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作 者:FENG Shuang1,WANG Yang1,WANG Xi1,WANG ZhaoYi3,CUI YuYing1,LIU Jing4,ZHAO ChunHui1,JIN Mei1,2 & ZOU Wei1,2 1 College of Life Science,Liaoning Normal University,Dalian 116029,China 2 Liaoning Key Laboratory of Biotechnology and Molecular Drug R&D,Dalian 116029,China 3 Cancer Center,Creighton University,2500 California Plaza,Omaha,NE 68178,USA 4 First Clinical Hospital of Dalian Medical University,Dalian 116011,China
出 处:《Science China(Life Sciences)》2010年第5期598-605,共8页中国科学(生命科学英文版)
基 金:supported by the National Natural Science Foundation of China (Grant No 30570225)
摘 要:ERα36,a variant of estrogen receptor-α,acts as a dominant-negative factor in both estrogen-dependent and estrogen-independent transactivation signaling pathways,and is a key factor in the promotion,progression and prognosis of breast cancers.Caveolin-1,a 22-to 24-kD integral membrane protein,may function as a tumor suppressor in inhibiting of many growth-promoting signaling pathways.It was shown that downregulation of Caveolin-1 strengthens the interaction of ERα and Caveolin-1.In conclusion,Caveolin-1 gene silencing activated the PI3K/AKT signaling pathway in an ERα36-dependent way.Our finding may provide a promising therapeutic target of breast cancer.ERα36,a variant of estrogen receptor-α,acts as a dominant-negative factor in both estrogen-dependent and estrogen-independent transactivation signaling pathways,and is a key factor in the promotion,progression and prognosis of breast cancers.Caveolin-1,a 22-to 24-kD integral membrane protein,may function as a tumor suppressor in inhibiting of many growth-promoting signaling pathways.It was shown that downregulation of Caveolin-1 strengthens the interaction of ERα and Caveolin-1.In conclusion,Caveolin-1 gene silencing activated the PI3K/AKT signaling pathway in an ERα36-dependent way.Our finding may provide a promising therapeutic target of breast cancer.
关 键 词:CAVEOLIN-1 ESTROGEN receptor PI3K/AKT
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