Targeting mTOR and Glycolysis in HER2-Positive Breast Cancer
Department of Biochemistry & Molecular Biology, Faculty of Medicine, Dalhousie University, Halifax, NS B3H 4R2, Canada
Author to whom correspondence should be addressed.
Academic Editor: Zhixiang Wang
Received: 10 May 2021
Revised: 9 June 2021
Accepted: 10 June 2021
Published: 11 June 2021
About one third of all breast cancers are classified as HER2-positive due to high levels of the HER2 cell surface protein. Drugs that target HER2 have been mostly successful, but this type of cancer returns at a high frequency once treatment has been completed. The high levels of HER2 also cause elevated activation of mechanistic target of rapamycin (mTOR) and enhanced glucose metabolism, both of which support cancer growth. Based on this, drugs have been developed to block mTOR and tested in clinical studies alone or in combination with drugs that target HER2. These treatments are successful but have more toxic effects and a higher chance that the cancer will return. Using drugs that mimic glucose deprivation in HER2-positive breast cancer patients has not been tested; however, preclinical studies have shown HER2-positive breast tumors are reduced by combining drugs that mimic glucose deprivation with mTOR inhibitors.