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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
MicroRNA-96 Promotes Tumor Invasion in Colorectal Cancer via RECK
Yasuhito Iseki1, Masatsune Shibutani2, Kiyoshi Maeda1
1Department of Surgical Oncology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Background:
miR-96 is reported to inhibit reversion cysteine-rich Kazal motif (RECK), which is associated with tumor invasion, in solid cancer types (e.g. breast cancer, non-small cell lung cancer, esophageal cancer). The purpose of this study is to clarify whether miR-96 is similarly associated with tumor invasion in colorectal cancer.
Materials And Methods:
We performed western blotting to investigate the expression of RECK when miR-96 mimics or inhibitors were transferred into HCT-116 colorectal cancer cells. The RECK mRNA level was assessed by a reverse transcription polymerase chain reaction. An invasion assay was used to evaluate tumor invasion.
Results:
The expression of RECK was inhibited by the transfection of miR-96 mimics. RECK mRNA level was reduced by miR-96 mimics and increased by miR-96 inhibitor. In the invasion assay, miR-96 mimics were shown to promote tumor invasion.
Conclusion:
miR-96 may be associated with tumor invasion through inhibition of RECK expression in colorectal cancer.
Insights
MicroRNA-96 (miR-96) may promote colorectal cancer invasion by inhibiting RECK expression. This study investigated miR-96
Area of Science:
- Molecular biology
- Oncology
- Cancer research
Background:
- MicroRNA-96 (miR-96) is known to inhibit RECK (reversion cysteine-rich Kazal motif) expression.
- RECK is implicated in tumor invasion in various solid cancers.
- The role of miR-96 in colorectal cancer invasion remains unclear.
Purpose of the Study:
- To investigate the association between miR-96 and tumor invasion in colorectal cancer.
- To determine if miR-96 affects RECK expression in colorectal cancer cells.
Main Methods:
- Western blotting to assess RECK protein levels.
- Reverse transcription polymerase chain reaction (RT-PCR) for RECK mRNA.
- Transfection of miR-96 mimics and inhibitors into HCT-116 cells.
- Invasion assays to evaluate cellular invasive potential.
Main Results:
- miR-96 mimics decreased RECK protein and mRNA expression.
- miR-96 inhibitor increased RECK mRNA expression.
- miR-96 mimics promoted tumor invasion in HCT-116 cells.
Conclusions:
- miR-96 may contribute to colorectal cancer invasion.
- The mechanism involves the inhibition of RECK expression by miR-96.
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