| الوصف: |
// Yunwei Ou 1, 2, 3, 4, 7 , Zitong Zhao 2 , Weimin Zhang 2 , Qingnan Wu 2 , Chuanyue Wu 5, 6 , Xuefeng Liu 2 , Ming Fu 2 , Nan Ji 1 , Dan Wang 1 , Jiaji Qiu 1 , Liwei Zhang 1 , Chunjiang Yu 4 , Yongmei Song 2 , Qimin Zhan 2 1 Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China 2 State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China 3 Beijing Neurosurgical Institute, Capital Medical University, Beijing 100050, China 4 Department of Neurosurgery, Beijing Sanbo Brain Hospital, Capital Medical University, Beijing 100093, China 5 Department of Pathology, University of Pittsburgh, Pittsburgh, PA 15261, USA 6 Department of Biology and Shenzhen Key Laboratory of Cell Microenvironment, South University of Science and Technology of China, Shenzhen, 518055, China 7 China National Clinical Research Center for Neurological Diseases, Beijing 100050, China Correspondence to: Chunjiang Yu, email: cjyu1955@sina.com Yongmei Song, email: symlh2006@163.com Qimin Zhan, email: zhanqimin@pumc.edu.cn Keywords: EGFR, glioma, Kindlin-2, transcription Received: April 20, 2016 Accepted: August 11, 2016 Published: October 04, 2016 ABSTRACT Kindlin-2 promotes carcinogenesis through regulation of cell-cell and cell-extracellular matrix adhesion. However, the role of Kindlin-2 in glioma has not been elucidated. We investigated Kindlin-2 expression in 188 human glioma tissue samples. High Kindlin-2 expression was correlated with high pathological grade and a worse prognosis. Kindlin-2 promoted glioma cell motility and proliferation both in vitro and in vivo . Importantly, Kindlin-2 activated the EGFR pathway and increased EGFR mRNA levels. In addition to up-regulating Y-box binding protein-1 (YB-1) and β-catenin expression, Kindlin-2 formed a transcriptional complex with YB-1 and β-catenin that bound to the EGFR promoter and enhanced transcription. The β-catenin/YB-1/EGFR pathway was required for Kindlin-2-mediated functions. Our data provide a better understanding of the mechanisms underlying glioma progression, and suggest that Kindlin-2 may be a biomarker and therapeutic target in glioma. |
