Rab11a promotes proliferation and invasion through regulation of YAP in non-small cell lung cancer
Metrics: PDF 3129 views | HTML 2545 views | ?
Qianze Dong1, Lin Fu1, Yue Zhao1, Yaming Du2, Qingchang Li1, Xueshan Qiu1, Enhua Wang1
1Department of Pathology, First Affiliated Hospital and College of Basic Medical Science, China Medical University, Shenyang, China
2Department of Cardiovascular Thoracic Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China
Enhua Wang, email: firstname.lastname@example.org
Keywords: Rab11a, Hippo, YAP, non-small cell lung cancer, proliferation
Received: October 26, 2016 Accepted: January 09, 2017 Published: February 15, 2017
Rab11a, an evolutionarily conserved Rab GTPases, plays important roles in intracellular transport and has been implicated in cancer progression. However, its role in human non-small cell lung cancer (NSCLC) has not been explored yet. In this study, we discovered that Rab11a protein was upregulated in 57/122 NSCLC tissues. Rab11a overexpression associated with advanced TNM stage, positive nodal status and poor patient prognosis. Rab11a overexpression promoted proliferation, colony formation, invasion and migration with upregulation of cyclin D1, cyclin E, and downregulation of p27 in NSCLC cell lines. Nude mice xenograft demonstrated that Rab11a promoted in vivo cancer growth. Importantly, we found that Rab11a induced YAP protein and inhibited Hippo signaling. Depletion of YAP abolished the effects of Rab11a on cell cycle proteins and cell proliferation. Furthermore, immunoprecipitation showed that Rab11a interacted with YAP in lung cancer cells. In conclusion, the present study suggestes that Rab11a serves as an important oncoprotein and a regulator of YAP in NSCLC.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.