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Updated: Dec 16, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
miR-1184 regulates the proliferation and apoptosis of colon cancer cells via targeting CSNK2A1
Shuo Chen1, Yan Wang2, Mingyue Xu1
1Department of Colorectal Surgery, Tianjin Union Medical Center, Nankai University, Tianjin, 300121, PR China.
Abstract:
MicroRNA (miRNA) exerts an important part in colon cancer cell proliferation and apoptosis. Meanwhile, the dysregulation of some miRNAs is detected in colon cancer cells. However, it remains unclear about the underlying mechanism of their effects on tumor pathogenesis. The current work aimed to examine the miR-1184 effect on colon cancer cells. The differentially expressed miRNAs (DEMs), including miR-9-3p, miR-1184, miR-492, miR-92a-1-5p and miR-20a-3p, were obtained from the GSE115108 and GSE132619 data sets using the 'GEO2R' online tool. Based on the findings, miR-1184 was significantly down-regulated within colon cancer cells and tissues. Moreover, the experimental results of CCK8, flow cytometry, colony formation and Western blotting assays showed that, miR-1184 over-expression suppressed colon cancer cell proliferation through inhibiting Ki67 expression and promoted their apoptosis through up-regulating cleaved caspase-3 and down-regulating Bcl-2 expression. By contrast, miR-1184 inhibition exerted the opposite effects. A total of 110 target genes of miR-1184 were predicted using the TargetScan and miRTarBase databases, which were then used to construct the protein-protein interaction (PPI) network based on the DAVID and STRING websites and to perform GO and KEGG pathway enrichment analyses. The MCODE plug-in of cytoscape was utilized to verify that CSNK2A1 was the target gene and key gene in significant modules. MiR-1184 directly targets CSNK2A1 via using RNA immunoprecipitation assay and luciferase reporter gene assay. According to the results, CSNK2A1 over-expression reversed the functions of miR-1184 over-expression in suppressing colon cancer cell proliferation and enhancing their apoptosis. In conclusion, over-expression of miR-1184 inhibits colon cancer cell proliferation but promotes their apoptosis through down-regulating CSNK2A1 expression.
Insights
MicroRNA-1184 (miR-1184) suppresses colon cancer cell growth and promotes apoptosis by targeting CSNK2A1. This finding offers a potential therapeutic strategy for colon cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) play a role in colon cancer, but their specific mechanisms are unclear.
- Dysregulation of miRNAs is observed in colon cancer cells, necessitating further investigation into individual miRNA functions.
Purpose of the Study:
- To investigate the role of miR-1184 in colon cancer cell proliferation and apoptosis.
- To elucidate the molecular mechanism underlying miR-1184's function in colon cancer pathogenesis.
Main Methods:
- Differential expression analysis of miRNAs using GEO datasets (GSE115108, GSE132619) via GEO2R.
- Functional assays including CCK8, flow cytometry, colony formation, and Western blotting to assess miR-1184's effects.
- Bioinformatic prediction of miRNA targets, PPI network construction, GO and KEGG pathway analysis.
- Validation of miR-1184 targeting CSNK2A1 using RNA immunoprecipitation and luciferase reporter assays.
Main Results:
- miR-1184 was significantly downregulated in colon cancer cells and tissues.
- Overexpression of miR-1184 inhibited cell proliferation (decreased Ki67) and promoted apoptosis (increased cleaved caspase-3, decreased Bcl-2).
- CSNK2A1 was identified as a direct target of miR-1184, and its overexpression reversed miR-1184's effects.
Conclusions:
- miR-1184 functions as a tumor suppressor in colon cancer.
- miR-1184 inhibits colon cancer cell proliferation and promotes apoptosis by directly targeting and downregulating CSNK2A1 expression.
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