ArticleProceedings of the National Academy of Sciences of the United States of America1994
Transcriptional regulation of basic fibroblast growth factor gene by p53 in human glioblastoma and hepatocellular carcinoma cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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Who cites it
38 citing papers in PubMed, 143 citations in OpenAlex.
- Elucidating the tumor microenvironment interactions in breast, cervical, and ovarian cancer through single-cell RNA sequencing.Scientific reports · 2025Article
- Potential enhancement of post-stroke angiogenic response by targeting the oligomeric aggregation of p53 protein.Frontiers in cellular neuroscience · 2023Review
- Clinical and therapeutic relevance of cancer-associated fibroblasts.Nature reviews. Clinical oncology · 2021Review
- A ZEB1/p53 signaling axis in stromal fibroblasts promotes mammary epithelial tumours.Nature communications · 2019Article
- Lymphatic vasculature in tumor metastasis and immunobiology.Journal of Zhejiang University. Science. B · 2019Review
- Molecular mechanisms underlying gliomas and glioblastoma pathogenesis revealed by bioinformatics analysis of microarray data.Medical oncology (Northwood, London, England) · 2017Article
- Fibroblast growth factor family as a potential target in the treatment of hepatocellular carcinoma.Journal of hepatocellular carcinoma · 2014Review
- Oncogenes and angiogenesis: a way to personalize anti-angiogenic therapy?Cellular and molecular life sciences : CMLS · 2013Review
- Article
- The role of stromal myofibroblast and extracellular matrix in tumor angiogenesis.Genes & cancer · 2011Article
- Defective p53 antiangiogenic signaling in glioblastoma.Neuro-oncology · 2010Article
- Involvement of stromal p53 in tumor-stroma interactions.Seminars in cell & developmental biology · 2010Review
- Inhibition of tumor angiogenesis by p53: a new role for the guardian of the genome.Journal of molecular medicine (Berlin, Germany) · 2007Review
- Fibroblast growth factor (FGF)-2 and FGF receptor 3 are required for the development of the substantia nigra, and FGF-2 plays a crucial role for the rescue of dopaminergic neurons after 6-hydroxydopamine lesion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- A dyad symmetry element in the fibroblast growth factor-2 gene promoter with different levels of activity in astrocytoma and hepatocelluar carcinoma cell lines.Journal of neuro-oncology · 2006Article
- Expression of basic fibroblast growth factor correlates with resistance to paclitaxel in human patient tumors.Pharmaceutical research · 2006Article
- FGF1 inhibits p53-dependent apoptosis and cell cycle arrest via an intracrine pathway.Oncogene · 2005Article
- Fate of UVB-induced p53 mutations in SKH-hr1 mouse skin after discontinuation of irradiation: relationship to skin cancer development.Oncogene · 2005Article
- Angiogenesis in gliomas: biology and molecular pathophysiology.Brain pathology (Zurich, Switzerland) · 2005Review
- Genetic and hypoxic regulation of angiogenesis in gliomas.Journal of neuro-oncology · 2004Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations of the p53 gene are found in various human cancers. The frequency of its mutation is reported to increase during tumor progression in most tumors. In human gliomas, mutations of the p53 gene are found in about one-third of the malignant forms and in few of the benign ones, indicating their possible involvement in tumor progression. On the other hand, we have recently shown that basic fibroblast growth factor (basic FGF) plays a crucial role in tumor progression as an autocrine growth factor in tissues of human gliomas. Therefore, we hypothesized that p53 might regulate the promoter activity of the basic FGF gene, which has several GC boxes and no typical TATA box. In this study, cotransfection assays using human glioblastoma and hepatocellular carcinoma cells and establishment of stable cell lines expressing mutant-type p53 were performed. The basic FGF gene promoter was demonstrated to be regulated by p53 at the transcriptional level and its basal core promoter was found to be responsive to p53. Expression of endogenous basic FGF was also demonstrated to be activated by mutant type p53. Wild-type p53 repressed gene expression of the basic FGF and its mutant activated it in vitro, implying one of the possible pathways in tumor progression.
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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.