Abstract 4413: Targeting glutamine metabolism in MUC1 expressing triple negative breast cancer

Abstract

Abstract Breast cancer, the second leading cause of cancer deaths in women, accounts for nearly 1 in 3 cancer cases diagnosed in the U.S. women. Triple negative breast cancer (TNBC) accounts for approximately 15-25% of all breast cancer cases and has an increased incidence of metastasis, high recurrence within 1-3 years and a high mortality rate. Therefore, identifying factors that facilitate tumor growth and metastasis have the potential to serve as novel molecular targets for breast cancer therapy. Mucin1 (MUC1), a glycoprotein associated with chemoresistance, is aberrantly overexpressed in TNBC and facilitates growth and metastasis of TNBC cells. Recent studies suggest a role for MUC1 in modulating cancer cell metabolism to support tumor growth. In the present study we examined the role that MUC1 plays in TNBC tumor metabolism; thus facilitating tumor growth. Our results indicate that MUC1 expression facilitates glutamine metabolism. A correlation between MUC1 expression, glutamine dependency, and amino-oxyacetate (AOA) sensitivity was established. These alterations can be attributed in part to alterations in the expression of genes regulating glutamine metabolism. Collectively, these findings suggest that MUC1 serves as a metabolic regulator in TNBC, facilitating metabolic reprogramming of glutamine that influences growth of TNBC. Additionally, the findings with AOA’s effectiveness provide evidence for potential therapeutic utility, particularly for MUC1 overexpressing TNBC. Citation Format: Gennifer D. Goode, Venugopal Gunda, Pankaj Singh. Targeting glutamine metabolism in MUC1 expressing triple negative breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4413. doi:10.1158/1538-7445.AM2017-4413