miR-223 promotes colon cancer by directly targeting p120 catenin
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Liwei Liu1,*, Chao Zhang1,*, Xiyu Li1, Wenjia Sun1, Shenghui Qin1, Lingzhi Qin1 and Xi Wang1
1Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
*These authors have contributed equally to this work
Xi Wang, email: [email protected]
Keywords: colon cancer, miR-223, p120, RhoA, β-catenin
Received: December 21, 2016 Accepted: June 19, 2017 Published: July 25, 2017
microRNA (miRNA) dysregulation is frequently observed in colon cancer. Previous studies found that miR-223 is upregulated in colon cancer and functions as an oncogene. Conversely, p120 is often downregulated or even absent in colon cancer, and is a likely tumor suppressor. The present study showed that increased miR-223 and decreased p120 levels are associated with colon cancer malignancy, and p120 expression is negatively correlated with miR-223 expression. A dual luciferase reporter assay showed that miR-223 directly targets p120. miR-223 upregulation in a colon cancer cell line upregulated c-Myc, cyclinD1, MMP7, and vimentin expression, downregulated E-cadherin, increased nuclear expression of β-catenin, and enhanced RhoA activation. We suggest miR-223 may promote colon cancer cell invasion and metastasis by downregulating p120, thereby reducing intercellular adhesion, promoting RhoA activity, and activating β-catenin signaling. Thus miR-223 functions as an oncogene in colon cancer and may be a potential diagnostic and therapeutic target for anti-colon cancer treatment.
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