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  P3.02 - Poster Session 3 - Novel Cancer Genes and Pathways (ID 149)

  • Event: WCLC 2013
  • Type: Poster Session
  • Track: Biology
  • Presentations: 1
  • Moderators:
  • Coordinates: 10/30/2013, 09:30 - 16:30, Exhibit Hall, Ground Level

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    P3.02-012 - Cysteine dioxygenase 1 (CDO1) : A novel tumor suppressor gene regulated by hypermethylation. (ID 2207)

    09:30 - 09:30  |  Author(s): J. Kwon
    • Abstract

    Background
    Lung cancer is one of the most common causes of cancer-related deaths worldwide. Effective early diagnosis and targeted therapies for lung cancer to reduce mortality and incidence would benefit from in-depth study on molecular mechanism of lung carcinogenesis, but these are largely unknown. In our previous study, we reported a novel hyper-methylated gene, CDO1, encoding cysteine dioxygenase 1 that involved in the conversion of cysteine to cysteine sulfinate, and plays a key role in taurine biosynthesis. In this study, we evaluated the functional characteristics of CDO1 in Lung squamous cell carcinoma (LSCC).

    Methods
    We analyzed expression levels of CDO1 mRNA and protein in tumor and normal tissue pairs from 12 LSCC patients were determined by RT-PCR and Western blot analysis. In order to determine whether high levels of CDO1 expression contributed to the LSCC cell proliferation, migration, invasion and colony formation, we employed a CDO1-expressing vector pEGFP_C3_CDO1 to transfect CDO1 into LSCC cell lines (HCC-95, HCC-1588). Furthermore, we performed gene expression profile analysis using human whole genome oligonucleotide chip (Agilent).

    Results
    Downregulation of CDO1 mRNA level was observed in LSCC cell lines and tumors derived from patient tissues. In cell proliferation assay, the number of HCC-95 and HCC-1588 cells transfected with pEGFP_C3_CDO1 decreased to 58-70% compared with pEGFP_C3 (p<0.05). Moreover, the forces expression of CDO1 in two different types of LSCC cell lines significantly decreased the cell migration, invasion, and colony formation ability (p<0.05). Furthermore, we showed that overexpression of CDO1 make change of several signal molecules in lung cancer cells using microarray analysis.

    Conclusion
    In this study, we found that CDO1 expression was regulated by DNA methylation, and this epigenetic regulated CDO1 might be a novel tumor suppressor gene and potentially valuable biomarker for lung squamous cell carcinoma.