Haiyan Li

Publications (4)10.36 Total impact

• Article: PDCD5 promotes cisplatin-induced apoptosis of glioma cells via activating mitochondrial apoptotic pathway.

  Haiyan Li, Xia Zhang, Xingguo Song, Faliang Zhu, Qun Wang, Chun Guo, Chunmei Liu, Yongyu Shi, Chunhong Ma, Xiaoyan Wang, Lining Zhang
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  ABSTRACT: Glioma is one of the most common primary brain tumors. Despite surgical resection, radiotherapy, and chemotherapy, the prognosis of patients with malignant glioma remains poor. Programmed cell death 5 (PDCD5) is a newly described pro-apoptotic protein. Our previous study showed that PDCD5 downregulation in gliomas was associated with higher pathological grade. Here, we investigated the effect of PDCD5 on chemosensitivity of glioma cells and its mechanism. We demonstrated that overexpression or knockdown of PDCD5 had no significant effect on the proliferation of glioma cell lines (U87, U251, and T98G) in the absence of chemotherapeutic agents. However, PDCD5 overexpression effectively sensitized U87 cells to chemotherapeutic drugs (cisplatin, carboplatin, and vincristine) in a concentration-dependent manner, while its knockdown resulted in decreased chemosensitivity in U251, T98G, and U87 cells. Importantly, expression of PDCD5 also markedly inhibited tumor cell proliferation and colony formation in the presence of low doses of cisplatin. Furthermore, we found that PDCD5 expression promoted cisplatin-induced apoptosis, increased markedly the activation of caspase-3 and caspase-9, and decreased significantly the ratio of Bcl-2/Bax proteins, but had no effect on the activation of caspase-8. Taken together, our findings indicate that PDCD5 promotes chemosensitivity by activating mitochondria-related apoptotic pathway, and that the combination of PDCD5 and chemotherapeutic drugs such as cisplatin, is expected to be an effective therapeutic strategy for the malignant glioma.
  Cancer biology & therapy 07/2012; 13(9):822-30. · 2.64 Impact Factor
• Article: Blockade of CD28 by a synthetical peptoid inhibits T-cell proliferation and attenuates graft-versus-host disease

  Na Li, Faliang Zhu, Fei Gao, Qun Wang, Xiaoyan Wang, Haiyan Li, Chunhong Ma, Wensheng Sun, Wenfang Xu, Chaodong Wang, Lining Zhang
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  ABSTRACT: CD28 is one of the costimulatory molecules crucial for T-cell activation and thus has become an attractive target for therapeutic immunomodulation. Conventional strategies for blocking CD28 activity using monoclonal antibodies, Fab fragments, antagonistic peptide and fusion proteins, have apparent disadvantages such as inherent immunogenicity, unwanted Fc signaling, poor tissue penetration and bioinstability. Recent research has been directed toward the creation of non-natural, sequence-specific biomimetic oligomers with bioinspired structures that capture the amino-acid interface of the targeted proteins. One such family of molecules is the poly-N-substituted glycines or peptoids, which have close structural similarity to peptides but are essentially invulnerable to protease degradation. To screen for peptoids that specifically target CD28, we first designed and chemically synthesized 19 candidate peptoids based on molecular modeling and docking. Using the phage-displaying system that expresses the extracellular domain of the CD28 homodimer and contains the core B7-binding motif, a peptoid (No. 9) with a molecular formula of C21H29N3O7, was identified to display the highest binding activity to CD28. This peptoid not only inhibited the lymphocyte proliferation in vitro, but suppressed immunoresponses against alloantigens in vivo, and attenuated the graft-versus-host disease in a mouse bone-marrow transplantation model. These results suggested that peptoids targeting CD28 are effective agents for blocking the CD28-mediated costimulation and suitable for development of novel therapeutic approaches for diseases involving this pathway.Keywords: CD28; peptoid; phage display
  Cellular & molecular immunology 02/2010; 7(2):133-142. · 2.99 Impact Factor
• Article: Reoxygenation of hypoxia-differentiated dentritic cells induces Th1 and Th17 cell differentiation.

  Qun Wang, Chunmei Liu, Faliang Zhu, Fengming Liu, Pin Zhang, Chun Guo, Xiaoyan Wang, Haiyan Li, Chunhong Ma, Wensheng Sun, Yun Zhang, Wanjun Chen, Lining Zhang
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  ABSTRACT: Dendritic cells (DCs) are often exposed to various oxygen tensions under physiological and pathological conditions. However, the effects of various oxygen tensions on DC functions remain unclear. In this study, we showed that hypoxia-differentiated DCs expressed lower levels of MHC-II molecule, co-stimulatory molecules (CD80, CD86) and proinflammatory cytokines (IL-1beta, IL-6, and TNF-alpha), but higher levels of immunoregulatory cytokine transforming growth factor-beta (TGF-beta) than normoxia-differentiated DCs. Unexpectedly, re-exposure of hypoxia-differentiated DCs to saturated oxygen (reoxygenation) completely restored their mature phenotype and function. Specifically, the reoxygenated DCs induced naïve CD4(+) T cells to differentiate into Th1 and Th17 effector cells, but deceased the generation of CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs). The data indicate that hypoxic microenvironment suppresses the maturation and function of murine DCs. Reoxygenation of hypoxia-differentiated DCs however results in complete recovery of their mature phenotype and function, and has strong ability to drive immune response toward a proinflammatory direction, suggesting reoxygenated DCs may contribute to inflammation of ischemia-reperfusion injury.
  Molecular Immunology 11/2009; 47(4):922-31. · 2.90 Impact Factor
• Article: Reduced expression of PDCD5 is associated with high-grade astrocytic gliomas.

  Haiyan Li, Qun Wang, Fei Gao, Faliang Zhu, Xiaoyan Wang, Chengjun Zhou, Chunmei Liu, Yingyu Chen, Chunhong Ma, Wensheng Sun, Lining Zhang
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  ABSTRACT: Programmed cell death 5 (PDCD5) is a novel apoptosis-promoting protein. Recently, a decreased expression of PDCD5 has been found in several types of human tumors. However, the expression level of PDCD5 in human gliomas has not been investigated. In the present study, we examined the expression of PDCD5 in 88 human glioma samples at both mRNA and protein levels by RT-PCR, Western blotting and immunohistochemistry. We found that 53.3% (16/30) of the glioma samples had a reduced expression of PDCD5 mRNA and 70.5% (62/88) had a reduced expression of the PDCD5 protein as compared to normal brain tissue. Furthermore, we studied the correlation of the expression level of PDCD5 with the clinicopathological grade and survival of patients with astrocytomas. Although longitudinal studies of a cohort of patients with astrocytoma revealed that PDCD5 expression was not able to predict clinical outcome (p>0.05), a decreased expression of PDCD5 correlated significantly with high-grade astrocytomas (p<0.001). In conclusion, our data suggest that reduced PDCD5 expression may contribute to the pathogenesis of human gliomas.
  Oncology Reports 09/2008; 20(3):573-9. · 1.84 Impact Factor