Yiming Li

Publications (3)8.07 Total impact

• Article: Antitumor effects obtained by autologous Lewis lung cancer cell vaccine engineered to secrete mouse Interleukin 27 by means of cationic liposome.

  Junfeng Zhang, Hongwei Tian, Can Li, Lin Cheng, Shuang Zhang, Xiaomei Zhang, Ruibo Wang, Fen Xu, Lei Dai, Gang Shi, Xiaolei Chen, Yiming Li, Tao Du, Jie Deng, Yu Liu, Yang Yang, Yuquan Wei, Hongxin Deng
  [show abstract] [hide abstract]
  ABSTRACT: Interleukin-27 (IL-27), a novel IL-6/IL-12 family cytokine, plays an important role in the early regulation of Th1 responses. The cytokine IL-27 can exert a variety of immune-regulatory functions including cytotoxic T lymphocyte (CTL), CD4(+), CD8+ T lymphocytes activation and interferon-γ (IFN-γ) production. In this study, we developed an effective and gene modified tumor cell vaccine. Lewis lung cancer cell LL/2 transfected with the DOTAP:cholesterol cationic liposome could express the mouse IL-27 (mIL-27) gene at a relative high level. The resultant transfectants were then irradiated with X-ray and used as a tumor cell vaccine. This tumor cell vaccine not only contained tumor associated antigen (TAA) of LL/2 cells but also secreted mIL-27 which could induce immune response in mice. The mice vaccinated with LL/2-mIL-27 performed strong tumor inhibiting effect accompanied with a high IFN-γ production. Both CD4+ and CD8+ T lymphocytes were significantly elevated in these mice vaccinated with LL/2-mIL-27 cell vaccine. Moreover, after depletion of CD4+, CD8+ T lymphocytes by injection of antibodies against CD4 and CD8, the vaccinated mice inoculated with autologous LL/2 cells were not protected from tumor challenge. In contrast, vaccinated mice inoculated with autologous LL/2 cells were treated with antibody against natural killer (NK)cells or normal rat IgG still possessed strong antitumor activity. Our data suggested that DOTAP:cholesterol cationic liposome was quite useful in generating an autologous tumor cell vaccine and mIL-27 could be therapeutically used to potentiate the host antitumor immunity.
  Molecular Immunology 03/2013; · 2.90 Impact Factor
• Article: Therapeutic upregulation of Class A scavenger receptor member 5 inhibits tumor growth and metastasis.

  Nv Yan, Shuang Zhang, Yang Yang, Lin Cheng, Can Li, Lixia Dai, Lei Dai, Xiaomei Zhang, Ping Fan, Hongwei Tian, Ruibo Wang, Xiaolei Chen, Xiaolan Su, Yiming Li, Junfeng Zhang, Tao Du, Yuquan Wei, Hongxin Deng
  [show abstract] [hide abstract]
  ABSTRACT: Class A scavenger receptor member 5 (SCARA5) is a new member of the Class A scavenger receptors that has been proposed recently as a novel candidate tumor suppressor gene in human hepatocellular carcinoma. In the present study, we found that SCARA5 expression was frequently downregulated in various cancer cell lines and tumor samples. In addition, upregulation of SCARA5 expression in human cancer cell line (U251) led to a significant decrease in cell proliferation, clone formation, migration, and invasion in vitro. Furthermore, systemic treatment of tumor-bearing mice with SCARA5-cationic liposome complex not only reduced the growth of subcutaneous human glioma tumors, but also markedly suppressed the spontaneous formation of lung metastases. Similar results were obtained in another experiment using mice bearing experimental A549 lung metastases. Compared with the untreated control group, mice treated with SCARA5 exhibited reductions in both spontaneous U251 and experimental A549 lung metastases rates of 77.3% and 70.2%, respectively. Western blot analysis was used to explore the molecular mechanisms involved and revealed that SCARA5 physically associated with focal adhesion kinase. Interestingly, upregulation of SCARA5 inactivated signal transducer and activator of transcription 3, as well as downstream signaling including cyclinB1, cyclinD1, AKT, survivin, matrix metalloproteinase-9 and vascular endothelial growth factor-A. Overall, the findings of the present study provide the first evidence that SCARA5 might be a promising target for the development of new antimetastatic agents for the gene therapy of cancer.
  Cancer Science 05/2012; 103(9):1631-9. · 3.33 Impact Factor
• Article: Suppression of epidermal growth factor receptor (EGFR) expression by small hairpin RNA inhibits the growth of human nonsmall cell lung cancers bearing wild-type and mutant EGFR.

  Shuang Zhang, Hongwei Tian, Qingyuan Jiang, Li Li, Yu Ding, Lei Dai, Yu Xiang, Guobo Shen, Lin Cheng, Qiaorong Huang, [......], Xiaomei Zhang, Yongping Ma, Na Zhang, Shengyong Liu, Wei Wang, Lixia Dai, Yiming Li, Xia Zhao, Yuquan Wei, Hongxin Deng
  [show abstract] [hide abstract]
  ABSTRACT: In the present study, we have used plasmid-based RNA interference (RNAi) strategy to downregulate the expression of epidermal growth factor receptor (EGFR) in EGFR wild-type (H292) and mutant (H1975) lung tumor models. The targeted knockdown of EGFR by small hairpin RNA not only inhibited growth of H292 xenograft but also inhibited H1975 lung cancer cell and xenograft, which bore L858R/T790M EGFR and was resistant to EGFR tyrosine kinase inhibitors. These data demonstrated that small hairpin RNA was an effective therapy against mutant EGFR-expressing cancer cells and thus considered to be a promising strategy in the treatment of lung cancers.
  Cancer Investigation 01/2011; 29(10):701-8. · 1.85 Impact Factor