Author of

• 28120

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  Poster Session (ID 8)

  • Event: ACLC 2018
  • Type: Poster Session
  • Track:
  • Presentations: 1
  • Moderators:
  • Coordinates: 11/07/2018, 00:00 - 00:00, Poster Hall

  • 28183

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    P029 - Circulating MDSCs Derived from Small Cell Lung Cancer Patients Secrete TGF - Beta 1 and Play Roles in Angiogenesis (ID 151)

    00:00 - 00:00  |  Author(s): S. Lan
    • Abstract

    Background:
    Studies showed that small cell lung cancer (SCLC) induced CD33+cells production in vitro and the CD33+ cells present typical features of myeloid-derived suppressor cells (MDSCs). We previously reported CD33+CD11b+HLA-DR-MDSCs level was elevated in peripheral blood of SCLC patients and has a prognostic value for SCLC patients. In this study we further explored the mechanisms of SCLC-derived MDSCs involved in angiogenesis.
    
    
    Method:
    Peripheral blood specimens from SCLC patients and healthy volunteer were collected and CD11b+/CD33+cells were separated using magnetic bead. Giemsa stain was used in morphological identification of the cells. CD11b+/CD33+cells were cultured in vitro for 72 hrs, then TGF-?1 in cell pellets and supernatant was detected using RT-PCR and western blot, or ELISA respectively. Endothelial tube formation was performed through culturing HUVEC cells on Matrigel using the supernatant as medium. The supernatant was added into HUVEC cells cultured on Matrigel to test angiogenesis effects.
    
    
    Results:
    RT-PCR data showed that CD33+ and CD11b+MDSCs from SCLC expressed higher level of TGF-?1 than those from healthy control, 0.349 vs 0.174 (P=0.000632) and 0.191 vs 0.105 (P=0.000867), respectively, and the expression of TGF-?1 in CD33+MDSCs was higher than that in CD11b+cells (P=0.0382). In addition, the western blot results showed that CD33+MDSCs from SCLC expressed higher TGF-?1 than that in control (0.391 vs 0.164?P=0.000491), however, the similar effects were not seen in CD11b+ cells. TGF-?1 expression in supernatant was higher in SCLC-derived CD33+ or CD11b+MDSCs than those in healthy control, 0.620 vs 0.324 (P=0.0155) and 0.482 vs 0.307 (P=0.0413), respectively), and the TGF-?1 level was higher in CD33+MDSCs than that in CD11b+MDSCs (P=0.00668). A significant decrease in tube formation and TGF-?1 level was found in SCLC patients after treatment compared to those before treatment.
    
    
    Conclusion:
    The TGF-?1 was highly expressed in both CD11b+ or CD33+MDSCs from SCLC in both transcription and translation levels, along with level change after treatment implying TGF-? signaling pathway may participate in MDSC-mediated angiogenesis in SCLC. Moreover, the expression level of TGF-?1 was discrepant in different phenotypes of MDSCs demonstrating the plastic phenotype of MDSCs in SCLC.