Regulatio of actin cytoskeleton by TIS21 vi downregulating reactive oxygen species (ROS) in the doxorubicin-induced premature senescenc

BTG2(B-cell translocation gene2)is a member of the BTG/Tob family of anti-proliferative genes and has been implicated in various cellular processes including cell cycle progression, differentiation and apoptosis. Cellular senescence is an irreversible arrest of proliferation, which is induced by replicative cell division (replicative senescence) or stress (stress induced premature senescence; SIPS). Cellular senescence is induced by DNA damage, telomere shortening or oncogene activation. During cellular senescence BTG2 is stabilized in response to telomere dysfunction. Doxorubicin is an effective anticancer drug that belongs to a class of anthracyclines and a commonly used inducer of DNA damage. Here, we show the role of BTG2 in doxorubicin induced senescence in human diploid fibroblast. We observed increase in SA-β-galstaining, change in cellular morphology, an increase in BTG2expression and ROS level in response to doxorubicin treatment along with F-actin distribution in HDF cells, suggesting doxorubicin induced senescence phenotypes. However, TIS21 over expression reduced the phenotypes characterized by the morphological change, SA-β-galstaining, F-actin re-distribution and ROS generations after doxorubicin treatment. The effect of TIS21 on the doxorubicin induced senescence phenotypes was further confirmed by knocking down of endogenous BTG2 expression. However, the underlying mechanism of BTG2 effect on stress induced senescence needs further studies.

Author dc:creator

• 김, 빛나

Contributors dc:contributor

• 임, 인경
• 대학원 의생명과학과
• 201124150

• 세포노화
• BTG2
• TIS21
• Doxorubicin
• Stress induced senescence

Language dc:language

ko

Identifier

http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000016361
000000016361

OAI identifier oai:identifier

oai:repository.ajou.ac.kr:201003/10848