Research Papers:

Altered Hepa1-6 cells by dimethyl sulfoxide (DMSO)-treatment induce anti-tumor immunity in vivo

Zhengyu Jiang, Hongxia Zhang, Ye Wang, Bin Yu, Chen Wang, Changcheng Liu, Juan Lu, Fei Chen, Minjun Wang, Xinlu Yu, Jiahao Lin, Xinghua Pan, Pin Wang _ and Haiying Zhu

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Oncotarget. 2016; 7:9340-9352. https://doi.org/10.18632/oncotarget.7009

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Zhengyu Jiang1,2,3, Hongxia Zhang1,2, Ye Wang1,2, Bin Yu1,2, Chen Wang1,2, Changcheng Liu1,2, Juan Lu4, Fei Chen1,2, Minjun Wang1,2, Xinlu Yu1,2, Jiahao Lin5, Xinghua Pan6, Pin Wang7, Haiying Zhu1,2

1Department of Cell Biology, Second Military Medical University, Shanghai, P.R. China

2Center for Stem Cell and Medicine, The Graduate School, Second Military Medical University, Shanghai, P.R. China

3Department of Anesthesiology, Second Military Medical University, Shanghai, P.R. China

4Training Department, Second Military Medical University, Shanghai, P.R. China

5School of Clinic Medicine, Second Military Medical University, Shanghai, P.R. China

6Department of Genetics, Yale University School of Medicine, New Haven, CT, USA

7National Key Laboratory of Medical Immunology and Institute of Immunology, Second Military Medical University, Shanghai, P.R. China

Correspondence to:

Pin Wang, e-mail: [email protected]

Haiying Zhu, e-mail: [email protected]

Keywords: cancer immunotherapy, DMSO, anti-tumor immunity

Received: July 14, 2015     Accepted: January 01, 2016     Published: January 25, 2016


Cancer immunotherapy is the use of the immune system to treat cancer. Our current research proposed an optional strategy of activating immune system involving in cancer immunotherapy. When being treated with 2% DMSO in culture medium, Hepa1-6 cells showed depressed proliferation with no significant apoptosis or decreased viability. D-hep cells, Hepa1-6 cells treated with DMSO for 7 days, could restore to the higher proliferation rate in DMSO-free medium, but alteration of gene expression profile was irreversible. Interestingly, tumors from D-hep cells, not Hepa1-6 cells, regressed in wild-type C57BL/6 mice whereas D-hep cells exhibited similar tumorigenesis as Hep1–6 cells in immunodeficient mice. As expected, additional Hepa1-6 cells failed to form tumors in the D-hep-C57 mice in which D-hep cells were eliminated. Further research confirmed that D-hep-C57 mice established anti-tumor immunity against Hepa1-6 cells. Our research proposed viable tumor cells with altered biological features by DMSO-treatment could induce anti-tumor immunity in vivo.

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