期刊
ONCOTARGET
卷 7, 期 3, 页码 3201-3216出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.6420
关键词
lncRNA; breast cancer; estrogen receptor; data integration; DSCAM-AS1
资金
- AIRC (Associazione Italiana per la Ricerca sul Cancro) [IG 15600]
- Fondazione CRT [2014.1854]
- Fondazione San Paolo grant GeneRNet
- Local University of Torino
Estrogen Receptor alpha (ER alpha) activation by estrogenic hormones induces luminal breast cancer cell proliferation. However, ER alpha plays also important hormone-independent functions to maintain breast tumor cells epithelial phenotype. We reported previously by RNA-Seq that in MCF-7 cells in absence of hormones ER alpha down-regulation changes the expression of several genes linked to cellular development, representing a specific subset of estrogen-induced genes. Here, we report regulation of long non-coding RNAs from the same experimental settings. A list of 133 Apo-ER alpha-Regulated lncRNAs (AER-lncRNAs) was identified and extensively characterized using published data from cancer cell lines and tumor tissues, or experiments on MCF-7 cells. For several features, we ran validation using cell cultures or fresh tumor biopsies. AER-lncRNAs represent a specific subset, only marginally overlapping estrogen-induced transcripts, whose expression is largely restricted to luminal cells and which is able to perfectly classify breast tumor subtypes. The most abundant AER-lncRNA, DSCAM-AS1, is expressed in ER alpha+ breast carcinoma, but not in pre-neoplastic lesions, and correlates inversely with EMT markers. Down-regulation of DSCAM-AS1 recapitulated, in part, the effect of silencing ER alpha, i.e. growth arrest and induction of EMT markers. In conclusion, we report an ER alpha-dependent lncRNA set representing a novel luminal signature in breast cancer cells.
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