title: ART3 regulates triple-negative breast cancer cell function via activation of Akt and ERK pathways.
abstract: 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.
authors.affiliation: Department of Breast, Pancreas, and Thyroid Surgery, Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Tan
authors.affiliation: Department of Breast, Pancreas, and Thyroid Surgery, Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
authors.forename: Xiaodan
authors.initials: X
authors.lastname: Song
authors.affiliation: Department of Bioengineering, College of Engineering, Northeastern University, Boston, MA, USA.
authors.forename: Xin
authors.initials: X
authors.lastname: Sun
authors.affiliation: Department of Breast, Pancreas, and Thyroid Surgery, Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
authors.forename: Ning
authors.initials: N
authors.lastname: Wang
authors.affiliation: Department of Surgery, Department of Obstetrics and Gynecology, Women's Cancer Program Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
authors.forename: Ying
authors.initials: Y
authors.lastname: Qu
authors.affiliation: Department of Breast, Pancreas, and Thyroid Surgery, Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
authors.forename: Zhijun
authors.initials: Z
authors.lastname: Sun
mesh_terms: D036002:ADP Ribose Transferases / Q000032:analysis / Q000502:physiology*; D000818:Animals; D017209:Apoptosis; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D048049:Extracellular Signal-Regulated MAP Kinases / Q000502:physiology*; D005260:Female; D058851:GPI-Linked Proteins / Q000032:analysis / Q000502:physiology; D006801:Humans; D020935:MAP Kinase Signaling System / Q000502:physiology*; D051379:Mice; D009361:Neoplasm Invasiveness; D051057:Proto-Oncogene Proteins c-akt / Q000502:physiology*; D064726:Triple Negative Breast Neoplasms / Q000401:mortality / Q000473:pathology*; D023041:Xenograft Model Antitumor Assays
chemical_list: D058851:GPI-Linked Proteins; D036002:ADP Ribose Transferases; C105233:ART3 protein, human; D051057:Proto-Oncogene Proteins c-akt; D048049:Extracellular Signal-Regulated MAP Kinases
keywords: ART3; Akt; ERK; triple-negative breast cancer