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)

  • 24041

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    P3.02-093 - Knockdown of BRM Causes Epithelial-Mesenchymal Transition in Lung Adenocarcinoma Cell Line H1975 (ID 8955)

    09:30 - 09:30  |  Author(s): M. Takahashi
    • Abstract
    • Slides

    Background:
    Recent genomic studies have identified mutations in the multiple subunits of the chromatin remodeling complex in various cancers. Expression of BRG1/BRM, the core subunit of the SWI/SNF complex, is frequently altered in lung cancer, and our group has previous shown that loss of BRG1/BRM is associated with the EMT phenotype and poor prognosis in lung adenocarcinomas (Cancer Sci 2013).
    
    Method:
    In this study, we explored the effect of BRM knockdown (KD) with lentiviral sh-RNA in lung cancer cell line H1975.
    
    Result:
    BRM KD with lentiviral sh-RNA caused profound changes in H1975; original polygonal cells became spindled shaped, and when injected subcutaneously into SCID mouse, BRM-KD cells formed tumors composed of uniform spindle cells, mimicking sarcomatoid carcinomas. qRT-PCR and Western blot analyses confirmed downregulation of E-cadherin and upregulation of vimentin. Analysis of signaling molecules showed that EMT occurred independent of the EGFR, MET, or TGF-β/SMAD pathway. Among the master regulators of EMT, ZEB-1 was most remarkably upregulated, as compared to snail or slug, by BRM knockdown.
    
    Conclusion:
    Loss of BRM caused EMT, which was due to upregulation of ZEB1. Figure 1
    
    
    
    

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