Author of

• 18974

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  P3.02 - Biology/Pathology (ID 620)

  • Event: WCLC 2017
  • Type: Poster Session with Presenters Present
  • Track: Biology/Pathology
  • Presentations: 1
  • Moderators:
  • Coordinates: 10/18/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)

  • 24035

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    P3.02-087 - Long Noncoding RNA FOXF1-AS1 Regulates Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer Cells (ID 8060)

    09:30 - 09:30  |  Author(s): L. Miao
    • Abstract
    • Slides

    Background:
    Lung cancer is still the leading cause of cancer related death in China and has become a severe public health problem. Two main subtypes of lung cancer are named as non-small cell lung cancer (NSCLC) and small cell lung cancer, which accounts for approximately 80-85% and 15-20% respectively. The high mortality is probably related to early metastasis, however the underlying mechanism remains unclear. The main critical changes of progression and metastasis are epithelial-to-mesenchymal transition (EMT). Long noncoding RNA (lncRNA) is consisted of more than 200 nucleotides in length. Recent evidence showed that lncRNAs trigger the initiation and progression of cancers. In this study, we aim to investigate whether lncRNA can regulate EMT in NSCLC.
    
    Method:
    Quantitive PCR was performed to investigate the different expression of lncRNA, FOXF1-AS1 in NSCLC and matched normal tissues. Full length FOXF1-AS1 cDNA was transfected into lung cancer cells by plasmid vectors to forced express the FOXF1-AS1. The morphology of cancer cells were observed after transfection with FOXF1-AS1. And transwell migration and invasion assay were performed using transwell chambers without (migration) or with (invasion) Matrigel.
    
    Result:
    We identified a panel of key factors dysregulated in lung cancer. Among them, the expression of FOXF1-AS1 was significantly downregulated in lung cancer.The loss expression FOXF1-AS1 in lung cancer tissues was further validated by real time qRT-PCR . When we stably overexpress FOXF1-AS1 in NSCLC, we observed the morphological changes of CALU1 and NCIH1975 cells from a fibroblastoid appearance elongated spindle shape to cobblestone shape after stable overexpression FOXF1-AS1.Then, CALU1-FOXF1-AS1 cell and H1975-FOXF1-AS1 cell that overexpressed FOXF1-AS1 or their negative control were allowed to migrate through a transwell membrane into complete media. Compared to the negative control, overexpression of FOXF1-AS1 induced the promotion of the motility of both two of the transfected cells. And FOXF1-AS1 overexpression also significantly promoted the invasion of the two transfected cells. And we also found that overexpression of FOXF1-AS1 decreased Vimentin and increased E-Cadherin in both CALU1 and NCIH1975 cells.
    
    Conclusion:
    FOXF1-AS1 regulates epithelial-mesenchymal transition in lung cancer cells.
    
    

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