Adipocytes promote malignant growth of breast tumours with monocarboxylate transporter 2 expression via β-hydroxybutyrate

Chun-Kai Huang, Po-Hao Chang, Wen-Hung Kuo, Chi-Long Chen, Yung-Ming Jeng, King-Jen Chang, Jin-Yuh Shew, Chun-Mei Hu and Wen-Hwa Lee ()
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Chun-Kai Huang: Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University
Po-Hao Chang: Genomics Research Center, Academia Sinica
Wen-Hung Kuo: National Taiwan University Hospital
Chi-Long Chen: Wan Fang Hospital, Taipei Medical University
Yung-Ming Jeng: National Taiwan University Hospital
King-Jen Chang: National Taiwan University Hospital
Jin-Yuh Shew: Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University
Chun-Mei Hu: Genomics Research Center, Academia Sinica
Wen-Hwa Lee: Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract Adipocytes are the most abundant stromal partners in breast tissue. However, the crosstalk between breast cancer cells and adipocytes has been given less attention compared to cancer-associated fibroblasts. Here we find, through systematic screening, that primary mammary gland-derived adipocytes (MGDAs) promote growth of breast cancer cells that express monocarboxylate transporter 2 (MCT2) both in vitro and in vivo. We show that β-hydroxybutyrate is secreted by MGDAs and is required to enhance breast cancer cells malignancy in vitro. Consistently, β-hydroxybutyrate is sufficient to promote tumorigenesis of a mouse xenograft model of MCT2-expressing breast cancer cells. Mechanistically we observe that upon co-culturing with MGDAs or treatment with β-hydroxybutyrate, breast cancer cells expressing MCT2 increase the global histone H3K9 acetylation and upregulate several tumour-promoting genes. These results suggest that adipocytes promote malignancy of MCT2-expressing breast cancer via β-hydroxybutyrate potentially by inducing the epigenetic upregulation of tumour-promoting genes.

Date: 2017
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DOI: 10.1038/ncomms14706

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