ArticleCancer gene therapy2004
E1A-induced apoptosis does not prevent replication of adenoviruses with deletion of E1b in majority of infected cancer cells.
Article in Cancer gene therapy, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Absent in melanoma 2 enhances anti-tumour effects of CAIX promotor controlled conditionally replicative adenovirus in renal cancer.Journal of cellular and molecular medicine · 2020Article
- Temozolomide renders murine cancer cells susceptible to oncolytic adenovirus replication and oncolysis.Cancer biology & therapy · 2018Article
- Adenovirus Lacking E1b Efficiently Induces Cytopathic Effect in HPV-16-Positive Murine Cancer Cells via Virus Replication and Apoptosis.Cancer investigation · 2018Article
- The role of JNK phosphorylation as a molecular target to enhance adenovirus replication, oncolysis and cancer therapeutic efficacy.Cancer biology & therapy · 2018Article
- Article
- Development of an Oncolytic Adenovirus with Enhanced Spread Ability through Repeated UV Irradiation and Cancer Selection.Viruses · 2016Article
- The E1B19K-deleted oncolytic adenovirus mutant AdΔ19K sensitizes pancreatic cancer cells to drug-induced DNA-damage by down-regulating Claspin and Mre11.Oncotarget · 2016Article
- Combined therapy of oncolytic adenovirus and temozolomide enhances lung cancer virotherapy in vitro and in vivo.Virology · 2016Article
- Oncolytic Replication of E1b-Deleted Adenoviruses.Viruses · 2015Review
- Virotherapy targeting cyclin E overexpression in tumors with adenovirus-enhanced cancer-selective promoter.Journal of molecular medicine (Berlin, Germany) · 2015Article
- Indole-3-carbinol (I3C) increases apoptosis, represses growth of cancer cells, and enhances adenovirus-mediated oncolysis.Cancer biology & therapy · 2014Article
- Adenoviral vectors for prodrug activation-based gene therapy for cancer.Anti-cancer agents in medicinal chemistry · 2014Review
- Molecular basis for viral selective replication in cancer cells: activation of CDK2 by adenovirus-induced cyclin E.PloS one · 2013Article
- Enhanced cancer cell killing by truncated E2F-1 used in combination with oncolytic adenovirus.Virology · 2012Article
- Article
- Dual E1A oncolytic adenovirus: targeting tumor heterogeneity with two independent cancer-specific promoter elements, DF3/MUC1 and hTERT.Cancer gene therapy · 2011Article
- 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
- Human telomerase reverse transcriptase promoter-driven oncolytic adenovirus with E1B-19 kDa and E1B-55 kDa gene deletions.Human gene therapy · 2008Article
- Adenovirus E1B55K region is required to enhance cyclin E expression for efficient viral DNA replication.Journal of virology · 2008Article
- Selective replication of E1B55K-deleted adenoviruses depends on enhanced E1A expression in cancer cells.Cancer gene therapy · 2006Article
Corrections and comments
- Expression of concern
Authors and funding
9 authors.
Funding
Abstract
Apoptotic pathways are initiated as a cellular defense mechanism to eliminate adenovirus-infected cells. We have investigated how E1A-induced apoptosis interferes with viral replication in cancer cells. We found that E1B19K alone can efficiently suppress E1A-induced apoptosis in cancer cells. Viruses deleted for both E1B19K and E1B55K resulted in cellular DNA degradation. However, less than 20% of human lung cancer cells infected with a virus deleted for both E1B19K and E1B55 K had evidence of chromatin condensation and multiple-micronuclei formation (apoptotic hallmarks); these cells could not produce infectious viral particles. The majority of cancer cells infected with viruses deleted for the entire E1b gene did not undergo extended apoptosis and produced abundant viral progeny. Thus, only a fraction of cancer cells underwent apoptosis and did not allow E1b-deleted viruses to replicate, while the majority of cancer cells were resistant to E1A-induced apoptosis and could support virus-selective replication. The results of this study imply that, in addition to inhibiting E1A-induced apoptosis, E1B proteins may contribute other important roles in the viral life cycle. Our results also suggest that combining virus-induced apoptosis and selective viral replication into one vector will be a novel approach to destroy cancer cells.
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