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EfficientIn VitroTRAIL-Gene Delivery in Drug-Resistant A2780/DDP Ovarian Cancer Cell Line via Magnetofection
Author(s) -
Fang Li,
Sumei Niu,
Jing Sun,
Huaishi Zhu,
BA Qiu-jie,
Yi Guo,
Donglu Shi
Publication year - 2011
Publication title -
journal of nanomaterials
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.463
H-Index - 66
eISSN - 1687-4129
pISSN - 1687-4110
DOI - 10.1155/2011/484589
Subject(s) - lipofectamine , transfection , cisplatin , apoptosis , viability assay , microbiology and biotechnology , cell culture , mtt assay , gene delivery , cancer cell , biology , western blot , cancer research , cancer , gene , biochemistry , recombinant dna , chemotherapy , vector (molecular biology) , genetics
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) presents great promise as an anticancer agent for human cancer therapy. In this study, a magnetofection agent (polyMAG-l000) was evaluated for in vitro delivery of TRAIL gene towards drug-resistant A2780/DDP ovarian cancer cells. Transfection experiments showed that polyMAG-l000 was able to transfect A2780/DDP cells in vitro, leading to a higher level of TRAIL gene expression in the presence of a static magnetic field as compared to other transfection agent, such as Lipofectamine 2000. TRAIL gene expression in the A2780/DDP cells was also confirmed by Western blot analysis. Moreover, the TRAIL gene expression exhibited remarkable decrease in the cell viability, as determined by MTT assay. Importantly, PolyMAG-l000-mediated TRAIL gene transfection in the presence of anticancer drug cisplatin (CDDP) induced much higher percentages of apoptotic A2780/DDP cells, compared to TRAIL gene transfection or CDDP treatment alone. A further study by Western blot analysis indicated that cytochrome c release and caspase-9 cleavage pathway were associated with the initiation of the apoptosis in A2780/DDP cells. The results of this study indicate that polyMAG-l000 can be used as an efficient agent for TRAIL gene transfection in ovarian cancer cells

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