Genome-wide study of ER-regulated lncRNAs shows AP000439.3 may function as a key regulator of cell cycle in breast cancer | Zendy

Yin Zhang | Zendy; Dan-Lan Wang | Zendy; Haiyan Yan | Zendy; JianYou Liao | Zendy; Jiehua He | Zendy; Kaishun Hu | Zendy; Weixi Deng | Zendy; Yanjie Wang | Zendy; Hongtao Xing | Zendy; H. Phillip Koeffler | Zendy; Dong Yin | Zendy

Open Access

Genome-wide study of ER-regulated lncRNAs shows AP000439.3 may function as a key regulator of cell cycle in breast cancer

Author(s) -

Yin Zhang,

Dan-Lan Wang,

Haiyan Yan,

JianYou Liao,

Jiehua He,

Kaishun Hu,

Weixi Deng,

Yanjie Wang,

Hongtao Xing,

H. Phillip Koeffler,

Dong Yin

Publication year - 2017

Publication title -

oncology reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.094

H-Index - 96

eISSN - 1791-2431

pISSN - 1021-335X

DOI - 10.3892/or.2017.5975

Subject(s) - biology , cell cycle , estrogen receptor , oncogene , gene silencing , carcinogenesis , cancer research , regulator , cancer , cell growth , cyclin d1 , breast cancer , gene , microbiology and biotechnology , genetics

Estrogen receptor (ER) plays important roles in cell growth, development and tumorigenesis. Although ER-regulated genes have been extensively investigated, little is known about roles of ER-regulated lncRNAs in breast cancer. Here, we conducted genome-wide study of ER-regulated lncRNAs by using RNA-seq, ChIP-seq and TCGA data. A total of identified 114 ER-regulated lncRNAs were identified, many of them were overexpressed in ER+ breast cancer and co-expressed with some key regulators. Silencing one of most prominent lncRNA, AP000439.3, resulted in inhibition of cell cycle progression and proliferation. Further study revealed AP000439.3 can regulate expression of CCND1 through enhancing estrogen receptor induction of CCND1. This finding revealed lncRNAs may serve as important effectors of ER in regulation of gene expression and cell phenotype in breast cancer.

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