Defect of Mitochondrial Translation Machinery Enhances Hepatoma Cell Invasiveness

I. INTRODUCTION 1 II. MATERIALS AND METHODS 4 1. Cell cultures, drug treatment and cell growth rate 4 2. Reverse transcription-polymerase chain reaction (RT-PCR) 4 3. Endogenous cellular oxygen consumption rate 5 4. Estimation of intracellular and mitochondrial ROS level 5 5. Total genomic DNA isolation and sequencing of mitochondrial DNA fragments 5 6. Western blot analysis 6 7. Real-time reverse transcription-polymerase chain reaction (qPCR) 7 8. Gene expression profiling and data analysis 7 9. siRNAs transfection. 8 10. Cell invasion assay 8 11. Cell imaging 9 III. RESULTS 10 1. Mitochondrial respiratory defect is associated with tumoral behavior in SNU hepatoma cells. 10 2. Mitochondrial protein homeostasis is associated with mitochondrial dysfunction. 12 3. Mitochondrial translation machinery defect may be a key event in mitochondrial dysfunction in hepatoma cells 14 4. Mt-TMD-related invasive behavior induced by doxycycline in SNU-387 cells 20 5. Claudin-1 regulates Mt-TMD-induced hepatoma cell invasiveness. 26 6. Impact of doxycycline on gene expression 30 IV. DISCUSSION 33 V. CONCLUSION 36 REFFERENCE 37 국문요약 43

Author dc:creator

• 임, 종진

Contributors dc:contributor

• 대학원 의생명과학과
• 200324514

• Mitochondrial translational machinery defect
• Tumorigenesis
• Doxycycline
• Claudin-1
• Mitochondrial retrograde signaling
• Hepatoma cell invasiveness

Language dc:language

en

Identifier

http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000021529
000000021529

OAI identifier oai:identifier

oai:repository.ajou.ac.kr:201003/13027