Title page for etd-0806117-173323


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URN etd-0806117-173323
Author Jheng-Yan Jhung
Author's Email Address No Public.
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Department Institute of Biomedical Sciences
Year 2017
Semester 1
Degree Master
Type of Document
Language zh-TW.Big5 Chinese
Title Studies on the oncogene of BCl6 effect in human bladder cancer cell lines through FOXO signaling pathway
Date of Defense 2017-08-28
Page Count 49
Keyword
  • FOXO3
  • BCL6
  • Urothelial
  • Cell cycle
  • bladder cancer
  • Abstract Bladder cancer is derived from urothelial, called urothelial carcinoma. It’s the most top ten cancer in Taiwan. In addition, the cancer with high mortality rate and cost of treatment. In past report, the BCL6 induced cell cycle progression and cell proliferation when the BCL6 highly expression in bladder cancer. According to the analysis of whole gene array (HumanHT-12v4 Expression BeadChip) find that 2900 genes regulated by the BCL6. Further analysis of intersection gets 1310 genes. Using the KEGG mapper analysis finds that cell cycle pathway and the FOXO pathway regulated by the BCL6. The BCL6 through the FOXO pathway effects the FOXO3 (Forkhead box O3) expression. To prove the BCL6 how to effect the FOXO3 expression level and nuclear/cytosol distribution, and then affect the cell cycle progression and cell proliferation. The FOXO3 regulates cell function and expression level through the phosphorylation site. For the reason that, to up regulates the BCL6 and add to LY294002 (PI3K inhibitor), AZD6244 (MEK inhibitor), Gefitinib (EGFR inhibitor) to observed the change of phosphorylation site and nuclear/cytosol distribution and cell cycle progression of the FOXO3. Understanding BCL6 effects the downstream genes and cell function through the MEK/ERK in T24 and BFTC905 bladder cancer cell lines. Therefore, to control the activity of BCL6 is a potential therapy.
    Advisory Committee
  • Chien-Feng Li - chair
  • Cheng-Tang Pan - co-chair
  • Hung-Wen Huang - co-chair
  • Yow-Ling Shiue - advisor
  • Files
  • etd-0806117-173323.pdf
  • Indicate in-campus at 99 year and off-campus access at 99 year.
    Date of Submission 2017-09-07

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