ArticleMolecular medicine reports2017
HSVtk/GCV system on hepatoma carcinoma cells: Construction of the plasmid pcDNA3.1‑pAFP-TK and targeted killing effect.
Article in Molecular medicine reports, 2017. 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, 11 citations in OpenAlex.
- β2-Adrenergic receptor agonist enhances the bystander effect of HSV-TK/GCV gene therapy in glioblastoma multiforme via upregulation of connexin 43 expression.Molecular therapy oncolytics · 2022Article
- Gene-Directed Enzyme Prodrug Therapy by Dendrimer-Like Mesoporous Silica Nanoparticles against Tumor Cells.Nanomaterials (Basel, Switzerland) · 2021Article
- Inorganic Nanomaterial-Mediated Gene Therapy in Combination with Other Antitumor Treatment Modalities.Advanced functional materials · 2021Article
- Article
- ApoE-modified liposomes mediate the antitumour effect of survivin promoter-driven HSVtk in hepatocellular carcinoma.Cancer gene therapy · 2020Article
- Specific driving of the suicide E gene by the CEA promoter enhances the effects of paclitaxel in lung cancer.Cancer gene therapy · 2020Article
- Strategies for Targeting Gene Therapy in Cancer Cells With Tumor-Specific Promoters.Frontiers in oncology · 2020Review
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies demonstrated that herpes simplex virus thymidine kinase (HSVtk) could phosphorylate non‑toxic gancyclovir (GCV) efficiently to produce phosphorylated products that result in cell apoptosis, to kill tumor cells. The present study aimed to construct a plasmid vector, pcDNA3.1‑pAFP‑TK, carrying the suicide gene driven by the alpha‑fetoprotein (AFP) promoter, to investigate the cytotoxicity of HSVtk/GCV suicide gene system on hepatoma carcinoma cells. Reverse transcription‑polymerase chain reaction and western blotting results demonstrated that the HSVtk gene was effectively expressed in HepG2 hepatoma carcinoma cells transfected with pcDNA3.1‑pAFP‑TK plasmid, whereas HSVtk gene expression was not detected in normal HL‑7702 liver cells. In addition, MTT assays indicated that cell viability of HepG2 cells with the plasmid pcDNA3.1‑pAFP‑TK decreased in a dose‑dependent manner following treatment with GCV for 48 h. Flow cytometry also revealed that the cell apoptosis rate and mitochondrial membrane potential reduction rate in the HepG2 cells treated with HSVtk/GCV suicide gene system were significantly higher than in the control group. Apoptosis rates in the control group and the pcDNA3.1‑pAFP‑TK group were (1.00±0.62%) and (38.70±6.03%), respectively. Mitochondrial membrane potential reduction rates in the control group and the pcDNA3.1-pAFP-TK group were (0.57±0.11%) and (22.84±5.79%), respectively. Caspase‑3 staining demonstrated that activated caspase‑3 increased significantly in the HepG2 cells treated with HSVtk/GCV suicide gene system, whereas in the control group activated caspase‑3 increase was not observed. The results of the present study, therefore, indicated that HSVtk suicide gene was obviously expressed in the HepG2 cells and that the HSVtk/GCV system was effective at killing HepG2 hepatoma carcinoma cells.
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