Guo Juncheng, Wang Kaiqiong, Sun Qigang, Liu Jun, Zheng Jinfang
Department of Hepatobiliary Surgery, Hainan General Hospital, No.19 Xinhua Road, Xiuying District, Haikou, 570311, Hainan Province, China.
Cell Biol Toxicol. 2025 Apr 5;41(1):67. doi: 10.1007/s10565-025-10013-x.
Examining the communications in the tumor microenvironment (TME) specific to hepatocellular carcinoma (HCC), this exploration looks into the role played by beta-1,4-Galactosyltransferase III (B4GALT3) in bone marrow mesenchymal stromal cell-derived extracellular vesicles (BMSCs-EVs) regarding the NF-κB pathway and the triggering of cancer-associated fibroblasts (CAF). Through a multidisciplinary approach combining transcriptome sequencing, bioinformatic analysis, and various experimental models, the involvement of B4GALT3 in regulating CAF activity by modulating NF-κB signaling was brought to light in our study. The outcomes suggest that targeting B4GALT3 could impede HCC cell migration and invasion, promote apoptosis, and dampen tumor progression and metastasis, offering novel insights into potential therapeutic strategies for combating HCC.
通过研究肝细胞癌（HCC）特有的肿瘤微环境（TME）中的通讯，本探索调查了β-1,4-半乳糖基转移酶III（B4GALT3）在骨髓间充质基质细胞衍生的细胞外囊泡（BMSCs-EVs）中对NF-κB途径及癌症相关成纤维细胞（CAF）触发所起的作用。通过结合转录组测序、生物信息学分析和各种实验模型的多学科方法，我们的研究揭示了B4GALT3通过调节NF-κB信号传导参与调节CAF活性。结果表明，靶向B4GALT3可能会阻碍HCC细胞的迁移和侵袭，促进细胞凋亡，并抑制肿瘤进展和转移，为对抗HCC的潜在治疗策略提供了新的见解。
