Caveolin-1 gene silencing promotes the activation of PI3K/AKT dependent on Eralpha36 and the transformation of MCF10ACE.
ERalpha36, a variant of estrogen receptor-alpha, acts as a dominant-negative factor in both estrogen-dependent and estrogenindependent 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 ERalpha and Caveolin-1. In conclusion, Caveolin-1 gene silencing activated the PI3K/AKT signaling pathway in an ERalpha36-dependent way. Our finding may provide a promising therapeutic target of breast cancer.
Feng
Shuang
S
College of Life Science, Liaoning Normal University, Dalian, 116029, China.
Wang
Yang
Y
Wang
Xi
X
Wang
Zhaoyi
Z
Cui
Yuying
Y
Liu
Jing
J
Zhao
Chunhui
C
Jin
Mei
M
Zou
Wei
W
D001943:Breast Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D051242:Caveolin 1 / Q000235:genetics* / Q000378:metabolism; D045744:Cell Line, Tumor; D002471:Cell Transformation, Neoplastic; D005260:Female; D020868:Gene Silencing; D006801:Humans; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism* / Q000502:physiology*; D015398:Signal Transduction / Q000187:drug effects / Q000235:genetics / Q000502:physiology
D051242:Caveolin 1; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt