Bevacizumab induces ferroptosis and enhances CD8⁺ T cell immune activity in liver cancer via modulating HAT1 and increasing IL-9.

ABSTRACT: Bevacizumab is a recombinant humanized monoclonal immunoglobulin (Ig) G1 antibody of VEGF, and inhibits angiogenesis and tumor growth in hepatocellular carcinoma (HCC). Ferroptosis, a new form of regulated cell death function independently of the apoptotic machinery, has been accepted as an attractive target for pharmacological intervention; the ferroptosis pathway can enhance cell immune activity of anti-PD1 immunotherapy in HCC. In this study we investigated whether and how bevacizumab regulated ferroptosis and immune activity in liver cancer. Firstly, we performed RNA-sequencing in bevacizumab-treated human liver cancer cell line HepG2 cells, and found that bevacizumab significantly altered the expression of a number of genes including VEGF, PI3K, HAT1, SLC7A11 and IL-9 in liver cancer,

SUBMITTER: Hou CY 

PROVIDER: S-EPMC11335855 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature