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Potent antitumor activity of the Ad5/11 chimeric oncolytic adenovirus combined with interleukin-24 for acute myeloid leukemia via induction of apoptosis
Author(s) -
Wei Xu-bin,
Li Liu,
Gang Wang,
Wei Li,
Ke Xu,
Hongyan Qi,
Hong Liu,
Jing Shen,
Zhongjie Li,
Jimin Shao
Publication year - 2014
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2014.3563
Subject(s) - oncolytic virus , oncolytic adenovirus , myeloid leukemia , cancer research , haematopoiesis , cytotoxic t cell , biology , leukemia , myeloid , genetic enhancement , interleukin 3 , immunology , cancer , progenitor cell , stem cell , t cell , in vitro , immune system , interleukin 21 , gene , microbiology and biotechnology , biochemistry , genetics , tumor cells
The Ad5/11 chimeric oncolytic adenovirus represents a promising new platform for anticancer therapy. Acute myeloid leukemia (AML) is a heterogeneous clonal disorder of hematopoietic progenitor cells and is the most common malignant myeloid disorder in adults. Myeloid and other hematopoietic cell lineages are involved in the process of clonal proliferation and differentiation. In the present study, we aimed to ascertain whether chimeric oncolytic adenovirus-mediated transfer of the human interleukin-24 (IL-24) gene induces enhanced antitumor potency. Our results showed that the Ad5/11 chimeric oncolytic adenovirus carrying hIL-24 (AdCN205‑11-IL-24) produced high levels of hIL-24 in AML cancer cells, as compared with the Ad5 oncolytic adenovirus expressing hIL-24 (AdCN205-IL-24). AdCN205-11-IL-24 specifically induced a cytotoxic effect on AML cancer cells, but had little or no effect on a normal cell line. AdCN205-11-IL-24 induced higher antitumor activity in AML cancer cells by inducing apoptosis in vitro. This study suggests that transfer of IL-24 by an Ad5/11 chimeric oncolytic adenovirus may be a potent antitumor approach for AML cancer therapy.

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