Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
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:
Correspondence to: Feng Zhang, MD, PhD, Department of Surgery, Hangzhou Women’s Hospital, Kunpeng Road 369, Hangzhou 310008, Zhejiang Province, China.
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

Adjuvant therapies for breast cancer have achieved great success in recent years and early breast cancer is now a curable or chronic disease. Targeted therapies, including endocrine therapy and human epidermal growth factor receptor-2 targeted therapy, marked a new era of breast cancer treatment. However, except for chemotherapy, an efficient drug treatment to improve the overall survival of breast cancer patients is still lacking for triple negative breast cancer. Furthermore, a certain proportion of breast cancer patients present with resistance to drug therapy, making it much more difficult to control the deterioration of the disease. Recently, altered energy metabolism has become one of the hallmarks of cancer, including breast cancer, and it may be linked to drug resistance. Targeting cellular metabolism is becoming a promising strategy to overcome drug resistance in cancer therapy. This review discusses metabolic reprogramming in breast cancer and the possible complex mechanism of modulation. We also summarize the recent advances in metabolic therapy targeted glycolysis, glutaminolysis and fatty acids synthesis in breast cancer.

Keywords: Breast cancer, Targeted therapy, Metabolism, Drug resistance, Chemotherapy

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.