ArticleJournal of cancer research and clinical oncology2012
Cyclin D1 degradation and p21 induction contribute to growth inhibition of colorectal cancer cells induced by epigallocatechin-3-gallate.
Article in Journal of cancer research and clinical oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 49 citations in OpenAlex.
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- Antitumor Effect of Epigallocatechin Gallate and Vincristine in Mice with L5178Y Lymphoma.Plants (Basel, Switzerland) · 2023Article
- Morin Sensitizes MDA-MB-231 Triple-Negative Breast Cancer Cells to Doxorubicin Cytotoxicity by Suppressing FOXM1 and Attenuating EGFR/STAT3 Signaling Pathways.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Theabrownin Alleviates Colorectal Tumorigenesis in Murine AOM/DSS Model via PI3K/Akt/mTOR Pathway Suppression and Gut Microbiota Modulation.Antioxidants (Basel, Switzerland) · 2022Article
- Article
- Inhibition and potential treatment of colorectal cancer by natural compoundsFrontiers in oncology · 2022Review
- Plant Natural Products: Promising Resources for Cancer Chemoprevention.Molecules (Basel, Switzerland) · 2021Review
- Periplocymarin Induced Colorectal Cancer Cells ApoptosisFrontiers in oncology · 2021Article
- Epigallocatechin gallate induces chemopreventive effects on rats with diethylnitrosamine‑induced liver cancer via inhibition of cell division cycle 25A.Molecular medicine reports · 2020Article
- Anti-proliferative activity of A. Oxyphylla and its bioactive constituent nootkatone in colorectal cancer cells.BMC cancer · 2020Article
- Nitro aspirin (NCX4040) induces apoptosis in PC3 metastatic prostate cancer cells via hydrogen peroxide (HFree radical biology & medicine · 2019Article
- Advances in the Antagonism of Epigallocatechin-3-gallate in the Treatment of Digestive Tract Tumors.Molecules (Basel, Switzerland) · 2019Review
- Anti-proliferative and anti-apoptotic potential effects of epigallocatechin-3-gallate and/or metformin on hepatocellular carcinoma cells: in vitro study.Molecular biology reports · 2019Article
- Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine.Chinese medicine · 2019Review
- Epigallocatechin-3-Gallate Promotes the Growth of Mink Hair Follicles Through Sonic Hedgehog and Protein Kinase B Signaling Pathways.Frontiers in pharmacology · 2018Article
- Polyphenols in Colorectal Cancer: Current State of Knowledge including Clinical Trials and Molecular Mechanism of Action.BioMed research international · 2018Review
- The cytotoxic mechanism of epigallocatechin gallate on proliferative HaCaT keratinocytes.Journal of biomedical science · 2017Article
- Therapeutic targeting of replicative immortality.Seminars in cancer biology · 2015Review
- Epigallocatechin-3-gallate prevents autoimmune-associated down- regulation of p21 in salivary gland cells through a p53-independent pathway.Inflammation & allergy drug targets · 2014Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
purposeThe public has paid attention to green tea due to its health benefits. Epigallocatechin-3-gallate (EGCG), the major component of green tea, is well documented to induce apoptosis and cell cycle arrest in cancer cells by targeting multiple signal transduction pathways. However, the detailed mechanism(s) of action needs to be determined.
methodsCell growth was evaluated by MTT assay, cell cycle analysis, and caspase 3/7 activity. Protein expression was analyzed through Western blotting. Reverse transcription polymerase chain reaction was used for examining mRNA expression of p21 and cyclin D1. The promoter activity of p21 was assessed by the luciferase reporter system.
resultsWe identified cyclin D1 and p21 as molecular targets of EGCG in human colorectal cancer cells. We observed that cyclin D1 was down-regulated, while p21 expression was up-regulated by EGCG in dose- and time-dependent manners. Furthermore, we found EGCG decreased cyclin D1 protein stability, therefore triggering ubiquitin-dependent proteasomal degradation. Meanwhile, EGCG increased p21 promoter activity, resulting in up-regulation of p21 mRNA and protein, which was likely dependent on extracellular-signal-regulated kinase (ERK), inhibitor of nuclear factor kappa-B kinase (IKK) and phosphoinositide 3-kinase (PI3 K).
conclusionThe data presented here details a novel mechanism by which EGCG inhibits cell growth of colorectal cancer cells. Namely, EGCG-induced cyclin D1 degradation and p21 transcriptional activation partially contribute to growth suppression in these cells.
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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.