Loss of microRNA-27b contributes to breast cancer stem cell generation by activating ENPP1

Ryou-u Takahashi, Hiroaki Miyazaki, Fumitaka Takeshita, Yusuke Yamamoto, Kaho Minoura, Makiko Ono, Makoto Kodaira, Kenji Tamura, Masaki Mori and Takahiro Ochiya ()
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Ryou-u Takahashi: National Cancer Center Research Institute
Hiroaki Miyazaki: National Cancer Center Research Institute
Fumitaka Takeshita: National Cancer Center Research Institute
Yusuke Yamamoto: National Cancer Center Research Institute
Kaho Minoura: Genomic Application Group, Japan Diagnostics and Genomics, Agilent Technologies Japan Ltd., 9-1
Makiko Ono: National Cancer Center Research Institute
Makoto Kodaira: National Cancer Center Hospital, 1-1
Kenji Tamura: National Cancer Center Hospital, 1-1
Masaki Mori: Graduated School of Medicine, Osaka University
Takahiro Ochiya: National Cancer Center Research Institute

Nature Communications, 2015, vol. 6, issue 1, 1-15

Abstract: Abstract Cancer stem cells (CSCs) have been identified in various types of cancer; however, the mechanisms by which cells acquire CSC properties such as drug resistance and tumour seeding ability are not fully understood. Here, we identified microRNA-27b (miR-27b) as a key regulator for the generation of a side-population in breast cancer cells that showed CSC properties, and also found that the anti-type II diabetes (T2D) drug metformin reduced this side-population via miR-27b-mediated repression of ectonucleotide pyrophosphatase/phosphodiesterase family member 1 (ENPP1), which is involved in T2D development. ENPP1 induced the generation of the side-population via upregulation of the ABCG2 transporter. ENPP1 was also identified as a substrate of the 26S proteasome, the activity of which is downregulated in CSCs. Overall, these results demonstrate that a T2D-associated gene plays an important role in tumour development and that its expression is strictly controlled at the mRNA and protein levels.

Date: 2015
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DOI: 10.1038/ncomms8318

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