ArticleJournal of cellular physiology2011
Regulation of non-classical FGF1 release and FGF-dependent cell transformation by CBF1-mediated notch signaling.
Article in Journal of cellular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 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
11 citing papers in PubMed, 19 citations in OpenAlex.
- Electrical stimulation induced pre-vascularization of engineered dental pulp tissue.Regenerative therapy · 2024Article
- Interaction between BEND5 and RBPJ suppresses breast cancer growth and metastasis via inhibiting Notch signaling.International journal of biological sciences · 2022Article
- Through the back door: Unconventional protein secretion.Cell surface (Amsterdam, Netherlands) · 2020Review
- AHNAK2 Participates in the Stress-Induced Nonclassical FGF1 Secretion Pathway.Journal of cellular biochemistry · 2015Article
- Neurodegeneration in Parkinson's disease: interactions of oxidative stress, tryptophan catabolites and depression with mitochondria and sirtuins.Molecular neurobiology · 2014Review
- HIV envelope protein gp120-induced apoptosis in lung microvascular endothelial cells by concerted upregulation of EMAP II and its receptor, CXCR3.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Dysregulation of pathways involved in the processing of cancer and microenvironment information in MCA + TPA transformed C3H/10T1/2 cells.In vitro cellular & developmental biology. Animal · 2013Article
- Nonclassically Secreted Regulators of Angiogenesis.Angiology: open access · 2013Article
- Protein-phospholipid interactions in nonclassical protein secretion: problem and methods of study.International journal of molecular sciences · 2013Article
- Sphingosine kinase 1 in cancer.Advances in cancer research · 2013Review
- Notch signaling modulates hypoxia-induced neuroendocrine differentiation of human prostate cancer cells.Molecular cancer research : MCR · 2012Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
FGF1, a widely expressed proangiogenic factor involved in tissue repair and carcinogenesis, is released from cells through a non-classical pathway independent of endoplasmic reticulum and Golgi. Although several proteins participating in FGF1 export were identified, genetic mechanisms regulating this process remained obscure. We found that FGF1 export and expression are regulated through Notch signaling mediated by transcription factor CBF1 and its partner MAML. The expression of a dominant negative (dn) form of CBF1 in 3T3 cells induces transcription of FGF1 and sphingosine kinase 1 (SphK1), which is a component of FGF1 export pathway. dnCBF1 expression stimulates the stress-independent release of transduced FGF1 from NIH 3T3 cells and endogenous FGF1 from A375 melanoma cells. NIH 3T3 cells transfected with dnCBF1 form colonies in soft agar and produce rapidly growing highly angiogenic tumors in nude mice. The transformed phenotype of dnCBF1 transfected cells is efficiently blocked by dn forms of FGF receptor 1 and S100A13, which is a component of FGF1 export pathway. FGF1 export and acceleration of cell growth induced by dnCBF1 depend on SphK1. Similar to dnCBF1, dnMAML transfection induces FGF1 expression and release, and accelerates cell proliferation. The latter effect is strongly decreased in FGF1 null cells. We suggest that the regulation of FGF1 expression and release by CBF1-mediated Notch signaling can play an important role in tumor formation.
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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 OpenQuestion graph.