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Updated: Jan 29, 2026

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-3191 promotes migration and invasion by downregulating TGFBR2 in colorectal cancer
Hongjuan He1,2, Xiaojuan Zhao1,2, Ziqing Zhu1,2
1Key Laboratory of Resource Biology and Biotechnology, School of Life Sciences, Northwest University, Xi'an, China.
Abstract:
Mutations in transforming growth factor beta receptor II (TGFBR2) are detected in up to 30% of overall colorectal cancer (CRC). Dysregulation of some microRNAs participated in the CRC pathogenesis. In this study, we used the gene ontology analyses, the Kyoto Encyclopedia of Genes and Genomes pathway analyses and gene set enrichment analysis to indicate that miR-3191 was involved in the regulation of transforming growth factor beta (TGF-BETA) signal pathway in CRC. These bioinformatics results were supported by data obtained from CRC samples and experiments in vitro. The luciferase reporter assay was used to confirm that miR-3191 modulates TGF-BETA signal pathway by targeting TGFBR2. By transwell migration and invasion assays, we showed that miR-3191 promoted CRC cell migration and invasion by downregulating TGFBR2. And it may serve as a novel therapeutic strategy for treating CRC patients.
Insights
MicroRNA-3191 promotes colorectal cancer (CRC) cell migration and invasion by targeting the transforming growth factor beta receptor II (TGFBR2). This finding suggests miR-3191 as a potential therapeutic target for CRC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Transforming growth factor beta receptor II (TGFBR2) mutations occur in up to 30% of colorectal cancer (CRC) cases.
- MicroRNA dysregulation is implicated in the pathogenesis of CRC.
Purpose of the Study:
- To investigate the role of miR-3191 in colorectal cancer.
- To determine if miR-3191 regulates the transforming growth factor beta (TGF-BETA) signaling pathway in CRC.
- To explore miR-3191 as a potential therapeutic strategy for CRC.
Main Methods:
- Bioinformatic analyses including Gene Ontology, Kyoto Encyclopedia of Genes and Genomes pathways, and Gene Set Enrichment Analysis.
- In vitro experiments using CRC samples.
- Luciferase reporter assays to confirm direct targeting.
- Transwell migration and invasion assays to assess cell motility.
Main Results:
- Bioinformatic analyses indicated miR-3191's involvement in the TGF-BETA signaling pathway in CRC.
- miR-3191 was confirmed to target TGFBR2, modulating the TGF-BETA pathway.
- miR-3191 promoted CRC cell migration and invasion by downregulating TGFBR2 expression.
Conclusions:
- miR-3191 plays a significant role in CRC progression by regulating TGFBR2.
- miR-3191 represents a potential novel therapeutic target for colorectal cancer treatment.
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