ArticlePloS one2012
A novel anticancer therapy that simultaneously targets aberrant p53 and Notch activities in tumors.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Recombinant human type-5 adenovirus (H101) combined with radiofrequency ablation versus traditional radiofrequency ablation for hepatocellular carcinoma ≤ 3 cm: a phase III randomized controlled trial.International journal of surgery (London, England) · 2025Article
- An Extensive Review on Preclinical and Clinical Trials of Oncolytic Viruses Therapy for Pancreatic Cancer.Frontiers in oncology · 2022Review
- Oncolytic Virotherapy: From Bench to Bedside.Frontiers in cell and developmental biology · 2021Review
- Treatment with retinoic acid and lens epithelial cell-conditioned mediumExperimental and therapeutic medicine · 2015Article
- Effects of inhibition of hedgehog signaling on cell growth and migration of uveal melanoma cells.Cancer biology & therapy · 2014Article
- Effects of dexamethasone on angiotensin II-induced changes of monolayer permeability and F-actin distribution in glomerular endothelial cells.Experimental and therapeutic medicine · 2013Article
- Detection and validation of circulating endothelial cells, a blood-based diagnostic marker of acute myocardial infarction.PloS one · 2013Article
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11 authors.
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Abstract
Notch signaling pathway plays an important role in tumorigenesis by maintaining the activity of self-renewal of cancer stem cells, and therefore, it is hypothesized that interference of Notch signaling may inhibit tumor formation and progression. H101 is a recombinant oncolytic adenovirus that is cytolytic in cells lacking intact p53, but it is unable to eradicate caner stem cells. In this study, we tested a new strategy of tumor gene therapy by combining a Notch1-siRNA with H101 oncolytic adenovirus. In HeLa-S3 tumor cells, the combined therapy blocked the Notch pathway and induced apoptosis in tumors that are p53-inactive. In nude mice bearing xenograft tumors derived from HeLa-S3 cells, the combination of H101/Notch1-siRNA therapies inhibited tumor growth. Moreover, Notch1-siRNA increased Hexon gene expression at both the transcriptional and the translational levels, and promoted H101 replication in tumors, thereby enhancing the oncolytic activity of H101. These data demonstrate the feasibility to combine H101 p53-targted oncolysis and anti-Notch siRNA activities as a novel anti-cancer therapy.
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