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Updated: Oct 4, 2025

Detection of a Circulating MicroRNA Custom Panel in Patients with Metastatic Colorectal Cancer
Published on: March 14, 2019
Relationship between miR-204 and ANGPTL2 expression and diagnosis, pathological stage, and prognosis in patients with
Chenliang Wang1, Rongfei Tan2, Lizi Peng1
1Department of Pathology, First People's Hospital of Jiujiang City, Jiujiang, China.
Background:
Angiopoietin-like protein 2 (ANGPTL2) is linked to various tumors. MicroRNA-204 (miR-204) is associated with colorectal cancer (CRC). Bioinformatic analysis has demonstrated a targeting relationship between miR-204 and ANGPTL2. The present study aimed to investigate the role of miR-204 in the proliferation and apoptosis of colorectal tumor cells.
Methods:
Colorectal tumor tissues were collected. Normal colon mucosa was used as a control. The relationship between miR-204 and ANGPTL2 expression and tumor stage and prognosis was analyzed. The dual-luciferase reporter assay confirmed targeted regulation between miR-204 and ANGPTL2. SW480 cells were allocated to the miR-NC group and the miR-204 mimic group, followed by apoptotic analysis using flow cytometry and cellular proliferation analysis using EdU staining.
Results:
Compared with normal colonic mucosa, miR-204 expression was decreased in colorectal tumor tissues and ANGPTL2 expression was increased, which correlated with TNM staging. The prognosis of patients with low miR-204 expression and high ANGPTL2 expression was worse than for patients with high miR-204 expression and low ANGPTL2 expression. The dual-luciferase reporter assay confirmed a targeting regulation relationship between miR-204 and ANGPTL2. Transfection of miR-204 mimic significantly inhibited the expression of ANGPTL2 and cell proliferation in SW480 cells and promoted apoptosis.
Conclusions:
Downregulating miR-204 expression plays a vital role in upregulating ANGPTL2 expression and promoting the pathogenesis of CRC. MiR-204 is able to hinder the proliferation of colorectal tumor cells and encourage apoptosis by targeting the inhibition of ANGPTL2 expression.
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