ArticleProceedings of the National Academy of Sciences of the United States of America2007
SHP-2 tyrosine phosphatase inhibits p73-dependent apoptosis and expression of a subset of p53 target genes induced by EGCG.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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
30 citing papers in PubMed, 50 citations in OpenAlex.
- Development and Application of Rapamycin-regulated Tyrosine Phosphatases.Journal of visualized experiments : JoVE · 2024Article
- Context-dependent activation of p53 target genes and induction of apoptosis by actinomycin D in aerodigestive tract cancers.Apoptosis : an international journal on programmed cell death · 2022Article
- CENPE Inhibition Leads to Mitotic Catastrophe and DNA Damage in Medulloblastoma Cells.Cancers · 2021Article
- A Review of the Antiviral Role of Green Tea Catechins.Molecules (Basel, Switzerland) · 2017Review
- The NAD(+) salvage pathway modulates cancer cell viability via p73.Cell death and differentiation · 2016Article
- Evasion of anti-growth signaling: A key step in tumorigenesis and potential target for treatment and prophylaxis by natural compounds.Seminars in cancer biology · 2015Review
- A multi-targeted approach to suppress tumor-promoting inflammation.Seminars in cancer biology · 2015Review
- Functions of Shp2 in cancer.Journal of cellular and molecular medicine · 2015Review
- FLLL12 induces apoptosis in lung cancer cells through a p53/p73-independent but death receptor 5-dependent pathway.Cancer letters · 2015Article
- T cell activation is reduced by the catalytically inactive form of protein tyrosine phosphatase SHP-2.International journal of clinical and experimental medicine · 2015Article
- Curcumin induces apoptosis of upper aerodigestive tract cancer cells by targeting multiple pathways.PloS one · 2015Article
- Multivariate signaling regulation by SHP2 differentially controls proliferation and therapeutic response in glioma cells.Journal of cell science · 2014Article
- Chemoprevention of oral cancer: Green tea experience.Journal of natural science, biology, and medicine · 2014Review
- Article
- RRM2 regulates Bcl-2 in head and neck and lung cancers: a potential target for cancer therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
- Going Green: The Role of the Green Tea Component EGCG in Chemoprevention.Journal of carcinogenesis & mutagenesis · 2013Article
- N-(phosphonacetyl)-L-aspartate induces TAp73-dependent apoptosis by modulating multiple Bcl-2 proteins: potential for cancer therapy.Oncogene · 2013Article
- Novel functions of the phosphatase SHP2 in the DNA replication and damage checkpoints.PloS one · 2012Article
- The chemopreventive and chemotherapeutic potentials of tea polyphenols.Current pharmaceutical biotechnology · 2012Review
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Green tea polyphenol, epigallocatechin-3-gallate (EGCG) differentially regulates the cellular growth of cancer cells in a p53-dependent manner through apoptosis and/or cell cycle arrest. In an effort to further elucidate the mechanism of differential growth regulation by EGCG, we have investigated the role of the tyrosine phosphatase, SHP-2. Comparing the responses of mouse embryonic fibroblasts (MEFs), expressing either WT or functionally inactive/truncated SHP-2, we find that inactivation of SHP-2 remarkably sensitizes cells to EGCG-mediated killing. MEFs lacking functional SHP-2 undergo massive apoptosis upon treatment with EGCG. By comparing gene expression profiles, we have identified a set of transcriptional targets of p53 that are differentially modulated in cells undergoing apoptosis. Western blot and real-time PCR analyses of a select group of genes further confirm that the expression is SHP-2-dependent. Similar observations were made in MEFs lacking p53, confirming that the expression of these "p53 target genes" is p53-independent. In addition, EGCG treatment induced the expression of p73 mRNA and protein in both cell types, but not p63. Inactivation of p73 in cells expressing nonfunctional SHP-2 markedly inhibited apoptosis and p53 target gene expression. Although phosphorylation of JNK is differentially regulated by SHP2, it was found to be dispensable for EGCG-induced apoptosis and p53 target gene expression. Our results have identified SHP-2 as a negative regulator of EGCG-induced-apoptosis and have identified a subset of p53 target genes whose expression is paradoxically not mediated by p53 but by one of its family members, p73.
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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.