ART3 regulates triple-negative breast cancer cell function via activation of Akt and ERK pathways
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Ling Tan1,*, Xiaodan Song1,*, Xin Sun2, Ning Wang1, Ying Qu3, Zhijun Sun1
1Department of Breast, Pancreas, and Thyroid Surgery, Second Affiliated Hospital of Chongqing Medical University, Chongqing, China
2Department of Bioengineering, College of Engineering, Northeastern University, Boston, MA, USA
3Department of Surgery, Department of Obstetrics and Gynecology, Women’s Cancer Program Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA
*These authors have contributed equally to this work
Zhijun Sun, email: firstname.lastname@example.org
Keywords: Akt, ART3, ERK, triple-negative breast cancer
Received: August 03, 2015 Accepted: June 02, 2016 Published: June 27, 2016
Triple-negative breast cancers (TNBCs) are defined by lack of expressions of estrogen, progesterone, and ERBB2 receptors. Because biology of TNBC is poorly understood, no targeted therapy has been developed for this breast cancer subtype and chemotherapy is its only systemic treatment modality. In this study, we firstly determined that the expression of human ecto-ADP-ribosyltransferase 3 (ART3) is significantly associated with the basal-like breast cancer subgroup, which is largely overlapped with TNBC, through analyzing published data sets. We also found that ART3 protein is significantly overexpressed in human TNBC tumors tissue and cell lines through using immunohistochemistry and immunoblotting. Overexpression of ART3 in MDA-MB-231 breast cancer cells increased cell proliferation, invasion, and survival in vitro and growth of xenograft tumors. Conversely, knockdown of ART3 in breast cancer cells inhibited cell proliferation and invasion. In addition, we showed that ART 3 overexpression activated AKT and ERK in vitro and in xenograft tumors. Together, our findings demonstrate that ART3 is a critical TNBC marker with functional significance.
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