MiR-625-3p promotes cell migration and invasion via inhibition of SCAI in colorectal carcinoma cells
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Hailun Zheng1,*, Renqiang Ma2,*, Qizhi Wang1, Pei Zhang3, Dapeng Li1, Qiangwu Wang1, Jianchao Wang1, Huabin Li2, Hao Liu3, Zhiwei Wang4
1Department of Gastroenterology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China
2Cancer Center, ENT Hospital, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China
3Faculty of Pharmacy, Bengbu Medical College, Biochemical Drugs Engineering and Technological Research Center of Anhui Province, Bengbu, Anhui, China
4The 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
Zhiwei Wang, e-mail: email@example.com
Hao Liu, e-mail: firstname.lastname@example.org
Huabin Li, e-mail: email@example.com
Keywords: miR-625-3p, SCAI, invasion, migration, colorectal carcinoma
Received: May 24, 2015 Accepted: July 16, 2015 Published: July 28, 2015
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.
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