ArticleGene therapy1999
Utilization of variant-type of human alpha-fetoprotein promoter in gene therapy targeting for hepatocellular carcinoma.
Article in Gene therapy, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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
11 citing papers in PubMed, 41 citations in OpenAlex.
- Engineering Cancer Selective Virotherapies: Are the Pieces of the Puzzle Falling into Place?Human gene therapy · 2022Review
- Oncolytic adenovirus programmed by synthetic gene circuit for cancer immunotherapy.Nature communications · 2019Article
- Review
- Hypoxia/hepatoma dual specific suicide gene expression plasmid delivery using bio-reducible polymer for hepatocellular carcinoma therapy.Journal of controlled release : official journal of the Controlled Release Society · 2013Article
- The EIIAPA chimeric promoter for tumor specific gene therapy of hepatoma.Molecular imaging and biology · 2012Article
- Promoter-defined isolation and identification of hepatic progenitor cells from the human fetal liver.Histochemistry and cell biology · 2008Article
- Plasmid engineering for controlled and sustained gene expression for nonviral gene therapy.Pharmaceutical research · 2006Review
- Construction of a targeting adenoviral vector carrying AFP promoter for expressing EGFP gene in AFP-producing hepatocarcinoma cell.World journal of gastroenterology · 2004Article
- A promoter region of the midkine gene that is frequently expressed in human hepatocellular carcinoma can activate a suicide gene as effectively as the alpha-fetoprotein promoter.British journal of cancer · 2003Article
- Transcriptional Targeting in Cancer Gene Therapy.Journal of biomedicine & biotechnology · 2003Article
- The promoting molecular mechanism of alpha-fetoprotein on the growth of human hepatoma Bel7402 cell line.World journal of gastroenterology · 2002Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported that the retroviral vector (LNAFW0.3TK) expressing the herpes simplex thymidine kinase (HSVtk) gene under the control of the 0.3 kb human alpha-fetoprotein (AFP) promoter provided the ganciclovir (GCV)-mediated cytotoxicity in the high AFP-producing (HuH-7) but not in the low AFP-producing (huH-1/cl.2) human hepatoma cells. In the present study, we constructed the retroviral vector (LNAFM0.3TK) in which the HSVtk gene expression is regulated by the variant-type of the 0.3 kb human AFP promoter with a G-to-A substitution at nucleotide -119, a point mutation responsible for hereditary persistence of human AFP and the vector was applied to three human hepatoma cell lines HuH-7, huH-1/cl.2 and intermediate AFP-producing cells (PLC/PRF/5). By the reporter gene transfection assay, the activity of the variant-type of the promoter was much higher than that of the wild-type of the promoter in both HuH-7 and huH-1/cl.2 cells. Consistent with this, LNAFM0.3TK infection could sensitize huH-1/cl.2 cells, as well as HuH-7 and PLC/PRF/5 cells to GCV, but did not affect cell growth of nonhepatoma cells (HeLa). In addition, the bystander effect was achieved more efficiently by LNAFM0.3TK infection than LNAFW0.3TK infection in HuH-7 cells. These results suggest that the variant-type of the human AFP promoter ensures the therapeutic gene expression in gene therapy particularly for the low AFP-producing hepatoma cells.
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