SLC25A3 promotes hepatocellular carcinoma progression by inducing mitochondrial dysfunction and chromatin remodeling

Hepatocellular carcinoma (HCC) represents one of the most life-threatening malignancies globally. Despite significant advancements in the treatment of HCC in recent years, therapeutic outcomes remain unsatisfactory, particularly for patients with advanced, inoperable HCC. Thus, there is an urgent need to identify novel therapeutic targets and develop combination therapies to enhance treatment efficacy. The aim of this study is to elucidate the role and mechanism of solute carrier family 25 member A3 (SLC25A3) in HCC.

In this study, we examined the expression profiles and prognostic implications of mitochondrial-related gene sets in HCC using data from The Cancer Genome Atlas (TCGA) database. Among these genes, SLC25A3, a mitochondrial membrane protein, was found to be significantly overexpressed in HCC and associated with poor prognosis. To explore the potential role of SLC25A3 in HCC, we conducted analyses of clinical samples and performed in vivo and in vitro experiments. The underlying mechanisms were further investigated using multi-omics sequencing techniques.

The experimental results confirmed that SLC25A3 plays an oncogenic role in hepatocarcinogenesis, potentially by inducing mitochondrial dysfunction. Further multi-omics analysis revealed that the oncogenic effects of SLC25A3 in HCC may be mediated through its regulation of mitochondrial function and chromatin remodeling.

These findings offer valuable insights for identifying potential therapeutic targets for HCC.