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World J Clin Oncol. Feb 10, 2016; 7(1): 122-130
Published online Feb 10, 2016. doi: 10.5306/wjco.v7.i1.122
Targeting metabolism in breast cancer: How far we can go?
Jing-Pei Long, Xiao-Na Li, Feng Zhang
Jing-Pei Long, Xiao-Na Li, Department of Surgery, Women’s Hospital, School of Medicine, Zhejiang University, Hangzhou 310006, Zhejiang Province, China
Feng Zhang, Department of Surgery, Hangzhou Women’s Hospital, Hangzhou 310008, Zhejiang Province, China
Author contributions: Long JP and Li XN drafted the manuscript; Zhang F was responsible for the conception of the manuscript and collected the literature.
Conflict-of-interest statement: The authors have no conflicts of interest for this manuscript.
Open-Access: This article is an open access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Feng Zhang, MD, PhD, Department of Surgery, Hangzhou Women’s Hospital, Kunpeng Road 369, Hangzhou 310008, Zhejiang Province, China. zhang3772@qq.com
Telephone: +86-571-89992095
Received: May 28, 2015
Peer-review started: May 30, 2015
First decision: August 16, 2015
Revised: October 16, 2015
Accepted: December 8, 2015
Article in press: December 11, 2015
Published online: February 10, 2016
Core Tip

Core tip: Breast cancer cells display distinct metabolic characteristics according to different molecular phenotypes. There may be crosstalk with the estrogen receptor and human epidermal growth factor receptor-2 signal pathways in the metabolic regulation in breast cancer cells that make it more complex to evaluate the efficiency of an anti-metabolic drug. On the other hand, the research on target metabolism in breast cancer will also largely help us to understand the complicated mechanism by which an anti-metabolic drug improves the efficacy of cancer therapy or overcomes drug resistance.