STOML2 inhibits sorafenib-induced ferroptosis in hepatocellular carcinoma via p-AKT signaling pathway.

ABSTRACT: Tyrosine kinase inhibitor resistance is a key factor affecting the prognosis of patients with advanced hepatocellular carcinoma (HCC). Previously, our group demonstrated that HCC patients with high stomatin-like protein 2 (STOML2) expression were poorly sensitive to systemic therapy. Whether STOML2 is involved in sorafenib resistance is unclear. Recent mechanistic studies have demonstrated that selective activation of ferroptosis pathways is expected to restore sorafenib sensitivity. The aim of the present study was to investigate the STOML2-ferroptosis axis and its contribution to sorafenib resistance. In this study, STOML2 expression was detected in tissue microarrays from patients with primary HCC and in human cell lines. Functional proliferative clone formation assay was used to study

SUBMITTER: Yin R 

PROVIDER: S-EPMC12070115 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature