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Molecular Profiling of the Invasive Tumor Microenvironment in a 3-Dimensional Model of Colorectal Cancer Cells and Ex vivo Fibroblasts
Published on: April 29, 2014
MiR-382 inhibits cell growth and invasion by targeting NR2F2 in colorectal cancer
Baoguo Zhou1, Jianwei Song1, Taotao Han2
1Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Abstract:
Colorectal cancer (CRC) is one of the leading causes of cancer death worldwide. MiR-382 has been found to have a decreased expression and the ability to suppress tumorigenesis in certain cancers. However, the role of miR-382 in CRC has not been sufficiently investigated. NR2F2 (also known as COUP-TFII), a member of the steroid/thyroid receptor superfamily, is often aberrantly activated in various tumors, but it is currently unclear whether NR2F2 may be a target of miR-382. In the present study, we investigated the role of miR-382 in CRC and identified the regulation of NR2F2 by miR-382. We observed that miR-382 was aberrantly downregulated in CRC. Transfection with miR-382 mimics impeded the growth, migration, and invasion of CRC cells. The direct binding of miR-382 to the 3' untranslated region (3' UTR) of NR2F2 was confirmed using a luciferase reporter gene assay. We showed that the relative expression levels of NR2F2 were significantly higher in CRC tissues compared with normal adjacent mucosa. A Kaplan-Meier analysis indicated that patients with high NR2F2 expression had a poor overall survival. Knockdown of NR2F2 inhibited CRC cell growth, migration, and invasion. Ectopic expression of NR2F2 mitigated miR-382 suppression of CRC cell proliferation, migration, and invasion. In conclusion, the present study describes a potential mechanism underlying a miR-382/NR2F2 link contributing to CRC development. Our results demonstrate that miR-382 represents a potential strategy against CRC. © 2016 Wiley Periodicals, Inc.
Insights
MicroRNA-382 (miR-382) is downregulated in colorectal cancer (CRC), suppressing tumor growth. It targets NR2F2, offering a potential therapeutic strategy against CRC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Colorectal cancer (CRC) is a major global health concern.
- MiR-382 shows tumor-suppressive roles in some cancers, but its function in CRC is understudied.
- NR2F2 (COUP-TFII) is frequently activated in tumors, with its link to miR-382 in CRC unclarified.
Purpose of the Study:
- To investigate the role of miR-382 in colorectal cancer.
- To determine if NR2F2 is a direct target of miR-382 in CRC.
- To elucidate the miR-382/NR2F2 regulatory axis in CRC pathogenesis.
Main Methods:
- Analysis of miR-382 expression in CRC tissues.
- Cell proliferation, migration, and invasion assays using miR-382 mimics and NR2F2 knockdown/overexpression.
- Luciferase reporter gene assay to confirm direct miR-382 binding to NR2F2 3' UTR.
- Correlation analysis between NR2F2 expression and patient survival.
Main Results:
- MiR-382 expression was significantly downregulated in CRC tissues.
- Overexpression of miR-382 inhibited CRC cell growth, migration, and invasion.
- NR2F2 was identified as a direct target of miR-382.
- High NR2F2 expression correlated with poor patient survival and promoted CRC progression.
- NR2F2 knockdown suppressed CRC cell behaviors, and its overexpression reversed miR-382's effects.
Conclusions:
- The study identifies a novel miR-382/NR2F2 regulatory pathway contributing to CRC development.
- MiR-382 acts as a tumor suppressor in CRC by targeting NR2F2.
- MiR-382 represents a potential therapeutic target for colorectal cancer treatment.
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