Potentiation of estrogen receptor transcriptional activity by breast cancer amplified sequence 2.
Breast cancer amplified sequence 2 (BCAS2) was initially identified as a gene that was overexpressed and amplified in some breast cancer cell lines. It was later found to be a component of the spliceosome. Here, we identified BCAS2 as an estrogen receptor (ER) alpha interacting protein by yeast two-hybrid screening. In addition to ER alpha, BCAS2 also interacted with ER beta, TR beta, PR, and PPAR gamma in a ligand-independent way. Transient transfection assays revealed that overexpression of BCAS2 enhanced while inhibition of BCAS2 expression attenuated the estrogen receptor-mediated transcription. BCAS2 potentiated the activation function-2 (AF-2) activity of ER alpha but had no effect on the AF-1 activity. This study suggested that BCAS2 might play an important role in breast cancer development by increasing the estrogen receptor's function.
Qi
Chao
C
Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Zhu
Yiwei Tony
YT
Chang
Jeffrey
J
Yeldandi
Anjana V
AV
Rao
M Sambasiva
MS
Zhu
Yi-Jun
YJ
D000818:Animals; D001943:Breast Neoplasms / Q000378:metabolism*; D045744:Cell Line, Tumor; D002467:Cell Nucleus / Q000378:metabolism; D002522:Chlorocebus aethiops; D047628:Estrogen Receptor alpha / Q000737:chemistry / Q000378:metabolism*; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007668:Kidney / Q000378:metabolism*; D009363:Neoplasm Proteins / Q000737:chemistry / Q000378:metabolism*; D015533:Transcriptional Activation
C120624:BCAS2 protein, human; D047628:Estrogen Receptor alpha; D009363:Neoplasm Proteins