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Abstract
Basal-like breast cancer (BLBC) is associated with a poor clinical outcome due to the few treatment options and absence of effective targeted agents. Here, we show that malic enzyme 1 (ME1) is dramatically upregulated in BLBC due to ME1 copy number amplification. ME1 expression increases glucose uptake and lactate production, and reduces oxygen consumption, leading to aerobic glycolysis. ME1 expression promotes, whereas knockdown of ME1 expression suppresses tumorigenicity. In breast cancer patients, ME1 expression is positively correlated with large tumor size, high grade, poor survival, and chemotherapy resistance. Our study not only contributes to a new understanding of how metabolic reprogramming contributes to BLBC progression, but also provides a potential prognostic marker and therapeutic target for this challenging disease.
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1 Department of Pathology and Pathophysiology, and Department of Surgical Oncology (breast center) of The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China; Zhejiang Key Laboratory for Disease Proteomics, Zhejiang University School of Medicine, Hangzhou, China
2 Department of Pathology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China