ArticleMolecular and cellular biochemistry2012
Potent growth-inhibitory effect of TRAIL therapy mediated by double-regulated oncolytic adenovirus on osteosarcoma.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 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
5 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- Adenovirus-mediated small interfering RNA targeting ezrin induces apoptosis and inhibits metastasis of human osteosarcoma MG-63 cells.Bioscience reports · 2018Article
- miR-155 promotes the growth of osteosarcoma in a HBP1-dependent mechanism.Molecular and cellular biochemistry · 2015Article
- TIKI2 suppresses growth of osteosarcoma by targeting Wnt/β-catenin pathway.Molecular and cellular biochemistry · 2014Article
- Oncolytic virotherapy for osteosarcoma using midkine promoter-regulated adenoviruses.Cancer gene therapy · 2014Article
Corrections and comments
- Erratum issuedChunbao, Li [corrected to Li, Chunbao]; Qianpeng, Cheng [corrected to Cheng, Qianpeng]; Jia, Liu [corrected to Liu, Jia]; Bin, Wang [corrected to Wang, Bin]; Dongfeng, Chen [corrected to Chen, Dongfeng]; Yujie, Liu [corrected to Liu, Yujie]
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteosarcoma (OS) severely threatens the health of young people and understanding on the molecular mechanisms of OS etiology enables gene therapy to become an effective therapeutic modality. However, insufficient expression level of genes using existing vectors limits the clinical application of gene therapy for OS. To solve the problem, we developed an oncolytic adenoviral vector, OAT, which can selectively and efficiently replicate in OS cells to enhance the expression of transferred genes. We demonstrated that OAT-mediated TRAIL expression is significantly elevated after infection of OS cells than replication-incompetent Ad5 vector. Increased antitumor capacity was observed in OS cells after OAT-TRAIL treatment both in vitro and in vivo. In normal cells, adenoviral replication, TRAIL expression and growth-inhibiting effect were quite limited when OAT-TRAIL was administrated, showing a high biosafety of this oncolytic adenoviral vector. Collectively, we generated an efficient and promising expression vector for OS gene therapy.
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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.