Title page for etd-0731117-120743


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URN etd-0731117-120743
Author Chien-Ting Chou
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 Study on ABT-751-suppressed growth on hepatocellular carcinoma-derived Hep-3B cells
Date of Defense 2017-08-28
Page Count 58
Keyword
  • Apoptosis
  • Autophagy
  • Microtubule
  • ABT-751
  • Hepatocellular carcinoma
  • Abstract One of the most prone to diagnosed cancer in the world, Hepatocellular carcinoma (HCC) is a common malignant tumor. Besides, the latest statistics show that HCC is the second most common cancer in men and forth in women in Taiwan. In this study, data show that in hepatocellular carcinoma cell line, Hep-3B, ABT-751 can induce autophagy and apoptosis. This study is aim to investigate the mechanism of ABT-751-induced autophagy and apoptosis in Hep-3B.ABT-751 is a novel oral administration of anti-microtubule drugs. In previous studies, it has been demonstrated that ABT-751 can bond with β-tubulin to inhibit microtubules. In our research, we decided to use 2 μM as the application concentration by MTT test. ABT-751 is found to inhibit the splitting of Hep-3B cells by affecting microtubules. Besides, results of Cyto-ID, Acridine orange staining and western blotting show that ABT-751 induced autophagy at 24 and 48 hours. By using the autophagy inhibitors 3-Methyladenine (3-MA) and bafilomycin A1 (BafA1), we tend to investigate the role of autophagy during this study, results show that when autophagy is inhibited, the percentage of apoptotic cell would increase. In all, results indicated that ABT-751 inhibited splitting of Hep-3B by affecting microtubules, still, ABT-751 induced the occurrence of autophagy. Additionally, the proportion of apoptotic cells will increase, when the autophagy is inhibited.
    Advisory Committee
  • Chien-Feng Li - chair
  • Cheng-Tang Pan - co-chair
  • Hung-Wen Huang - co-chair
  • Yow-Ling Shiue - advisor
  • Files
  • etd-0731117-120743.pdf
  • Indicate in-campus at 99 year and off-campus access at 99 year.
    Date of Submission 2017-08-31

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