ArticleCancer medicine2016
Antitumor activity of combined endostatin and thymidine kinase gene therapy in C6 glioma models.
Article in Cancer medicine, 2016. 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, 13 citations in OpenAlex.
- rAAV9-UPII-TK-EGFP can precisely transduce a suicide gene and inhibit the growth of bladder tumors.Cancer biology & therapy · 2020Article
- MiR-210-3p Inhibits Proliferation and Migration of C6 Cells by Targeting Iscu.Neurochemical research · 2020Article
- XCHD Inhibits C6 Cell Growth Primarily via the p53/Caspase Pathway.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Production and Application of Multicistronic Constructs for Various Human Disease Therapies.Pharmaceutics · 2019Review
- Article
- The effect of gene therapy on postoperative recurrence of small hepatocellular carcinoma (less than 5cm).Cancer gene therapy · 2019Article
- Apoptotic effects of ε-viniferin in combination with cis-platin in C6 cells.Cytotechnology · 2018Article
- Extracellular Matrix, a Hard Player in Angiogenesis.International journal of molecular sciences · 2016Review
- Antitumor activity of combined endostatin and thymidine kinase gene therapy in C6 glioma models.Cancer medicine · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The combination of Endostatin (ES) and Herpes Simplex Virus thymidine kinase (HSV-TK) gene therapy is known to have antitumor activity in bladder cancer. The potential effect of ES and TK therapy in glioma has not yet been investigated. In this study, pTK-internal ribosome entry site (IRES), pIRES-ES, and pTK-IRES-ES plasmids were constructed; pIRES empty vector served as the negative control. The recombinant constructs were transfected into human umbilical vein endothelial cells (HUVECs) ECV304 and C6 rat glioma cell line. Ganciclovir (GCV) was used to induce cell death in transfected C6 cells. We found that ECV304 cells expressing either ES or TK-ES showed reduced proliferation, decreased migration capacity, and increased apoptosis, as compared to untransfected cells or controls. pTK-IRES-ES/GCV or pTK-IRES/GCV significantly suppressed cell proliferation and induced cell apoptosis in C6 cells, as compared to the control. In addition, the administration of pIRES-ES, pTK-IRES/GCV, or pTK-IRES-ES/GCV therapy improved animal activity and behavior; was associated with prolonged animal survival, and a lower microvessel density (MVD) value in tumor tissues of C6 glioma rats. In comparison to others, dual gene therapy in form of pTK-IRES-ES/GCV had a significant antitumor activity against C6 glioma. These findings indicate combined TK and ES gene therapy was associated with a superior antitumor efficacy as compared to single gene therapy in C6 glioma.
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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.