caffeine에 의한 HGF-induced G2 delay 촉진효과 확인 및 기전분석

In the present study, we explored the role of caffeine in G2 delay induced by HGF. Previously, we have shown that HGF induced transient G2 delay via ERK pathway. To address the involvement of ATM/ATR kinases in HGF-induced G2 delay, caffeine was used as an inhibitor. Interestingly, caffeine couldn't inhibit the HGF-induced G2 delay but rather augmented the HGF-induced delay while caffeine itself did not affect the duration of G2 phase significantly. Same observation was obtained by FACS analysis and mitotic index study. Increased G2 delay by caffeine was also accompanied with the delay in cdk1 activation and in cyclin B nuclear localization. Western blot analysis also showed delayed degradation of cyclin A and B. ATM/ATR knock-down cells did not show the augmentation of HGF-induced G2 delay, strongly suggesting that inhibitory activity of caffeine on ATM/ATR pathway was not related with increased G2 delay. Inhibitor study revealed that ERK pathway but not p38 MAPK, JNK, PI3K pathways, was involved in increased G2 delay. Western blot analysis revealed corroborating data with the inhibitor study. In caffeine and HGF co-treated cells, only ERK was more phosphorylated than in HGF treated cells. In addition, whether caffeine affects the duration of mitosis was addressed. Interestingly, caffeine itself could increase the mitosis duration, which was not influenced by HGF. In conclusion, we found that caffeine augmented HGF-induced G2 delay through ERK pathway.

Author dc:creator

• 이, 민우

Contributors dc:contributor

• 이, 재호
• 대학원 의학과
• 200424194

• HGF(hepatocyte growth factor)
• caffeine
• G2 delay
• 간세포 성장인자(HGF)
• G2 지연현상

Language dc:language

ko

Identifier

http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000001009
000000001009

OAI identifier oai:identifier

oai:repository.ajou.ac.kr:201003/1477