2. Academic Validation
  3. Long non-coding RNA MIAT is estrogen-responsive and promotes estrogen-induced proliferation in ER-positive breast cancer cells

Long non-coding RNA MIAT is estrogen-responsive and promotes estrogen-induced proliferation in ER-positive breast cancer cells

  • Biochem Biophys Res Commun. 2018 Sep 3;503(1):45-50. doi: 10.1016/j.bbrc.2018.05.146.
Yuehua Li 1,  Baohong Jiang 2,  Xiaoping Wu 3,  Qin Huang 4,  Wenqi Chen 5,  Hongbo Zhu 1,  Xiaofei Qu 1,  Liming Xie 1,  Xin Ma 6,  Guo Huang 7
Affiliations

Affiliations

  • 1 Department of Medical Oncology, The First Affiliated Hospital, University of South China, Hengyang City, Hunan Province, 421001, China.
  • 2 Department of Pharmacy, The First Affiliated Hospital, University of South China, Hengyang City, Hunan Province, 421001, China.
  • 3 Department of Medical Oncology, The First Affiliated Hospital, University of South China, Hengyang City, Hunan Province, 421001, China. Electronic address: wuxiaoping11120@163.com.
  • 4 Department of Histology and Embryology, Laboratory of Reproductive Medicine, University of South China, Hengyang City, Hunan Province, China.
  • 5 Department of Oncology, Shenzhen Hospital, University of Hong Kong, Shenzhen City, 518000, China.
  • 6 Department of Pathology, The First Affiliated Hospital, University of South China, Hengyang City, Hunan Province, China.
  • 7 Department of Breast and Thyroid Surgery, The Second Affiliated Hospital, University of South China, Hengyang City, Hunan Province, China.
PMID: 29792859 DOI: 10.1016/j.bbrc.2018.05.146
Abstract

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.

Keywords

Breast cancer; Cell cycle; Estrogen receptor; Long non-coding RNA; MIAT; Proliferation.

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