Fig 1: Effects of BA on YY1/FAS, ERβ, insulin/IGF‐1, MAPK/ERK, and Notch signalling pathways regulating UBE2T expression in glioma cells. (A) WB assay show that BA suppresses the YY1/FAS axis, decreasing cleaved caspase‐8 and YY1 nuclear accumulation (red arrows); FASL co‐treatment failed to restore UBE2T (black arrows). (B) WB assay show that BA inhibits ERβ nuclear localization and ERK1/2 phosphorylation (red arrows); ERβ activation by DPN re‐stimulated p‐ERK1/2 and elevated UBE2T (red arrows). (C) WB assay show that the insulin/IGF‐1 pathway is unaffected by BA (black arrows), but IGF‐1 treatment enhances IGF‐1Rβ phosphorylation, increases p‐ERK1/2, and up‐regulates UBE2T (red arrows). (D) WB assay show that direct ERK activation (ERK agonist) increases UBE2T expression (red arrows), confirming ERK as a convergent effector. (E) BA does not alter Notch signalling, and DLL4‐Fc–induced Notch activation shows no impact on UBE2T. β‐Actin served as loading controls of total protein, and Lamin B1 for nuclear extracts. (F–H) The relative mRNA levels of UBE2T are detected by qPCR in U87MG (F), LN229 (G) and U251 glioma cell lines (H) additionally treated with agonists of the pathway mentioned above. “*” indicates significant difference compared with BA+CDDP group.