TRIM11, a direct target of miR-24-3p, promotes cell proliferation and inhibits apoptosis in colon cancer

// Yan Yin 1, * , Jun Zhong 2, * , Si-Wei Li 3, * , Jian-Zhe Li 4 , Min Zhou 1 , Yin Chen 1 , Yi Sang 5 , Lijuan Liu 1 1 Department of Pharmacy, Jiangxi Cancer Hospital, Nanchang, China 2 Department of Radiotherapy, Jiangxi Cancer Hospital, Nanchang, China 3 Department of Radiation Oncology, The Affiliated Hospital of Guilin Medical University, Guilin, China 4 Department of Pharmacy, Ruikang Hospital, Guangxi University of Chinese Medicine, Nanning, China 5 Nanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, The Third Affiliated Hospital, Nanchang University, Nanchang, China * These authors have contributed equally to this work Correspondence to: Lijuan Liu, email: Liu_lijuanpharm@163.com Yi Sang, email: sangyi10@foxmail.com Keywords: TRIM11, colon cancer, miR-24-3p Received: July 18, 2016      Accepted: November 07, 2016      Published: November 24, 2016 ABSTRACT TRIM11 (tripartite motif-containing protein 11) is an E3 ubiquitin ligase recently identified as an oncogene in malignant glioma and lung cancer. In the present study, we report that expression of TRIM11 was increased in colon cancer (CC) tissue relative to paired normal tissues and that higher TRIM11 levels predicted poor overall survival (OS) and disease-free survival (DFS) in CC patients. Mechanistically, we showed that miR-24-3p downregulation contributes to TRIM11 upregulation in CC. We also demonstrated that TRIM11 overexpression promotes cell proliferation and colony formation and inhibits apoptosis in CC, while knocking down TRIM11 using CRISPR/Cas9-mediated genome editing inhibited cell proliferation and induced apoptosis. Silencing TRIM11 in vivo decreased tumor growth. These findings indicate that TRIM11 facilitates CC progression by promoting cell proliferation and inhibiting apoptosis and that the novel miR-24-3p/TRIM11 axis may be a useful new target for treating patients with CC.