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Increased Expression of Estrogen Receptor a-36 by Breast Cancer Oncogene IKKe Promotes Growth of ER-Negative Breast Cancer Cells
Author(s) -
Qihong Li,
Haiyan Sun,
Jingcai Zou,
Ge Cheng,
Kaitao Yu,
Yuan Cao,
Quan Hong
Publication year - 2013
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000350101
Subject(s) - estrogen receptor , transactivation , oncogene , cancer research , breast cancer , iκb kinase , estrogen receptor alpha , signal transduction , cancer , kinase , estrogen receptor beta , transcription factor , biology , chemistry , medicine , cell cycle , nf κb , microbiology and biotechnology , genetics , gene
The expression of estrogen receptor-α (ERα) is one of the most important diagnostic and prognostic factors of breast cancer. Recently, ERα-36 has been identified as a novel variant of ER-α. ERα-36 lacks intrinsic transcription activity and mainly mediates non-genomic estrogen signaling. The noncanonical IKK family member IKKε is essential for regulating antiviral signaling pathways and is recently discovered as a breast cancer oncogene. IKKε interacts with and phosphorylates ERα on serine 167, induces ERα transactivation activity and enhances ERα binding to DNA in ER-positive breast cancer cells. However, the correlation between IKKε and the ERα-36 signaling pathway in ER-negative breast cancer cells remains unclear.

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