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MiR-625-3p promotes cell migration and invasion via inhibition of SCAI in colorectal carcinoma cells

2015; Impact Journals LLC; Volume: 6; Issue: 29 Linguagem: Inglês

10.18632/oncotarget.4738

1949-2553

Hailun Zheng, Renqiang Ma, Qizhi Wang, Pei Zhang, Dapeng Li, Qiangwu Wang, Jianchao Wang, Huabin Li, Hao Liu, Zhiwei Wang,

Cancer-related molecular mechanisms research

// Hailun Zheng 1, * , Renqiang Ma 2, * , Qizhi Wang 1 , Pei Zhang 3 , Dapeng Li 1 , Qiangwu Wang 1 , Jianchao Wang 1 , Huabin Li 2 , Hao Liu 3 , Zhiwei Wang 4 1 Department of Gastroenterology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China 2 Cancer Center, ENT Hospital, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China 3 Faculty of Pharmacy, Bengbu Medical College, Biochemical Drugs Engineering and Technological Research Center of Anhui Province, Bengbu, Anhui, China 4 The Cyrus Tang Hematology Center and Collaborative Innovation Center of Hematology, Jiangsu Institute of Hematology, The First Affiliated Hospital, Soochow University, Suzhou, China * These authors have contributed equally to this work Correspondence to: Zhiwei Wang, e-mail: zwang6@bidmc.harvard.edu Hao Liu, e-mail: liuhao6886@foxmail.com Huabin Li, e-mail: allergyli@163.com Keywords: miR-625-3p, SCAI, invasion, migration, colorectal carcinoma Received: May 24, 2015 Accepted: July 16, 2015 Published: July 28, 2015 ABSTRACT MicroRNAs (miRNAs) play a critical role in controlling tumor invasion and metastasis via regulating the expression of a variety of targets, which act as oncogenes or tumor suppressor genes. Abnormally expressed miR-625-3p has been observed in several types of human cancers. However, the molecular mechanisms of miR-625-3p-mediated tumorigenesis are largely elusive. Therefore, the aim of this study was to evaluate the biological function and molecular insight on miR-625-3p-induced oncogenesis in colorectal carcinoma (CRC). The effects of miR-625-3p in cell migration and invasion were analyzed by wound healing assay and transwell assay, respectively. In addition, the expression of miR-625-3p and its targets was detected in five human CRC cell lines. In the present study, we found that overexpression of miR-625-3p promoted migration and invasion in SW480 cells, whereas downregulation of miR-625-3p inhibited cell motility in SW620 cells. More importantly, we observed potential binding sites for miR-625-3p in the 3′-untranslated region of suppressor of cancer cell invasion (SCAI). Notably, we identified that overexpression of miR-625-3p inhibited the expression of SCAI, while depletion of miR-625-3p increased SCAI level, suggesting that SCAI could be a target of miR-625-3p. Additionally, we revealed that miR-625-3p exerts its oncogenic functions through regulation of SCAI/E-cadherin/MMP-9 pathways. Our findings indicate the pivotal role of miR-625-3p in invasion that warrants further exploration whether targeting miR-625-3p could be a promising approach for the treatment of CRC.