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  2. Targeting B4GALT3 in BMSCs-EVs for Therapeutic Control of HCC via NF-κB pathway inhibition

Targeting B4GALT3 in BMSCs-EVs for Therapeutic Control of HCC via NF-κB pathway inhibition

  • Cell Biol Toxicol. 2025 Apr 5;41(1):67. doi: 10.1007/s10565-025-10013-x.
Juncheng Guo 1 Kaiqiong Wang 1 Qigang Sun 1 Jun Liu 1 Jinfang Zheng 2
Affiliations

Affiliations

  • 1 Department of Hepatobiliary Surgery, Hainan General Hospital, No.19 Xinhua Road, Xiuying District, Haikou, 570311, Hainan Province, China.
  • 2 Department of Hepatobiliary Surgery, Hainan General Hospital, No.19 Xinhua Road, Xiuying District, Haikou, 570311, Hainan Province, China. zhengjfhnyxy@163.com.
Abstract

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.

Keywords

Beta-1; Bone Marrow Mesenchymal Stromal Cells; Extracellular Vesicles; Hepatocellular Carcinoma; Tumor Microenvironment.

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