Long non-coding RNA MIAT is estrogen-responsive and promotes estrogen-induced proliferation in ER-positive breast cancer cells
- Department of Medical Oncology, The First Affiliated Hospital, University of South China, Hengyang City, Hunan Province, 421001 (China)
- Department of Pharmacy, The First Affiliated Hospital, University of South China, Hengyang City, Hunan Province, 421001 (China)
- Department of Histology and Embryology, Laboratory of Reproductive Medicine, University of South China, Hengyang City, Hunan Province (China)
- Department of Oncology, Shenzhen Hospital, University of Hong Kong, Shenzhen City, 518000 (China)
- Department of Pathology, The First Affiliated Hospital, University of South China, Hengyang City, Hunan Province (China)
- Department of Breast and Thyroid Surgery, The Second Affiliated Hospital, University of South China, Hengyang City, Hunan Province (China)
Highlights: • lncRNA MIAT was over-expressed in ER-positive breast cancer tissues and cells. • Breast cancer cell MIAT expression was estrogen-dependent. • lncRNA MIAT promoted breast cancer cell growth. • lncRNA MIAT was required for breast cancer cell cycle progression. Estrogen drives the development and progression of estrogen receptor (ER)-positive breast cancer. However, the detailed mechanism underlying ER-driven carcinogenesis remains unclear despite extensive studies. Previously reports indicated higher expression of long non-coding RNA (lncRNA) myocardial infarction associated transcript (MIAT) in ER-positive breast cancer tissues than in ER-negative tissues. However, the functional relevance of MIAT in ER-positive breast cancer tumorigenesis was poorly understood. Here, we investigated the role of lncRNA MIAT in ER-positive breast cancer cells. MIAT was over-expressed in ER-positive breast cancer tissues and ER-positive breast cancer cell line MCF-7. Activating estrogen signaling by diethylstilbestrol (DES) led to a dose- and time-dependent up-regulation of MIAT in MCF-7 cells that was dependent on ERα, as evidenced by ERα silencing and pharmacological inhibition using ER antagonist ICI 182780. Silencing MIAT decreased DES-induced MCF-7 cell proliferation while overexpressing MIAT increased MCF-7 cell proliferation. Further mechanistic study identified that MIAT was critical for G1 to S phase cell cycle transition. Taken together, these results suggest that lncRNA MIAT is an estrogen-inducible lncRNA and a key regulator in ER-positive breast cancer cell growth. MIAT could serve as a potential biomarker and promising therapeutic target for ER-positive breast cancer.
- OSTI ID:
- 23105705
- Journal Information:
- Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 1 Vol. 503; ISSN BBRCA9; ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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