AAV-mediated gene transfer of human pigment epithelium-derived factor inhibits Lewis lung carcinoma growth in mice
Autor: | Sha-Sha He, Lian Lu, Huashan Shi, Yuquan Wei, Qin-Jie Wu, Li-Li Yang, Tao Yin, Shun-Tao Luo, Yong-Xia Li |
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Rok vydání: | 2012 |
Předmět: |
Male
Cancer Research Pathology medicine.medical_specialty Time Factors Angiogenesis AAV-PEDF viruses Genetic Vectors Apoptosis Biology Transfection angiogenesis Carcinoma Lewis Lung Mice PEDF Cell Line Tumor Human Umbilical Vein Endothelial Cells medicine Animals Humans Nerve Growth Factors Eye Proteins Lung cancer Serpins Neovascularization Pathologic Oncogene tumour Cell growth Lewis lung carcinoma Cancer Articles Genetic Therapy General Medicine Dependovirus medicine.disease Capillaries Tumor Burden Mice Inbred C57BL Oncology Cancer research LLC |
Zdroj: | Oncology Reports |
ISSN: | 1791-2431 1021-335X |
DOI: | 10.3892/or.2012.1621 |
Popis: | Pigment epithelium-derived factor (PEDF) is the most potent inhibitor of angiogenesis in the mammalian eye, and mechanisms through which PEDF exerts its antitumour activity have recently been defined. The aim of our research was to evaluate the ability of adeno-associated virus (AAV) vector-mediated transfer of human PEDF to inhibit lewis lung carcinoma (LCC) cell growth. Intratumoural injection of AAV-PEDF caused significant reduction of the tumour volume and prolonged the survival time of mice bearing LLC cells, which were associated with decreased microvessel density and increased apoptosis in the tumours. AAV vectors represent a very promising tool for cancer gene therapy. No noticeable toxicity concerning AAV was detected as inferred from monitoring changes in animal body weight as well as basic organ structure and histological morphology, and by analyzing mouse liver and kidney function. Our findings indicate that AAV-mediated PEDF gene expression may offer an active approach to inhibit LLC growth and that treatment with AAV-PEDF may provide a promising therapeutic strategy in lung cancer treatment. |
Databáze: | OpenAIRE |
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