Positive regulation of TAZ expression by EBV-LMP1 contributes to cell proliferation and epithelial-mesenchymal transition in nasopharyngeal carcinoma
Metrics: PDF 1482 views | HTML 1877 views | ?
Jiang He1,2, Feiyu Tang1, Liyu Liu1,2, Lin Chen1, Jiang Li1, Danming Ou1, Lu Zhang1,2, Zhi Li1,2, Deyun Feng3, Wenzheng Li4 and Lun-Quan Sun1,2
1Center for Molecular Medicine, Xiangya Hospital, Collaborative Innovation Center for Cancer Medicine, Central South University, Changsha, 410008, China
2Key Laboratory of Molecular Radiation Oncology Hunan Province, Changsha, 410008, China
3Department of Pathology, Xiangya Hospital, Central South University, Changsha, 410008, China
4Department of Radiology, Xiangya Hospital, Central South University, Changsha, 410008, China
Lun-Quan Sun, email: email@example.com
Wenzheng Li, email: firstname.lastname@example.org
Keywords: EBV, LMP1, TAZ, nasopharyngeal carcinoma
Received: September 27, 2016 Accepted: November 20, 2016 Published: December 02, 2016
The Epstein-Barr virus latent membrane protein 1 (LMP1) is an integral membrane protein. LMP1 has been reported to activate the NF-κB and mitogen-activated protein kinase pathways. However, these effects alone are unable to account for the profound oncogenic properties of LMP1. TAZ is one of the nuclear effectors of Hippo-related pathways and highly expressed in many human tumors. Here, we reported that TAZ was frequently expressed in LMP1-positive nasopharyngeal carcinoma. In NPC cell lines, we showed that LMP1 promoted TAZ expression. Gelsolin is an important inhibitor of TAZ activity. Our studies showed that LMP1 interacted with gelsolin, resulting in inhibition of Lats1/2 phosphorylation and improvement of TAZ stability. Furthermore, we revealed that TAZ is important for LMP1-mediated cell proliferation, cancer stem cell-like properties and epithelial-mesenchymal transition. These findings provide new insights into the carcinogenic roles of LMP1 and contribute to further understanding of its oncogenic mechanism.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.