Decrease of miR-622 expression suppresses migration and invasion by targeting regulation of DYRK2 in colorectal cancer cells
Authors Wang Y, Sun J, Wei X, Luan L, Zeng X, Wang C, Zhao W
Received 25 October 2016
Accepted for publication 12 January 2017
Published 22 February 2017 Volume 2017:10 Pages 1091—1100
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Manfred Beleut
Peer reviewer comments 4
Editor who approved publication: Dr Ingrid Espinoza
Yong Wang,1,* Jie Sun,2,* Xilin Wei,3 Lan Luan,2 Xiandong Zeng,4 Cuifang Wang,2 Wei Zhao1
1The 4th Department of Orthopedic Surgery, Central Hospital affiliated to Shenyang Medical College, Shenyang, 2Department of Pathology, Central Hospital affiliated to Shenyang Medical College, Shenyang, 3The 3rd Department of General Surgery, Central Hospital affiliated to Shenyang Medical College, Shenyang, 4Department of Surgical Oncology, Central Hospital affiliated to Shenyang Medical College, Shenyang, People’s Republic of China
*These authors contributed equally to this work
Background: More and more evidence indicates that microRNAs are present and involved in many tumor-related diseases. The function of microRNA-622 (miR-622) in colorectal cancer (CRC) remains controversial. Dual specificity tyrosine phosphorylation-regulated kinase 2 (DYRK2) has been reported as a tumor suppressor gene in different cancers. The detailed regulation mechanism of DYRK2 in CRC remains unclear.
Methods: miR-622 and DYRK2 expression levels were detected at tissue and cellular level respectively by using real time polymerase chain reaction (PCR), Western blot, and immunohistochemical staining. Pearson’s correlation analysis was used to evaluate the correlation between miR-622 and DYRK2. Transwell assay was applied to measure the effect of miR-622 on migration and invasion of SW1116 and SW480. We used dual luciferase reporter assay to confirm the targeted binding effect of miR-622 and DYRK2 3'-untranslated region (3'UTR). An antisense experiment was executed to further confirm the role miR-622 had played with regard to migration and invasion by targeting regulation of DYRK2 pathway in CRC cells.
Results: In our research, we found that the expression of miR-622 was elevated in CRC tissues and cell lines compared to that of nonCRC tissues and the normal human colon epithelial cell line NCM460. Correspondingly, the expression of DYRK2 in CRC tissues and cell lines showed a contrary tendency. The different expression level of DYRK2 was closely correlated with clinicopathological characteristics of CRC patients. We demonstrated that down-regulation of miR-622 could inhibit the ability of migration and invasion of CRC cell lines SW1116 and SW480. Also, we confirmed that DYRK2 was negatively regulated by miR-622 via a specific targeted binding site within the 3'UTR. We finally verified that the migration and invasion ability of CRC cells in the conducted DYRK2 3'UTR defect plasmid transfection group were lower compared to miR-622 and cotransfection group.
Conclusion: The findings of this study indicate that a decrease of miR-622 expression could suppress migration and invasion by targeting regulation of DYRK2 and miR-622/DYRK2 could be a potential molecular treating target of CRC.
Keywords: miR-622, DYRK2, migration, invasion, colorectal cancer
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