Abstract 4470: Loss of ARL6IP4 induces the epithelial mesenchymal transition in breast cancer metastasis by transcriptionally phosphorylating NF-kB

Abstract

Abstract The epithelial mesenchymal transition EMT is the major mechanism involved in cancer metastasis. During EMT, epithelial cells lose cell-cell adhesions to gain mesenchymal-like properties, such as increased invasive abilities. The function of ARL6IP4 in the EMT of breast cancers has not yet been studied. Here we show that the ARL6IP4 controls EMT in breast cancer metastasis. we demonstrate that the role of ARL6IP4 by analysis of ARL6IP4 conditional knockout animals, various in vitro and in vivo models of EMT and metastasis, a mouse mammary tumor virus-polyoma middle T antigen (MMTV-PyMT) model of breast cancer metastasis. We identified that loss of ARL6IP4 phosphorylated of nuclear factor-κB (NF-κB) by increasing the expression of the SNAIL and ZEB1 EMT transcription factors (EMT-TFs). Taken together, our findings establish that ARL6IP4 is a potential tumor suppressor by regulation the phosphorylation of NF-κB. Citation Format: Mi Kyung Park, Ji Yun Jang, Hyun Jung Byun, Hyun Ji Kim, Ho Lee, Chang Hoon Lee. Loss of ARL6IP4 induces the epithelial mesenchymal transition in breast cancer metastasis by transcriptionally phosphorylating NF-kB [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 4470.