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Sci Rep. 2016 Aug 17;6:31534. doi: 10.1038/srep31534.

Recombinant adenovirus of human p66Shc inhibits MCF-7 cell proliferation.

Yang X1,2, Xu R1,2, Lin Y2, Zhen Y3, Wei J2, Hu G2, Sun H1.

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Tianjin Key Laboratory of Biomaterial Research, Institute of Biomedical Engineering, Peking Union Medical College &Chinese Academy of Medical Sciences, Tianjin 300192, China.
The key Laboratory of Geriatrics, Beijing Hospital &Beijing Institute of Geriatrics, Ministry of Health, Beijing, 100730, China.
Department of Histology and Embryology, College of Basic Medical, Hebei United University, Tangshan, 063000, China.


The aim of this work was to construct a human recombinant p66Shc adenovirus and to investigate the inhibition of recombinant p66Shc adenovirus on MCF-7 cells. The recombinant adenovirus expression vector was constructed using the Adeno-X Adenoviral System 3. Inhibition of MCF-7 cell proliferation was determined by MTT. Intracellular ROS was measured by DCFH-DA fluorescent probes, and 8-OHdG was detected by ELISA. Cell apoptosis and the cell cycle were assayed by flow cytometry. Western blot were used to observe protein expression. p66Shc expression was upregulated in 4 cell lines after infection. The inhibitory effect of p66Shc recombinant adenovirus on MCF-7 cells was accompanied by enhanced ROS and 8-OHdG. However, no significant differences were observed in the cell apoptosis rate. The ratio of the cell cycle G2/M phase showed a significant increase. Follow-up experiments demonstrated that the expressions of p53, p-p53, cyclin B1 and CDK1 were upregulated with the overexpression of p66Shc. The Adeno-X Adenoviral System 3 can be used to efficiently construct recombinant adenovirus containing p66Shc gene, and the Adeno-X can inhibit the proliferation of MCF-7 cells by inducing cell cycle arrest at the G2/M phase. These results suggested that p66Shc may be a key target for clinical cancer therapy.

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