PBRM1 knockdown is associated with NRF2‑dependent ALDOA upregulation and metabolic reprogramming in HCCC‑9810 intrahepatic cholangiocarcinoma cells

PBRM1 knockdown made HCCC-9810 intrahepatic cholangiocarcinoma cells more proliferative, migratory and invasive, altered glucose-metabolism readouts, and raised aldolase A (ALDOA) expression. ALDOA silencing attenuated several metabolic and survival-related changes, and NRF2 overexpression increased ALDOA while NRF2 knockdown reduced it, indicating NRF2-dependent ALDOA regulation. In HCCC-9810-derived xenografts, PBRM1 knockdown produced greater tumor growth, higher ALDOA expression and higher Ki67 signal.