Technical Articles

This article focuses on the gain-of-function mechanisms and pro-metastatic effects of the p53 R175H hotspot mutant protein, systematically elaborating its specific protein interaction features that distinguish it from other p53 hotspot mutant subtypes, analyzing the molecular mechanism by which it binds to the transcription factor BACH1 and recruits the histone demethylase LSD2 to form a ternary regulatory complex, thereby achieving selective regulation of BACH1's inhibitory and activating targets, and exploring the dual effects of this mechanism in antagonizing ferroptosis and promoting tumor metastasis, as well as the validation evidence from mouse genetic models.