Overexpression of CAPN2 promotes cell metastasis and proliferation via AKT/mTOR signaling in renal cell carcinoma.

摘要: // Chenkui Miao 1, * , Chao Liang Ye Tian Aiming Xu 1 Jundong Zhu Kai Zhao 2 Jianzhong Zhang Yibo Hua Shouyong Liu Huiyu Dong Shifeng Su Pu Li Qin and Zengjun Wang State Key Laboratory of Reproductive Medicine Department Urology, The First Affiliated Hospital Nanjing Medical University, Nanjing, China Hospital, These authors contributed equally to this work Correspondence to: Wang, email: zengjunwang@njmu.edu.cn Qin, 13776678978@163.com Keywords: CAPN2; renal cell carcinoma; metastasis/proliferation; EMT; AKT/mTOR signaling Received: May 17, 2017      Accepted: October 11, Published: 26, 2017 ABSTRACT calpain (CAPN2) is upregulated in various malignant carcinomas. Previous studies have reported that CAPN2 functioned as an oncogenic factor human cancers. However, its clinical role potential effects on metastasis proliferation carcinoma (RCC) remain unknown. In study, we evaluated the mRNA protein levels RCC specimens, matched normal lines using quantitative Real-time PCR (RT-PCR) western blot. Immunohistochemistry 74 tissues a tissue microarrays (TMAs) kidney were performed. Kaplan-Meier survival curve analyses conducted measure correlation between tumor prognosis. Cell migration, invasion detected by transwell assays Counting Kit-8 (CCK-8) assays. exhibited significant overexpression compared with adjacent non-tumor proximal tubule epithelial line HK-2. Strong staining was associated higher stage histological grade. addition, sh-CAPN2 could significantly inhibit 769-P CAKI-1 cells. Conversely, increased biological behaviors observed CAPN2-OV CAKI-2 Moreover, subsequent mechanism investigation suggested promoted progression activating signaling, enhancing mesenchymal transition (EMT) MMP9 levels. present study indicates may act prominent indicator for novel therapeutic target patients.