HER3 and LINC00052 interplay promotes tumor growth in breast cancer

// Ahmad Salameh 1 , Xuejun Fan 1 , Byung-Kwon Choi 2 , Shu Zhang 3 , Ningyan Zhang 1 , Zhiqiang An 1 1 Texas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, Texas, USA 2 Department of Molecular and Human Genetics Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA 3 Clinical Research Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China Correspondence to: Ningyan Zhang, email: ningyan.zhang@uth.tmc.edu Zhiqiang An, email: Zhiqiang.An@uth.tmc.edu Keywords: lncRNA, MCF7, T47D, HER3, NRG-1 Received: October 26, 2016 Accepted: December 13, 2016 Published: December 27, 2016 ABSTRACT Here we report that the lncRNA LINC00052 expression correlates positively with HER3/ErbB3 levels in breast cancer cells. Gene silencing of LINC00052 diminished both LINC00052 and HER3 expression and reduced cancer cell growth in vitro and in vivo . LINC00052 overexpression promoted cancer cell growth in vitro and in vivo and increased HER3-mediated downstream signaling. Importantly, neutralization of HER3 signaling with HER3 targeting monoclonal antibodies blocked LINC00052 mediated cancer cell proliferation in vitro and tumor growth in vivo , suggesting LINC00052 promoting cancer growth through HER3 signaling. Taken together, our results indicate that high LINC00052 levels predict activation of HER3-mediated signaling, and LINC00052 expression level may serve as a potential biomarker for HER3 targeted antibody cancer therapies.