Dongqing Zhang, Liu Qian, Jiying Zhang and Ping Wang
Shanghai Jiao Tong University, China
Posters & Accepted Abstracts: J Cancer Sci Ther
Multiple myeloma (MM) is a plasma cell disorder (plasma cell dyscrasia) caused by bone lesions and production of a paraprotein.
Our findings show high expression levels of B-lymphocyte stimulator (BLyS) and its receptor on B cells both of the peripheral
blood and the bone marrow in MM patients when compared to monoclonal gammopathy of unknown significance (MGUS) and
healthy control donors, and may involve the immunopathogenesis of MM. Serum BLyS in MM patients were significantly higher than
that in MGUS and healthy controls and coincided with the evaluation of increased BLyS expression in bone marrow specimens from
patients with MM by immunofluorescence. Furthermore, BLyS significantly promoted multiple myeloma cell proliferation and its
receptor BAFFR, together with IL-2 and IL-6 when compared with the control group. Bortezomib is an approved clinical treatment
for relapsed MM as a therapeutic proteasome inhibitor. In this study, Bortezomib induced apoptosis to repress the proliferation
of RPMI8226 and U266 cells expressed high level of BLyS through the inhibition of NF�ºB p65 and I�ºB�±. So, our findings confirm
that BLyS and its receptors are expressed by B lymphocytes in peripheral blood and in the bone marrow of patients with MM. In
addition, the ability of BLyS binding to B cells and the finding of elevated serum soluble BLyS levels suggest that it may be seen as
hallmark of MM. The same as that Bortezomib induced apoptosis in MM cells and suggest it might be involved in the mechanism of
the regulation of BLyS. We hypothesize that abnormal BLyS signaling and NF�ºB activity form a positive feedback loop which may be
crucial in elucidating further mechanisms in MM pathogenesis and could provide future therapeutic targets for MM.
Recent Publication
1. Dong-Qing Zhang, Rong Zhao, Ni-Nan Chen, Xiao-Wei Zhou, Ping Miao, Chao-Ying Hu, Liu Qian, Qi-Wen Yu, Ji-Ying Zhang,
Hong Nie, Xue-hua Chen, Pu Li, Rong Xu, Lian-Bo Xiao, Xin Zhang and Jian-Ren Liu (2014) Intervention with exogenous IFNbeta
regulates RANKL-c-Fos-IFN-beta signaling pathway in collagen antibody-induced arthritis model. Journal of translational
medicine, 12(1):330.
2. Dongqing Zhang, Ping Wang, Liu Qian, Xiangliang Yuan, Chaoying Hu, Liansheng Huang, PingMiao, Qiwen YU, Yanhui Ma,
Jiying Zhang, Xuehua Chen, Bingya Liu and Lisong Shen (2013) Blys: A potential hallmark of multiple myeloma. Frontiers in
Bioscience 18(1):324-331.
3. Zhang D, Cheng W, Ma Y, Gong F, Hu C, Qian L, Huang Q, Yu Q, Zhang J, Chen S, Liu Z, Chen X and Zhou T (2013) Crossreactivity
of auto-reactive T cells with MBP and viral antigens in patients with MS. Front Biosci 17:1648-1658.
4. Zhang D, Hu C, Qian L, Miao Y, Huang Q, Miao P, Wang P, Yu Q, Nie H, Zhang J, He D, Xu R, Chen X and Liu B (2012) Antigenpresenting
effects of effector memory V�³9V�´2 T cells in rheumatoid arthritis. Cell Mol Immunol 9:245-254.
5. Zhang D Q, Ma Y H, Cheng W Z, Gong F, Ma A L, Yu Q W, Zhang J Y, Hu C Y and Chen X H (2008) Active Chinese mistletoe
lectin-55 enhances colon cancer surveillance through regulating innate and adaptive immune responses. World J Gastroenterol
14(34):5274-5281.
Dongqing Zhang is a Principle Investigator, Research Professor at Shanghai Institute of Immunology, Shanghai Jiaotong University Medical School. His research interests are: Tumor immunology and autoimmune disease are induced by many factors which seriously affect human health like genetic, environmental, endocrine, cell apoptosis and virus infection. His team is committed to study the pathogenesis of gastric cancer and autoimmune diseases-like RA, including T/B cells and their associated signaling molecules expression; and the feasibility of clinical application.
Email: dqzhang1333@163.com
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