OncoTargets and Therapy · 2017 · 47 citations · 24 references
Life SciencesMolecular BiologyOncologyGene ExpressionMetastasisMolecular OncologyCancer Cell SignalingColorectal CancerMicrorna BiologyMicrorna-mediated RegulationSignal Transduction In CancerTumor Suppressor GenesDual-luciferase AssaysImmunohistochemical DetectionImmunohistochemical StainingLuciferase Reporter AssaysLuciferase ReportersMicrorna Function In CancerMicrorna In CancerMicrorna Regulation In Cancer
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.
24
Real-time quantification of microRNAs by stem-loop RT-PCR
C. Chen · Nucleic Acids Research · 2005 · 5K citations · Full text
Annual report on status of cancer in China, 2010
Wanqing, Chen, Rongshou et al. · 中国癌症研究:英文版 · 2014 · 565 citations
Annual report on status of cancer in China, 2010.
Wanqing Chen, Rongshou Zheng, Siwei Zhang et al. · PubMed · 2014 · 380 citations · Full text
miR-22 represses cancer progression by inducing cellular senescence
Dan Xu, Fumitaka Takeshita, Yumiko Hino et al. · The Journal of Cell Biology · 2011 · 289 citations · Full text