ArticleMolecular carcinogenesis2008
Fyn is a novel target of (-)-epigallocatechin gallate in the inhibition of JB6 Cl41 cell transformation.
Article in Molecular carcinogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 88 citations in OpenAlex.
- Dihydromyrcenol Modulates Involucrin Expression through the Akt Signaling Pathway.International journal of molecular sciences · 2024Article
- Epigallocatechin-3-Gallate Therapeutic Potential in Cancer: Mechanism of Action and Clinical Implications.Molecules (Basel, Switzerland) · 2023Review
- In Silico Investigation of the Anti-Tumor Mechanisms of Epigallocatechin-3-Gallate.Molecules (Basel, Switzerland) · 2019Article
- TFAP2C-Activated MALAT1 Modulates the Chemoresistance of Docetaxel-Resistant Lung Adenocarcinoma Cells.Molecular therapy. Nucleic acids · 2019Article
- Nuclear factor-erythroid 2-related factor 3 (NRF3) is low expressed in colorectal cancer and its down-regulation promotes colorectal cancer malignance through activating EGFR and p38/MAPK.American journal of cancer research · 2019Article
- Molecular Targets of Epigallocatechin-Gallate (EGCG): A Special Focus on Signal Transduction and Cancer.Nutrients · 2018Review
- MNAT1 is overexpressed in colorectal cancer and mediates p53 ubiquitin-degradation to promote colorectal cancer malignance.Journal of experimental & clinical cancer research : CR · 2018Article
- In Vitro and In Silico Studies of the Molecular Interactions of Epigallocatechin-3-Molecules (Basel, Switzerland) · 2018Review
- Protective and Restorative Effects of Nutrients and Phytochemicals.The open biochemistry journal · 2018Review
- Cancer Preventive Activities of Tea Catechins.Molecules (Basel, Switzerland) · 2016Review
- Suppressive Effects of Tea Catechins on Breast Cancer.Nutrients · 2016Review
- Lessons learned from cancer prevention studies with nutrients and non-nutritive dietary constituents.Molecular nutrition & food research · 2016Review
- Review
- Niflumic acid exhibits anti-tumor activity in nasopharyngeal carcinoma cells through affecting the expression of ERK1/2 and the activity of MMP2 and MMP9.International journal of clinical and experimental pathology · 2015Article
- Green tea compounds in breast cancer prevention and treatment.World journal of clinical oncology · 2014Review
- The P110 subunit of PI3-K is a therapeutic target of acacetin in skin cancer.Carcinogenesis · 2014Article
- A chrysin derivative suppresses skin cancer growth by inhibiting cyclin-dependent kinases.The Journal of biological chemistry · 2013Article
- Signal transduction and molecular targets of selected flavonoids.Antioxidants & redox signaling · 2013Review
- Mycalamide A shows cytotoxic properties and prevents EGF-induced neoplastic transformation through inhibition of nuclear factors.Marine drugs · 2012Article
- Health-promoting effects of green tea.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
The cancer preventive action of (-)-epigallocatechin gallate (EGCG), found in green tea, is strongly supported by epidemiology and laboratory research data. However, the mechanism by which EGCG inhibits carcinogenesis and cell transformation is not clear. In this study, we report that EGCG suppressed epidermal growth factor (EGF)-induced cell transformation in JB6 cells. We also found that EGCG inhibited EGF-induced Fyn kinase activity and phosphorylation in vitro and in vivo. Fyn was implicated in the process because EGF-induced JB6 cell transformation was inhibited by small interfering RNA (siRNA)-Fyn-JB6 cells. With an in vitro protein-binding assay, we found that EGCG directly bound with the GST-Fyn-SH2 domain but not the GST-Fyn-SH3 domain. The K(d) value for EGCG binding to the Fyn SH2 domain was 0.367 +/- 0.122 microM and B(max) was 1.35 +/- 0.128 nmol/mg. Compared with control JB6 Cl41 cells, EGF-induced phosphorylation of p38 MAP kinase (p38 MAPK) (Thr180/Tyr182), ATF-2 (Thr71) and signal transducer and activator of transcription 1 (STAT1) (Thr727) was decreased in siRNA-Fyn-JB6 cells. EGCG could inhibit the phosphorylation of p38 MAPK, ATF-2, and STAT1. The DNA binding ability of AP-1, STAT1, and ATF-2 was also decreased in siRNA-Fyn-JB6 cells. Overall, these results demonstrated that EGCG interacted with Fyn and inhibited Fyn kinase activity and thereby regulated EGF-induced cell transformation. Inhibition of Fyn kinase activity is a novel and important mechanism that may be involved in EGCG-induced inhibition of cell transformation.
Indexed as
Identifiers
What OpenQuestion holds
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.