HER3 and LINC00052 interplay promotes tumor growth in breast cancer
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Ahmad Salameh1, Xuejun Fan1, Byung-Kwon Choi2, Shu Zhang3, Ningyan Zhang1, Zhiqiang An1
1Texas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, Texas, USA
2Department of Molecular and Human Genetics Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA
3Clinical Research Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
Ningyan Zhang, email: email@example.com
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
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.
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