MCT4 drives HCC progression by activating MMPs and polarizing M2 macrophages

To explore the role of MCT4 in hepatocellular carcinoma (HCC) progression and its impact on the tumor immune microenvironment.

Bioinformatic Analysis: Integrated analysis of multiple datasets (TCGA-LIHC, GSE46408, GSE36411) to identify differentially expressed lactate metabolism-related genes.
Experimental Validation: Conducted functional assays in HCC cell lines (Huh7, MHCC97-H) and a murine xenograft model to validate findings.
Immune Cell Analysis: Analyzed immune cell infiltration and polarization using CIBERSORT and single-cell RNA sequencing data.

MCT4 is significantly upregulated in HCC tissues and correlates with advanced tumor stage and poor survival.
MCT4 expression is associated with matrix metalloproteinase (MMP) pathways.
Knockdown of MCT4 reduces MMP1, MMP2, and MMP9 expression, inhibiting HCC cell migration and invasion.
High MCT4 expression correlates with M2 macrophage polarization in the tumor microenvironment.
In vivo MCT4 knockdown inhibits tumor growth and reduces CD206+ M2 macrophage infiltration.

MCT4 drives HCC progression through enhancing MMP-mediated invasion and promoting immunosuppressive M2 macrophage polarization.

MCT4 is implicated in HCC progression and may influence tumor immune responses.