Circ-EIF3I Promotes Hepatocellular Carcinoma Progression Through Modulating miR-361-3p/DUSP2 Axis

Area of Science:

• Oncology
• Molecular Biology
• Gene Regulation

Background:

• Hepatocellular carcinoma (HCC) is a prevalent global malignancy.
• Circular RNAs (circRNAs) are increasingly recognized for their roles in cancer development.
• The specific function and regulatory mechanisms of circ-EIF3I in HCC remain largely unknown.

Purpose of the Study:

• To investigate the biological role and underlying molecular mechanisms of circ-EIF3I in hepatocellular carcinoma (HCC) progression.
• To identify the downstream targets and regulatory pathways influenced by circ-EIF3I in HCC.

Main Methods:

• Bioinformatics analysis, luciferase reporter assays, Transwell migration assays, Cell Counting Kit-8 (CCK-8), and 5-Ethynyl-2'-deoxyuridine (EdU) assays were used.
• In vivo tumorigenesis and metastasis assays were performed to validate the findings.
• Expression levels of circ-EIF3I, miR-361-3p, and Dual-specificity phosphatase 2 (DUSP2) were analyzed.

Main Results:

• Circ-EIF3I expression was significantly upregulated in HCC cell lines.
• Downregulation of circ-EIF3I markedly suppressed HCC cell proliferation and migration in vitro and in vivo.
• Bioinformatics and luciferase assays confirmed miR-361-3p and DUSP2 as direct downstream targets of circ-EIF3I.
• Restoration of DUSP2 expression or inhibition of miR-361-3p reversed the suppressive effects of circ-EIF3I downregulation on HCC cells.

Conclusions:

• Circ-EIF3I promotes HCC progression by sponging miR-361-3p and subsequently upregulating DUSP2.
• Targeting the circ-EIF3I/miR-361-3p/DUSP2 axis represents a potential therapeutic strategy for HCC.