
Identification and Analysis of Estrogen Receptor α Promoting Tamoxifen Resistance-Related lncRNAs
Author(s) -
Xiulei Zhang,
Shanjun Gao,
Zhen Li,
Wei Wang,
Guangzhi Liu
Publication year - 2020
Publication title -
biomed research international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 126
eISSN - 2314-6141
pISSN - 2314-6133
DOI - 10.1155/2020/9031723
Subject(s) - tamoxifen , breast cancer , antiestrogen , estrogen receptor , chromatin immunoprecipitation , cancer research , estrogen receptor alpha , biology , cancer , drug resistance , oncology , bioinformatics , medicine , gene expression , genetics , gene , promoter
70-75% breast cancer patients are estrogen receptor alpha positive (ER α +), and the antiestrogen drug tamoxifen has been used for the past three decades. However, in 20-30% of these patients, tamoxifen therapy fails due to intrinsic or acquired resistance. A previous study has showed ER α signaling still exerts significant roles in the development of tamoxifen resistance and several lncRNAs have been demonstrated important roles in tamoxifen resistance. But ER α directly regulated and tamoxifen resistance related lncRNAs remain to be discovered. We reanalyze the published ER α chromatin immunoprecipitation-seq (ChIP-seq) and RNA-seq data of tamoxifen-sensitive (MCF-7/WT) and tamoxifen-resistant (MCF-7/TamR) breast cancer cells. We demonstrate that there are differential ER α recruitment events and the differentials may alert the expression profile in MCF-7/WT and MCF-7/TamR cells. Furthermore, we make an overlap of the ER α binding lncRNAs and differentially expressed lncRNAs and get 49 ER α positively regulated lncRNAs. Among these lncRNAs, the expression levels of AC117383.1, AC144450.1, RP11-15H20.6, and ATXN1-AS1 are negatively correlated with the survival probability of breast cancer patients and ELOVL2-AS1, PCOLCE-AS1, ITGA9-AS1, and FLNB-AS1 are positively correlated. These lncRNAs may be potential diagnosis or prognosis markers of tamoxifen resistance.