ArticleCancer biotherapy & radiopharmaceuticals2013
Targeting and eradicating hepatic cancer cells with a cancer-specific vector carrying the Buforin II gene.
Article in Cancer biotherapy & radiopharmaceuticals, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- The investigation of the death-inducing potency of a recombinant Adenovector expressing Mda-7-tlyp-1 on different cancer cell lines.Gastroenterology and hepatology from bed to bench · 2024Article
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe aim of this study was to investigate the suppressive effects of Buforin II on the growth of HepG2 cells. To accomplish this, we created a recombinant plasmid (pSUR-Buforin2) in which the survivin promoter was modified to drive the Buforin II gene.
methodsThe DNA fragment encoding the Buforin II gene was obtained by gene synthesis and cloned into the pSUR-Luc plasmid behind the survivin promoter. The vector was subsequently transfected into HepG2 and LO2 cells. Cell proliferation was measured by the MTT assay, cell cytotoxicity detected by the LDH assay, and cell apoptosis determined by flow cytometry, DNA ladder assays, and immunoblot analysis.
resultsThe pSUR-Buforin2 vector effectively suppressed the proliferation of HepG2 cells. The MTT and LDH assay demonstrated that under control of the survivin promoter, Buforin II was not expressed in LO2 cells, but it was expressed in tumor cells where cell death was also observed. AnnexinV-PI staining, DNA ladder assays, and western blots showed massive apoptosis in HepG2 cells transfected with pSUR-Buforin2.
conclusionpSUR-Buforin2 can significantly inhibit the growth of HepG2 cells, resulting in increased cancer cell apoptosis. Thus, this newly designed plasmid might provide a potent and selective anticancer therapy.
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