Title page for etd-0605118-111049


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URN etd-0605118-111049
Author HUI-CHUN WU
Author's Email Address No Public.
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Department Biological Sciences
Year 2017
Semester 2
Degree Master
Type of Document
Language zh-TW.Big5 Chinese
Title Autophagy inducers modulated ATG4B expression in human brain tumor cells
Date of Defense 2018-07-17
Page Count 46
Keyword
  • Rapamycin
  • Chloroquine
  • Glioma
  • Autophagy
  • ATG4B
  • Abstract Autophagy is a self-eating mechanism in cells through which damaged proteins and organelles are recruited to autophagosomes and fused with lysosome for their bulk degradation and recycling during nutrient deprivation. Dysregulation of autophagy is associated with various diseases, including cancer. ATG4B is a cysteine protease required for autophagy machinery. Recent reports have shown that elevated ATG4B promoted tumorigenesis, malignancy and drug resistance, suggesting ATG4B might modulate autophagy to facilitate tumor progression. However, the role of autophagy on ATG4B in cancer cells remains unknown. In this study, we found ATG4B protein level was decreased in glioma H4 and SHSY5Y cells during autophagy inducing conditions, including rapamycin and starvation. Moreover, autophagy inhibitors chloroquine or BafA1and proteosome inhibitor MG132 modestly recovered autophagy downregulated ATG4B in cells. Silencing ATG7 also partially recovered ATG4B protein level in cell treated with rapamycin, whereas it had no recovery effects in starved cells. Furthermore, mRNA level of ATG4B was decreased in rapamycin-treated H4 cells, but not starved cells. Luciferase fusion with 3’UTR of ATG4B as reporter assay was used to evaluate the effects of miRNA on ATG4B in cells during autophagy conditions. The luciferase activity was significantly decreased in H4 cells treated with rapamycin. However, the luciferase activity had little effects on recovery. The miR-34a was accordingly increased in the rapamycin-treated cells, while miR-34a was inhibited in BafA1 and CQ pretreated cells. Taken together, rapamycin may regulate autophagy and miR-34a to reduce ATG4B in glioma cells. Our results may shed a light on potential mechanisms of rapamycin on tumor suppression.
    Advisory Committee
  • Ming-Hong Tai - chair
  • Pei-Feng Liu - co-chair
  • Chih-Wen Shu - advisor
  • Chen, Chun-Lin - advisor
  • Files
  • etd-0605118-111049.pdf
  • Indicate in-campus at 3 year and off-campus access at 3 year.
    Date of Submission 2018-08-15

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