ArticleJournal of virology2001
Inactivation of p21 by E1A leads to the induction of apoptosis in DNA-damaged cells.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 54 citations in OpenAlex.
- Resveratrol potentiates chemotherapeutic efficacy of olaparib in MCF7 human breast cancer cells by inducing apoptosis.Irish journal of medical science · 2026Article
- Recent Advances in Novel Antiviral Therapies against Human Adenovirus.Microorganisms · 2020Review
- Article
- Histone Deacetylase Inhibitor Suberoylanilide Hydroxamic Acid Suppresses Human Adenovirus Gene Expression and Replication.Journal of virology · 2019Article
- Article
- Camptothecin exhibits topoisomerase1-independent KMT1A suppression and myogenic differentiation in alveolar rhabdomyosarcoma cells.Oncotarget · 2018Article
- miRNAs as Potential Treatment Targets and Treatment Options in Cancer.Molecular diagnosis & therapy · 2018Review
- Article
- Article
- The dynamics of E1A in regulating networks and canonical pathways in quiescent cells.BMC research notes · 2011Article
- Armoring CRAds with p21/Waf-1 shRNAs: the next generation of oncolytic adenoviruses.Cancer gene therapy · 2010Article
- Oncolytic adenoviral mutants with E1B19K gene deletions enhance gemcitabine-induced apoptosis in pancreatic carcinoma cells and anti-tumor efficacy in vivo.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Article
- Paclitaxel and vincristine potentiate adenoviral oncolysis that is associated with cell cycle and apoptosis modulation, whereas they differentially affect the viral life cycle in non-small-cell lung cancer cells.Cancer gene therapy · 2006Article
- Identification of p53-46F as a super p53 with an enhanced ability to induce p53-dependent apoptosis.Cancer science · 2006Article
- Involvement of Bcl-X(L) deamidation in E1A-mediated cisplatin sensitization of ovarian cancer cells.Oncogene · 2006Article
- Recent lessons in gene expression, cell cycle control, and cell biology from adenovirus.Oncogene · 2005Review
- Epstein-Barr virus can inhibit genotoxin-induced G1 arrest downstream of p53 by preventing the inactivation of CDK2.Oncogene · 2003Article
- Apoptosis or growth arrest: modulation of the cellular response to p53 by proliferative signals.Oncogene · 2003Article
- The adenovirus e3 promoter is sensitive to activation signals in human T cells.Journal of virology · 2003Article
- Comparative sequence analysis of the largest E1A proteins of human and simian adenoviruses.Journal of virology · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
A major impediment to successful chemotherapy is the propensity for some tumor cells to undergo cell cycle arrest rather than apoptosis. It is well established, however, that the adenovirus E1A protein can sensitize these cells to the induction of apoptosis by anticancer agents. To further understand how E1A enhances chemosensitivity, we have made use of a human colon carcinoma cell line (HCT116) which typically undergoes cell cycle arrest in response to chemotherapeutic drugs. As seen by the analysis of E1A mutants, we show here that E1A can induce apoptosis in these cells by neutralizing the activities of the cyclin-dependent kinase inhibitor p21. E1A's ability to interact with p21 and thereby restore Cdk2 activity in DNA-damaged cells correlates with the reversal of G(1) arrest, which in turn leads to apoptosis. Analysis of E1A mutants failing to bind p300 (also called CBP) or Rb shows that they are almost identical to wild-type E1A in their ability to initially overcome a G(1) arrest in cells after DNA damage, while an E1A mutant failing to bind p21 is not. However, over time, this mutant, which can still target Rb, is far more efficient in accumulating cells with a DNA content greater than 4N but is similar to wild-type E1A and the other E1A mutants in releasing cells from a p53-mediated G(2) block following chemotherapeutic treatment. Thus, we suggest that although E1A requires the binding of p21 to create an optimum environment for apoptosis to occur in DNA-damaged cells, E1A's involvement in other pathways may be contributing to this process as well. A model is proposed to explain the implications of these findings.
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.