Mechanistic interplay between aflatoxin B1 and tissue inhibitor of metalloproteinase-3 in hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is a major global health challenge, particularly in regions with high aflatoxin B1 (AFB1) exposure. This editorial explores the mechanistic interplay between AFB1 and tissue inhibitor of metalloproteinase-3 (TIMP-3) in AFB1-related HCC. TIMP-3, frequently downregulated in HCC due to promoter methylation, is linked to increased tumor aggressiveness and poor prognosis. We propose that AFB1 induces epigenetic silencing of TIMP-3, potentially <i>via</i> DNA adducts and oxidative stress, exacerbating AFB1-related HCC progression. This AFB1-TIMP-3 axis highlights TIMP-3's potential as a prognostic biomarker and therapeutic target. Future research should focus on elucidating these molecular pathways and integrating TIMP-3 into clinical practice for early detection and targeted therapies in AFB1-prevalent regions.