Published online Apr 7, 2025. doi: 10.3748/wjg.v31.i13.100566
Revised: December 27, 2024
Accepted: March 11, 2025
Published online: April 7, 2025
Processing time: 224 Days and 0.9 Hours
Liver hepatocellular carcinoma (LIHC) is a highly aggressive cancer with poor prognosis due to its complex tumor microenvironment (TME) and immune eva
To explore how the SOCS2 affects Treg activity in LIHC and its impact on tumor growth and metastasis.
LIHC transcriptome data from The Cancer Genome Atlas database were analyzed using Gene Set Enrichment Analysis, Estimation of Stromal and Immune Cells in Malignant Tumors Using Expression Data, and Cell-Type Identification by Esti
SOCS2 overexpression inhibited Treg cell activity, reducing LIHC cell migration and invasion while increasing apoptosis. In vivo, SOCS2 suppressed tumor growth and metastasis, confirming its therapeutic potential.
SOCS2 modulates CD4+ T function in the TME, contributing to LIHC progression. Targeting SOCS2 presents a potential therapeutic strategy for treating LIHC.
Core Tip: This study provides novel insights into the role of the suppressor of cytokine signaling 2 (SOCS2) in inhibiting liver hepatocellular carcinoma (LIHC) growth and metastasis by modulating regulatory T-cell (Treg) activity. Through comprehensive bioinformatics analysis and both in vitro and in vivo experiments, we demonstrated that SOCS2 overexpression suppresses Treg cell activity, enhances cancer cell apoptosis, and reduces tumor migration and invasion. These findings highlight SOCS2 as a potential therapeutic target for improving LIHC prognosis by modulating immune responses in the tumor microenvironment.