Abstract

Abstract TRAF3 (TNF Receptor Associated Factor 3) is a regulator of NF-κB signaling, acting mainly as an inhibitor of the alternative NF-κB pathway through the interaction with other TRAF molecules and the downregulation of NIK (MAP3K14) kinase. While NF-κB has a well-established role in breast cancer development and progression, TRAF3 which acts as a ubiquitin-ligase in the NF-κB cascade has never been studied in mammary carcinomas. Here by employing breast cancer cell lines in invasion and colony formation assays, we show that TRAF3 forced expression inhibits aggressive traits of breast cancer cells. In addition, immunohistochemistry (IHC) for TRAF3 protein in breast cancer FFPE samples and analysis of TRAF3 gene expression from publicly available data sets, indicates that TRAF3 mRNA and protein expression in breast cancer tissue correlates with Recurrence Free Survival (RFS), Overall Survival (OS) and other clinicopathological parameters such as Histological Grade and proliferation index (ki-67). To our knowledge this is the first report on TRAF3 protein in breast cancer providing preliminary evidence for an inhibitory role of this protein in breast cancer development and progression. Citation Format: Anastasios Papanastasiou, Chaido Sirinian, Maria Theakou, Stavros Peroukidis, Dimitrios Chaniotis, Haralabos Kalofonos, Angelos Koutras. TRAF3 as a regulator of breast cancer aggressiveness [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P2-26-03.

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