ArticleOncotarget2017
Selective eradication of cancer cells by delivery of adenovirus-based toxins.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Bacterial defense systems: Mechanisms, homology to eukaryotic immune systems, and applications.Zoological research · 2026Review
- Bacterial Toxin-Antitoxin Systems' Cross-Interactions-Implications for Practical Use in Medicine and Biotechnology.Toxins · 2023Review
- Article
- Limited-angle tomographic phase microscopy utilizing confocal scanning fluorescence microscopy.Biomedical optics express · 2021Article
- Toxin-antitoxin systems and their medical applications: current status and future perspective.Applied microbiology and biotechnology · 2021Review
- Developmental Landscape of Potential Vaccine Candidates Based on Viral Vector for Prophylaxis of COVID-19.Frontiers in molecular biosciences · 2021Review
- Applications of phage-derived RNA-based technologies in synthetic biology.Synthetic and systems biotechnology · 2020Review
- Viral Vector-Based Melanoma Gene Therapy.Biomedicines · 2020Review
- New frontiers in oncolytic viruses: optimizing and selecting for virus strains with improved efficacy.Biologics : targets & therapy · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectiveKRAS mutation is an early event in colorectal cancer carcinogenesis. We previously reported that a recombinant adenovirus, carrying a pro-apoptotic gene (PUMA) under the regulation of Ets/AP1 (RAS-responsive elements) suppressed the growth of cancer cells harboring hyperactive KRAS. We propose to exploit the hyperactive RAS pathway, rather than to inhibit it as was previously tried and failed repeatedly. We aim to improve efficacy by substituting PUMA with a more potent toxin, the bacterial MazF-MazE toxin-antitoxin system, under a very tight regulation.
resultsA massive cell death, in a dose-dependent manner, reaching 73% at MOI 10 was seen in KRAS cells as compared to 22% in WT cells. Increase expression of MazE (the anti-toxin) protected normal cells from any possible internal or external leakage of the system and confirmed the selectivity, specificity and safety of the targeting system. Considerable tumor shrinkage (61%) was demonstrated in vivo following MazEF-encoding adenovirus treatment without any side effects.
designEfficient vectors for cancer-directed gene delivery were constructed; "pAdEasy-Py4-SV40mP-mCherry-MazF""pAdEasy-Py4-SV40mP-mCherry-MazF-IRES-TetR-CMVmp-MazE-IRES-EGFP","pAdEasy-ΔPy4-SV40mP-mCherry-MazF-IRES-TetR-CMVmp-MazE-IRES-EGFP "and "pAdEasy-mCherry". Virus particles were produced and their potency was tested. Cell death was measured qualitatively by using the fluorescent microscopy and colony formation assay, and was quantified by MTT. FACS analysis using annexin V and RedDot2 dyes was performed for measuring apoptotic and dead cells, respectively. In vivo tumor formation was measured in a xenograft model.
conclusionsA proof of concept for a novel cancer safe and effective gene therapy exploiting an aberrant hyperactive pathway is achievable.
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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.