CircRSF1 Promoted HepG2 Cell Proliferation, Migration and Invasion Depending on EIF4A3

Area of Science:

• Oncology
• Molecular Biology
• Hepatology

Background:

• Hepatocellular carcinoma (HCC) is a prevalent malignancy with high mortality.
• Inflammation significantly contributes to HCC initiation and progression.
• Circular RNA circRSF1 is linked to liver diseases and inflammation.

Purpose of the Study:

• To investigate the role of inflammation-related circRSF1 in HCC development in vitro.
• To explore the interaction between circRSF1 and EIF4A3 in HCC progression.

Main Methods:

• Established an in vitro HCC model using IL-1β-treated HepG2 cells.
• Quantified circRSF1 and EIF4A3 expression via RT-qPCR and Western blot.
• Assessed cell proliferation, migration, and invasion.
• Confirmed circRSF1-EIF4A3 binding using RIP and pull-down assays.
• Evaluated in vivo effects in a nude mouse xenograft model.

Main Results:

• IL-1β upregulated circRSF1 in HepG2 cells and HCC tissues.
• circRSF1 knockdown inhibited HCC cell proliferation, migration, and invasion.
• circRSF1 and EIF4A3 bind, with EIF4A3 stabilizing circRSF1.
• EIF4A3 knockdown reduced tumor growth, reversed by circRSF1 overexpression.

Conclusions:

• circRSF1, stabilized by EIF4A3, drives malignant progression in HCC.
• circRSF1 acts as an oncogene in inflammation-mediated HCC.
• circRSF1 represents a potential therapeutic target for HCC.