HELLS controls mitochondrial dynamics and genome stability in liver cancer by collusion with MIEF1.

ABSTRACT: Dysregulated chromatin remodelers have emerged as critical disease targets. However, owing to the pleiotropic functions of chromatin remodelers, the underlying mechanisms of their effects on cancer have been difficult to elucidate. Here, we investigated the helicase lymphoid-specific (HELLS) oncogenic mechanism by identifying a new direct transcriptional target. Using loss or gain experiments, we identified Mitochondrial elongation factor 1 (MIEF1) as a critical target of the HELLS molecular network in liver cancer. Liver cancer patients with a poor prognosis exhibited upregulated expression of MIEF1, and MIEF1 knockdown led to the loss of tumor capabilities, indicating MIEF1 as an oncogene in liver cancer. Suppressing the HELLS-MIEF1 axis caused mitochondrial hyperfusion, energy deprivati

SUBMITTER: Choi SK 

PROVIDER: S-EPMC11965466 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature