TRIM27-Cas9-loaded EVs suppress HCC proliferation and enhance responsiveness to anti-PD-1 therapy by promoting ACSL4-mediated ferroptosis.
It is suggested that TRIM27 confers ferroptosis resistance via facilitating K48-linked ubiquitination and subsequent proteasomal degradation of ACSL4 and developed TRIM27-Cas9-loaded EVs with robust editing efficiency.