Shaohong Chen

Publications (3)11.25 Total impact

• Article: Re-expression of miR-150 induces EBV-positive Burkitt lymphoma differentiation by modulating c-Myb in vitro.

  Shaohong Chen, Zhiqiang Wang, Xinzhen Dai, Jianhua Pan, Juan Ge, Xiqun Han, Zijing Wu, Xinhua Zhou, Tong Zhao
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  ABSTRACT: Burkitt lymphoma (BL) is a highly aggressive B-cell lymphoma including 2 forms of BL differing in Epstein-Barr virus (EBV) infection status: EBV-positive and EBV-negative BL. Recent years, although many efforts, such as high-intensity, short-duration combination chemotherapy, have been devoted to improve therapy for this rapidly proliferating neoplasm, there are still significant treatment-associated toxicities. Therefore, there remains a need for novel effective therapeutic strategies. MicroRNAs (miRNAs) play a role of "fine tuning" in the physiological and pathological differentiation process, by which cells can rapidly regulate dynamic events such as cell-lineage decisions and morphogenesis. This unique miRNA feature shifts the traditional one drug target paradigm to a novel one drug multiple targets paradigm. Here, we found that BL cell lines exhibited an extremely low expression of miR-150, and then restored miR-150 expression at physiologic levels in BL cell lines, i.e. Daudi, Raji, BJAB and Ramos. The results showed that re-expression of miR-150 reduced proliferation of Daudi and Raji cells. Furthermore, Daudi and Raji, both of which are EBV-positive germinal center B-cell (GC B) origin, transduced with miR-150 can be rescued to differentiate toward B-cell terminal stage. However, no significant changes were observed in BJAB and Ramos cells which are EBV-negative GC B origin. Of note, re-expression of miR-150 also resulted in decreasing c-Myb protein levels. Additionally, c-Myb knockdown in Daudi and Raji cell lines recapitulated the partial characteristics similar to that caused by re-expression of miR-150. Taken together, our findings demonstrate that miR-150 can induce EBV-positive BL differentiation by targeting c-Myb.
  Cancer Science 03/2013; · 3.33 Impact Factor
• Article: CD99 triggers upregulation of miR-9-modulated PRDM1/BLIMP1 in Hodgkin/Reed-Sternberg cells and induces redifferentiation.

  Xueping Huang, Xinhua Zhou, Zhiqiang Wang, Feng Li, Fanrong Liu, Lin Zhong, Xiangzhao Li, Xiqun Han, Ziqing Wu, Shaohong Chen, Tong Zhao
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  ABSTRACT: CD99 is a 32-kDa transmembrane glycoprotein that is encoded by the MIC2 gene. Our study was carried out to examine the role of CD99 in tumor progression of classical Hodgkin lymphoma (cHL). Here, we showed that lowly expressed CD99 protein in cHL cell lines and primary cHL cases correlates with the deficient expression of the positive regulatory domain 1 (PRDM1/BLIMP1). In addition, cHL cell lines showed high levels of miR-9 expression. We determined that the upregulation of CD99 induced expression of transcription factor PRDM1, a master regulator of plasma-cell differentiation, which is also a target for miR-9-mediated downregulation. Indeed, inhibition of miR-9 also triggered upregulation of PRDM1 expression. Furthermore, overexpression of CD99 resulted in changed growth features and reorganization of actin cytoskeleton. As upregulation of CD99 led to a decrease in cHL diagnosis marker CD30 and CD15 and an increase in plasma-cell differentiation marker CD38 and the restoration of B-cell makers PAX5, CD79α and CD19, we suggest that downregulated CD99 leads to the prevention of plasma-cell differentiation in Hodgkin/Reed-Sternberg (H/RS) cells. Furthermore, these data indicate that CD99 may control miR-9 expression, which directly targets PRDM1. Altogether, these results reveal a CD99-miR-9-PRDM1 molecule axis in lymphomagenesis of cHL and suggest that upregulation of CD99 in H/RS cells induces terminal B-cell differentiation, which may provide a novel therapeutic strategies for cHL.
  International Journal of Cancer 10/2011; 131(4):E382-94. · 5.44 Impact Factor
• Article: Down-regulation of Wnt signaling could promote bone marrow-derived mesenchymal stem cells to differentiate into hepatocytes.

  Zunfu Ke, Feng Zhou, Liantang Wang, Shaohong Chen, Fang Liu, Xinjuan Fan, Fang Tang, Dawei Liu, Guoqiang Zhao
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  ABSTRACT: Bone marrow-derived mesenchymal stem cells (BMSCs) have been demonstrated to be able to differentiate into hepatocytes, but the precise mechanisms controlling this process are unclear. Our aim is try to explore the role of Wnt signaling on the differentiation of BMSCs into hepatocytes. Our study demonstrated that BMSCs could successfully differentiate into hepatocytes under in vitro induction of the tissue extract of damaged liver. The mRNA level of Wnt-1, Wnt-5a, Frizzled1, DSH (disheveled), GSK-3beta (glycogen synthase kinase 3 beta) and beta-catenin on day 21 when the differentiation direction was determined, was lower than that on days 0, 7, and 11. Furthermore, blocking Wnt-1 signaling by treating BMSCs with Dkk1 could induce BMSCs to express albumin earlier and up-regulation of Wnt signaling by treating BMSCs with Wnt-1 could inhibit BMSCs to differentiate into hepatocytes. Above results indicated that inhibition on Wnt signaling can promote BMSCs to differentiate into hepatocytes.
  Biochemical and Biophysical Research Communications 04/2008; 367(2):342-8. · 2.48 Impact Factor