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Estrogen receptor α promotes breast cancer by reprogramming choline metabolism

Jia, Min; Andreassen, Trygve; Jensen, Lasse; Bathen, Tone Frost; Sinha, Indranil; Gao, Hui; Zhao, Chunyan; Haldosen, Lars-Arne; Cao, Yihai; Girnita, Leonard; Moestue, Siver Andreas; Dahlman-Wright, Karin
Journal article, Peer reviewed
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Postprint_Jia+2016.pdf (13.61Mb)
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http://hdl.handle.net/11250/2407728
Utgivelsesdato
2016
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  • Institutt for sirkulasjon og bildediagnostikk [1007]
  • Publikasjoner fra CRIStin - NTNU [19694]
Originalversjon
Cancer Research 2016   10.1158/0008-5472.CAN-15-2910
Sammendrag
Estrogen receptor α (ERα) is a key regulator of breast growth and breast cancer development. Here, we report how ERα impacts these processes by reprogramming metabolism in malignant breast cells. We employed an integrated approach, combining genome-wide mapping of chromatin-bound ERα with estrogen-induced transcript and metabolic profiling, to demonstrate that ERα reprograms metabolism upon estrogen stimulation, including changes in aerobic glycolysis, nucleotide and amino acid synthesis, and choline (Cho) metabolism. Cho phosphotransferase CHPT1, identified as a direct ERα-regulated gene, was required for estrogen-induced effects on Cho metabolism, including increased phosphatidylcholine synthesis. CHPT1 silencing inhibited anchorage-independent growth and cell proliferation, also suppressing early-stage metastasis of tamoxifen-resistant breast cancer cells in a zebrafish xenograft model. Our results showed that ERα promotes metabolic alterations in breast cancer cells mediated by its target CHPT1, which this study implicates as a candidate therapeutic target. Cancer Res; 76(19); 1–13. ©2016 AACR
Tidsskrift
Cancer Research

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