promote tenascin-C-dependent fibroblast migration.
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 31 papers.
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The trial behind it
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Who cites it
31 citing papers in PubMed.
- Deciphering the Tenascin-C Nexus: A Comprehensive Review of Its Involvement in Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- The role of PRX1-expressing cells in periodontal regeneration and wound healing.Frontiers in physiology · 2023Review
- Tenascin-C in fibrosis in multiple organs: Translational implications.Seminars in cell & developmental biology · 2022Review
- Tenascin-C promotes bladder cancer progression and its action depends on syndecan-4 and involves NF-κB signaling activation.BMC cancer · 2022Article
- Revisiting the Tenascins: Exploitable as Cancer Targets?Frontiers in oncology · 2022Review
- Article
- Mesenchymal proteases and tissue fluidity remodel the extracellular matrix during airway epithelial branching in the embryonic avian lung.Development (Cambridge, England) · 2019Article
- TheBiology open · 2019Article
- Homeobox B7 accelerates the cancer progression of gastric carcinoma cells by promoting epithelial-mesenchymal transition (EMT) and activating Src-FAK pathway.OncoTargets and therapy · 2019Article
- A positive feedback loop bi-stably activates fibroblasts.Nature communications · 2018Article
- Transcriptional signatures of schizophrenia in hiPSC-derived NPCs and neurons are concordant with post-mortem adult brains.Nature communications · 2017Article
- Paired related homeobox protein 1 regulates PDGF-induced chemotaxis of hepatic stellate cells in liver fibrosis.Laboratory investigation; a journal of technical methods and pathology · 2017Article
- PIAS1-FAK Interaction Promotes the Survival and Progression of Non-Small Cell Lung Cancer.Neoplasia (New York, N.Y.) · 2016Article
- Functional Genomics Identifies Tis21-Dependent Mechanisms and Putative Cancer Drug Targets Underlying Medulloblastoma Shh-Type Development.Frontiers in pharmacology · 2016Article
- The sulfiredoxin-peroxiredoxin (Srx-Prx) axis in cell signal transduction and cancer development.Cancer letters · 2015Review
- Hydrogen peroxide - production, fate and role in redox signaling of tumor cells.Cell communication and signaling : CCS · 2015Review
- Down-regualtion of miR-106b induces epithelial-mesenchymal transition but suppresses metastatic colonization by targeting Prrx1 in colorectal cancer.International journal of clinical and experimental pathology · 2015Article
- The Axolotl Fibula as a Model for the Induction of Regeneration across Large Segment Defects in Long Bones of the Extremities.PloS one · 2015Article
- Tenascin-C: Form versus function.Cell adhesion & migration · 2015Review
- Crosstalk between breast cancer stem cells and metastatic niche: emerging molecular metastasis pathway?Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Fibroblast migration depends, in part, on activation of FAK and cellular interactions with tenascin-C (TN-C). Consistent with the idea that FAK regulates TN-C, migration-defective FAK-null cells expressed reduced levels of TN-C. Furthermore, expression of FAK in FAK-null fibroblasts induced TN-C, whereas inhibition of FAK activity in FAK-wild-type cells had the opposite effect. Paired-related homeobox 1 (Prx1) encodes a homeobox transcription factor that induces TN-C by interacting with a binding site within the TN-C promoter, and it also promotes fibroblast migration. Therefore, we hypothesized that FAK regulates TN-C by controlling the DNA-binding activity of Prx1 and/or by inducing Prx1 expression. Prx1-homeodomain binding site complex formation observed with FAK-wild-type fibroblasts failed to occur in FAK-null fibroblasts, yet expression of Prx1 in these cells induced TN-C promoter activity. Thus, FAK is not essential for Prx1 DNA-binding activity. However, activated FAK was essential for Prx1 expression. Functionally, Prx1 expression in FAK-null fibroblasts restored their ability to migrate toward fibronectin, in a manner that depends on TN-C. These results appear to be relevant in vivo because Prx1 and TN-C expression levels were reduced in FAK-null embryos. This paper suggests a model whereby FAK induces Prx1, and subsequently the formation of a TN-C-enriched ECM that contributes to fibroblast migration.
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