ArticleCancer letters2010
p53-Dependent p21-mediated growth arrest pre-empts and protects HCT116 cells from PUMA-mediated apoptosis induced by EGCG.
Article in Cancer letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- 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
- EGCG binds intrinsically disordered N-terminal domain of p53 and disrupts p53-MDM2 interaction.Nature communications · 2021Article
- The Role of the Cyclin Dependent Kinase Inhibitor p21Cancers · 2019Review
- Adenovirus-mediated small interfering RNA targeting ezrin induces apoptosis and inhibits metastasis of human osteosarcoma MG-63 cells.Bioscience reports · 2018Article
- miRNA‑222 promotes liver cancer cell proliferation, migration and invasion and inhibits apoptosis by targeting BBC3.International journal of molecular medicine · 2018Article
- Silencing microRNA-143 protects the integrity of the blood-brain barrier: implications for methamphetamine abuse.Scientific reports · 2016Article
- Article
- An Association Map on the Effect of Flavonoids on the Signaling Pathways in Colorectal Cancer.International journal of medical sciences · 2016Review
- PUMA mediates ER stress-induced apoptosis in portal hypertensive gastropathy.Cell death & disease · 2014Article
- Anticancer effects and molecular mechanisms of epigallocatechin-3-gallate.Integrative medicine research · 2014Review
- Epigallocatechin-3-gallate prevents autoimmune-associated down- regulation of p21 in salivary gland cells through a p53-independent pathway.Inflammation & allergy drug targets · 2014Article
- Lifestyle Modifications and Colorectal Cancer.Current colorectal cancer reports · 2014Review
- EGCG suppresses Fused Toes Homolog protein through p53 in cervical cancer cells.Molecular biology reports · 2013Article
- Going Green: The Role of the Green Tea Component EGCG in Chemoprevention.Journal of carcinogenesis & mutagenesis · 2013Article
- Article
- Identifying molecular targets of lifestyle modifications in colon cancer prevention.Frontiers in oncology · 2013Article
- Role of Ku70 and Bax in epigallocatechin-3-gallate-induced apoptosis of A549 cells in vivo.Oncology letters · 2013Article
- Cyclin D1 degradation and p21 induction contribute to growth inhibition of colorectal cancer cells induced by epigallocatechin-3-gallate.Journal of cancer research and clinical oncology · 2012Article
- Green tea polyphenols increase p53 transcriptional activity and acetylation by suppressing class I histone deacetylases.International journal of oncology · 2012Article
- Green tea polyphenols induce p53-dependent and p53-independent apoptosis in prostate cancer cells through two distinct mechanisms.PloS one · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
The tumor suppressor protein p53 plays a key role in regulation of negative cellular growth in response to EGCG. To further explore the role of p53 signaling and elucidate the molecular mechanism, we employed colon cancer HCT116 cell line and its derivatives in which a specific transcriptional target of p53 is knocked down by homologous recombination. Cells expressing p53 and p21 accumulate in G1 upon treatment with EGCG. In contrast, same cells lacking p21 traverse through the cell cycle and eventually undergo apoptosis as revealed by TUNEL staining. Treatment with EGCG leads to induction of p53, p21 and PUMA in p21 wild-type, and p53 and PUMA in p21(-/-) cells. Ablation of p53 by RNAi protects p21(-/-) cells, thus indicating a p53-dependent apoptosis by EGCG. Furthermore, analysis of cells lacking PUMA or Bax with or without p21 but with p53 reveals that all the cells expressing p53 and p21 survived after EGCG treatment. More interestingly, cells lacking both PUMA and p21 survived ECGC treatment whereas those lacking p21 and Bax did not. Taken together, our results present a novel concept wherein p21-dependent growth arrest pre-empts and protects cells from otherwise, in its absence, apoptosis which is mediated by activation of pro-apoptotic protein PUMA. Furthermore, we find that p53-dependent activation of PUMA in response to EGCG directly leads to apoptosis with out requiring Bax as is the case in response to agents that induce DNA damage. p21, thus can be used as a molecular switch for therapeutic intervention of colon cancer.
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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.