ArticleCancer gene therapy2002
Impaired expression of a human septin family gene Bradeion inhibits the growth and tumorigenesis of colorectal cancer in vitro and in vivo.
Article in Cancer gene therapy, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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.
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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, 34 citations in OpenAlex.
- Aberrant circulating tumor DNA methylation and exosomal microRNA biomarkers for early detection of colorectal cancer.Molecular biology reports · 2023Review
- Adenosine Kinase on Deoxyribonucleic Acid Methylation: Adenosine Receptor-Independent Pathway inFrontiers in pharmacology · 2022Review
- Acute myeloid leukemia withSAGE open medical case reports · 2018Article
- Septin Mutations in Human Cancers.Frontiers in cell and developmental biology · 2016Review
- Septin functions in organ system physiology and pathology.Biological chemistry · 2014Review
- Linking the septin expression with carcinogenesis.Molecular biology reports · 2010Article
- Conquering the complex world of human septins: implications for health and disease.Clinical genetics · 2010Review
- Do septins have a role in cancer?British journal of cancer · 2005Review
- Maxizyme-mediated specific inhibition on mutant-type p53 in vitro.World journal of gastroenterology · 2003Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have identified a novel human septin family gene Bradeion, which is specifically expressed in human colorectal cancer and malignant melanoma. In order to analyze the implications of tumor-specific gene expression, ribozymes and its derivatives were specifically designed and transfected into various colorectal adenocarcinoma cell lines for Bradeion inactivation. We constructed ribozyme expression plasmids controlled by a human tRNA(Val) promoter, and both hammerhead ribozyme and its allosteric derivative maxizyme were used for two different forms of Bradeion mRNA. The sequence-specific cleavage of Bradeion mRNA resulted in significant growth inhibition and G2 arrest in human cancer cell lines, detected by flow cytometry analysis. In addition, in vivo mice studies demonstrated marked tumor growth suppression by the Bradeion-specific ribozymes. Thus, the tumor-specific and selective marker Bradeion also provides valuable tools as a potential target for colorectal cancer therapy.
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Registered trials
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