The following is a summary of “ZMIZ2 facilitates hepatocellular carcinoma progression via LEF1 mediated activation of Wnt/β-catenin pathway,” published in the January 2024 issue of Hematology by Ding et al.

Hepatocellular carcinoma (HCC) stands as a prevalent and highly lethal malignancy, necessitating an in-depth exploration of contributing factors. This study discusses the role of ZMIZ2, a transcriptional co-activator implicated in various human diseases, in HCC. Leveraging public databases and employing bioinformatic analyses, investigators scrutinized the expression and prognostic implications of ZMIZ2 in HCC. The findings were further validated through quantitative RT-PCR, western blotting, and immunohistochemistry. Through a series of loss and gain-of-function experiments in vitro and in vivo, the investigators elucidated that ZMIZ2, highly expressed in HCC, significantly curtails cell proliferation, cell cycle progression, migration, and invasion. 

Notably, its expression in HCC was linked to immune cell infiltration. Somatic mutation analysis revealed a joint impact of ZMIZ2 and TP53 mutations on HCC progression. Mechanistically, ZMIZ2 demonstrated an interaction with LEF1, influencing the malignant progression of HCC by activating the Wnt/β-catenin pathway. The study concludes that ZMIZ2, serving as a potential prognostic biomarker, is overexpressed in HCC, correlating with a malignant phenotype and facilitating disease progression through the LEF1-mediated activation of the Wnt/β-catenin pathway. This sheds light on ZMIZ2 as a promising therapeutic target for HCC, offering new avenues for prognosis and intervention in this challenging malignancy.

Source: ehoonline.biomedcentral.com/articles/10.1186/s40164-024-00475-w