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Title: miR-206 is down-regulated in breast cancer and inhibits cell proliferation through the up-regulation of cyclinD2

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [2];  [1];  [1];  [3];  [4];  [3];  [5];  [1];  [1];  [1]
  1. Department of Oncology, Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu (China)
  2. Department of Hepatobiliary Surgery, Affiliated Yijishan Hospital of Wannan Medical College, Wuhu, Anhui (China)
  3. Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, Jiangsu (China)
  4. Department of Obstetrics and Gynaecology, Jiangsu Province Hospital, Nanjing, Jiangsu (China)
  5. School of Pharmacy, Nanjing Medical University, Nanjing, Jiangsu (China)

Highlights: ► miR-206 was downexpressed in tumor samples compared with matched normal samples. ► Enhanced expression of miR-206 could inhibit breast cancer growth in vitro. ► Luciferase confirmed miR-206 functions as an anti-oncogene by targeting cyclinD2. ► A reverse correlation between miR-206 and cyclinD2 in breast cancer was found. -- Abstract: MicroRNAs act as important gene regulators in human genomes, and their aberrant expression is linked to many malignancies. Aberrant expression of miR-206 has been frequently reported in cancer studies; however, the role and mechanism of its function in breast cancer remains unclear. Quantitative real-time PCR was performed to detect the relative expression levels of miR-206 in breast cancer and normal breast tissues. Lower expression of miR-206 in breast cancer tissues was associated with larger tumour size and a more advanced clinical stage. Further in vitro observations showed that the enforced expression of miR-206 in MCF-7 breast cancer cells inhibited cell growth by blocking the G1/S transition and suppressed cell proliferation and colony formation, implying that miR-206 functions as a tumour suppressor in the progression of breast cancer. Interestingly, Luciferase assays first revealed that miR-206 inhibited cyclinD2 expression by targeting two binding sites in the 3′-untranslated region of cyclinD2 mRNA. qRT-PCR and Western blot assays verified that miR-206 reduced cyclinD2 expression at both the mRNA and protein levels. A reverse correlation between miR-206 and cyclinD2 expression was noted in breast cancer tissues. Altogether, our results identify a crucial tumour suppressive role of miR-206 in the progression of breast cancer, at least partly via up-regulation of the expression of cyclinD2, and suggest that miR-206 might be a candidate prognostic predictor or an anticancer therapeutic target for breast cancer patients.

OSTI ID:
22239534
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 433, Issue 2; Other Information: Copyright (c) 2013 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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