MicroRNA-7 Exerts Antiangiogenic Effect on Colorectal Cancer via ERK Signaling
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Updated: Jan 27, 2026

Detection of a Circulating MicroRNA Custom Panel in Patients with Metastatic Colorectal Cancer
Published on: March 14, 2019
Xuepeng Fan1, Mei Liu2, Hao Tang2
1Department of Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Department of Intensive Care Unit, Wuhan NO.1 Hospital, Wuhan, China.
Background:
Recent studies have suggested that microRNA-7 (miR-7) family members may play important roles in human cancer by regulating cell proliferation, apoptosis, migration, and invasion. Therefore, the present study aimed to investigate the clinical significance and biological function of miR-7 in colorectal cancer (CRC).
Methods:
Initially, cancer and adjacent tissues were collected from 76 patients with CRC. Then, microvascular density was detected using the Weidner counting method. The functional role of miR-7 in CRC was determined using ectopic expression, knockdown, and reporter assay experiments. The vasculogenic mimicry density was determined. Expression of miR-7, epidermal growth factor receptor (EGFR), extracellular signal-regulated kinase (ERK1/2), vascular endothelial growth factor, and thrombospondin-1 was determined. 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assays, scratch tests, and Transwell assays were conducted to examine cell proliferation, migration, and invasion, respectively. Finally, flow cytometry was applied to evaluate cell apoptosis.
Results:
CRC tissues showed increased microvascular density and EGFR expression, activated ERK signaling, and miR-7 downregulation. EGFR was a target gene of miR-7. miR-7 overexpression and EGFR silencing decreased vasculogenic mimicry density, cell migration, and cell invasion, but increased cell apoptosis. In addition, miR-7 overexpression and EGFR silencing upregulated thrombospondin-1 and downregulated EGFR, ERK1/2, and vascular endothelial growth factor. Furthermore, we observed that the effect of miR-7 inhibition was abolished after EGFR silencing.
Conclusions:
Overexpressed miR-7 suppresses angiogenesis of CRC cells through ERK signaling by downregulating EGFR. It may identify new targets for CRC treatment.
Insights
MicroRNA-7 (miR-7) suppresses colorectal cancer (CRC) angiogenesis by downregulating epidermal growth factor receptor (EGFR) via ERK signaling. This finding may offer new therapeutic targets for CRC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNA-7 (miR-7) family members are implicated in human cancer, influencing cell proliferation, apoptosis, migration, and invasion.
- The specific role of miR-7 in colorectal cancer (CRC) requires further investigation.
Purpose of the Study:
- To investigate the clinical significance of miR-7 in colorectal cancer (CRC).
- To elucidate the biological function of miR-7 in CRC progression and angiogenesis.
Main Methods:
- Analysis of microvascular density and expression of miR-7, EGFR, ERK1/2, VEGF, and TSP-1 in 76 CRC patient tissues.
- Functional assays including ectopic expression, knockdown, reporter assays, MTT, scratch, Transwell, and flow cytometry to assess cell behavior and apoptosis.
- Determination of vasculogenic mimicry density.
Main Results:
- CRC tissues exhibited increased microvascular density, EGFR expression, activated ERK signaling, and downregulated miR-7.
- EGFR was identified as a direct target gene of miR-7.
- miR-7 overexpression and EGFR silencing reduced vasculogenic mimicry, migration, and invasion, while increasing apoptosis.
- miR-7 and EGFR modulation affected TSP-1, EGFR, ERK1/2, and VEGF expression, with miR-7's effects being dependent on EGFR.
Conclusions:
- Overexpressed miR-7 suppresses CRC cell angiogenesis by downregulating EGFR through the ERK signaling pathway.
- miR-7's role in regulating EGFR presents potential new therapeutic targets for colorectal cancer treatment.
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