Eif3h, eukaryotic translation initiation factor 3 subunit h, is crucial in regulating translational initiation. It is involved in multiple cellular pathways and has been associated with various biological processes and diseases. Genetic models, such as KO/CKO mouse models, are valuable for studying its functions [1,2].

Conditional Eif3h deletion suppresses colorectal tumorigenesis in the AOM/DSS model, uncovering its role in promoting colorectal cancer progression [2]. In esophageal squamous cell carcinoma (ESCC), Eif3h promotes cell proliferation, migration, and invasion, and its knockdown represses tumor growth and metastasis in vitro and in vivo. Eif3h acts as a deubiquitinating enzyme for Snail, stabilizing it and promoting the Snail-mediated EMT process [1]. In hepatocellular carcinoma (HCC), Eif3h promotes progression by stabilizing O-GlcNAc transferase (OGT) and inhibiting ferroptosis. Its knockdown reduces OGT expression, cell proliferation, and invasion, and causes G1/S arrest and ferroptosis [3].

In summary, Eif3h plays a significant role in the development and progression of multiple cancers, including colorectal, esophageal, and hepatocellular carcinomas. Conditional knockout mouse models have been instrumental in revealing its oncogenic functions in these disease areas, highlighting its potential as a therapeutic target and prognostic marker.