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L. Miao



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    MINI 21 - Novel Targets (ID 133)

    • Event: WCLC 2015
    • Type: Mini Oral
    • Track: Biology, Pathology, and Molecular Testing
    • Presentations: 1
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      MINI21.04 - HS3ST3B1 Is a Novel Regulator of TGF-Beta Mediated EMT and Regulated by miR-218 in Lung Cancer (ID 827)

      17:00 - 17:05  |  Author(s): L. Miao

      • Abstract
      • Presentation
      • Slides

      Background:
      Heparan sulfate D-glucosamine 3-O-sulfotransferase 3B1 (HS3ST3B1) participates in the biosynthetic steps of heparan sulfate (HS) and found to target VEGF in acute myeloid leukemia(AML) cells thus contributing the angiogenesis and proliferation of AML cells . However, the role of HS3ST3B1 in NSCLC has never been reported. In this study, we aim to investigate the role of HS3ST3B1 in NSCLC epithelial-to-mesenchymal transition.

      Methods:
      Expression of HS3ST3B1 was investigated by qRT-PCR in specimens of tumor and matched normal tissues of NSCLC patients and also in epithelial and mesenchymal NSCLC cell lines. A549 and HCC827 cell lines was induced to mesenchymal phenotype by TGF-β, and expression of HS3ST3B1, CDH1, and VIM were studied by PCR. HS3ST3B1 was knockdown by siRNA to analyze the effect of HS3ST3B1 on EMT. Computational predicting software was used to predict potential regulators of HS3ST3B1 and dual luciferase report system demonstrated that miR-218 may target HS3ST3B1 in cells. MiR-218 was tranfected into cells to analyze the association of miR-218 and HS3ST3B1 in cells.

      Results:
      HS3ST3B1 was significantly up-regulated in tumors compared with matched normal tissues(P=0.002). Its expression was also up-regulated in mesenchymal phenotype NSCLC cells lines compared with epithelial phenotype(P＜0.05). When epithelial phenotype NSCLC cells transformed to mesenchymal phenotype induced by TGF-β, HS3ST3B1 was also significantly up-regulated. Moreover, when HS3ST3B1 was knockdown by siRNA in mesenchymal phenotype NSCLC cell lines, cells were reversed to epithelial phenotype morphologically. With Targetscan, we found that HS3ST3B1 was one potential targets of miR-218 and dual luciferase report system demonstrated that HS3ST3B1 was direct target of miR-218 in cells. When miR-218 was transfected into cells, we found that HS3ST3B1 was down-regulated. Figure 1 Figure 2





      Conclusion:
      HS3ST3B1 may regulate EMT and it can be regulated by miR-218 in NSCLC.

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