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In vitro and in vivo delivery of novel anticancer fusion protein MULT1E/FasTI via adenoviral vectors

Cancer Gene Therapy volume 17, pages 164–170 (2010)Cite this article

Abstract

We previously demonstrated that a novel fusion protein MULT1E/FasTI expressed by TC-1 tumor cells inhibited tumor growth by simultaneously activating NKG2D expressing cells, such as NK cells, through the MULT1E portion and sending a death signal into cells through the Fas portion (Kotturi et al., Gene Therapy, 2008). In this study, an adenoviral gene delivery system was used to deliver this fusion protein. Our data indicate that adenoviral vector can efficiently deliver the MULT1E/FasTI fusion protein into TC-1 cells both in vitro and in vivo as assayed by RT-PCR, FACS analysis, caspase-3 activity and decreased in vivo tumor growth. This study further confirms that MULTE/FasTI represents a powerful bi-functional, therapeutic protein for the treatment of cancers.

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Acknowledgements

We thank Eric Holle and his staff for the professional care of the mice used in this study, Lakendra Workman for her administrative contribution in this study and Angela Howing for her help in preparation of frozen tissue sections. This study was supported in part by the GHS Oncology Foundation and the New Hope fund.

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Author notes

  1. H S R Kotturi

    Present address: 3Current address: Dr Hari Shankar R. Kotturi, Department of Biology, University of Central Oklahoma, 100 North University Drive, Edmond, OK 73034.,

Authors and Affiliations

  1. Department of Biological Sciences, Clemson University, Clemson, SC, USA

    H S R Kotturi, M Branham-O'Connor, X Yu, T E Wagner & Y Wei

  2. Oncology Research Institute, Greenville Hospital System, Greenville, SC, USA

    J Li, X Yu, T E Wagner & Y Wei

Authors
  1. H S R Kotturi
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  2. J Li
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  3. M Branham-O'Connor
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  4. X Yu
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  5. T E Wagner
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  6. Y Wei
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Correspondence to Y Wei.

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Kotturi, H., Li, J., Branham-O'Connor, M. et al. In vitro and in vivo delivery of novel anticancer fusion protein MULT1E/FasTI via adenoviral vectors. Cancer Gene Ther 17, 164–170 (2010). https://doi.org/10.1038/cgt.2009.69

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