ArticleOncogene1999
Inhibition of the putative tumor suppressor gene TIMP-3 by tumor-derived p53 mutants and wild type p53.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 40 citations in OpenAlex.
- Tumor suppressors in Sox2-mediated lung cancers promote distinct cell-intrinsic and immunologic remodeling.JCI insight · 2025Article
- The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024Review
- Mutant p53 in cell-cell interactions.Genes & development · 2021Review
- p53's Extended Reach: The Mutant p53 Secretome.Biomolecules · 2020Review
- Mutant p53 in Cancer Progression and Targeted Therapies.Frontiers in oncology · 2020Review
- Anti-inflammatory macrophages activate invasion in pancreatic adenocarcinoma by increasing the MMP9 and ADAM8 expression.Medical oncology (Northwood, London, England) · 2014Article
- Modulation of NKG2D ligand expression and metastasis in tumors by spironolactone via RXRγ activation.The Journal of experimental medicine · 2013Article
- Clinicopathological and prognostic significance of Ki-67, caspase-3 and p53 expression in gastric carcinomas.Oncology letters · 2013Article
- Multivalent pseudopeptides targeting cell surface nucleoproteins inhibit cancer cell invasion through tissue inhibitor of metalloproteinases 3 (TIMP-3) release.The Journal of biological chemistry · 2012Article
- [Expressions and significance of TIMP-3 and mtp53 in non-small cell lung cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2012Article
- Increased expression of the heterogeneous nuclear ribonucleoprotein K in pancreatic cancer and its association with the mutant p53.International journal of cancer · 2010Article
- Predicting invasive phenotype with CDH1, CDH13, CD44, and TIMP3 gene expression in primary breast cancer.Cancer science · 2009Article
- TIMP-3 deficiency in the host, but not in the tumor, enhances tumor growth and angiogenesis.Oncogene · 2006Article
- Expression of tissue inhibitor of matrix metalloproteinases (TIMP)-3 protein in invasive breast carcinoma: relation to tumor phenotype and clinical outcome.Breast cancer research : BCR · 2006Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p53 gene is a tumor suppressor that regulates the expression of genes required for cell cycle arrest or apoptosis. Mutations in p53 have been observed in over 60% of all human cancers. Certain classes of mutant p53 proteins maintain some of their activities or acquire novel activities and thus may contribute to the transformed phenotype. By carrying out an analysis of differential gene expression using cDNA expression arrays, we compared the expression patterns of cells expressing no p53 to isogenic lines expressing the codon 248 Arg to Trp mutant p53 allele (R248W). In this report, we show that the R248W and D281G p53 mutants, two of the more commonly occurring mutations, as well as wild type p53, repress transcription of the tissue inhibitor of metalloproteinases type 3 (TIMP-3) gene by greater than tenfold. TIMP-3 expression has been observed to be repressed in many tumors and its reduced expression is thought to contribute to tumor metastasis and invasiveness by allowing increased activity of metalloproteinases in the extracellular matrix. Since mutant forms of p53 tend to be expressed at greatly elevated levels in many human tumors, the retention of their ability to repress TIMP-3 illustrate one mechanism by which mutant forms of the p53 gene may contribute to tumorigenesis.
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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.