ZNF207 in human diseases: Molecular mechanisms, signalling networks, and emerging therapeutic opportunities.
TL;DR
Mechanistically, ZNF207 contributes to tumour development and progression through modulation of major oncogenic signalling pathways, including phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin signalling, nuclear factor erythroid 2-related factor 2 (NRF2)-related ferroptosis, spindle checkpoint and immune-regulatory pathways.
Abstract
Zinc finger protein 207 (ZNF207), a member of the Cys2His2 (C2H2)-type zinc finger protein family, functions as a transcriptional regulator involved in key cellular processes, including proliferation, differentiation, and tumourigenesis. Through its zinc finger motifs, microtubule-binding region, GLEBS motif, intrinsically disordered region, and nuclear localization signal, ZNF207 participates in mitotic regulation, pluripotency maintenance, RNA processing, and context-dependent transcriptional control. Aberrant ZNF207 expression has been associated with disease progression and adverse clinical outcomes in several cancer types, although the strength of evidence varies across disease contexts. Mechanistically, ZNF207 contributes to tumour development and progression through modulation of major oncogenic signalling pathways, including phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR) signalling, nuclear factor erythroid 2-related factor 2 (NRF2)-related ferroptosis, spindle checkpoint and immune-regulatory pathways. Given its multifaceted regulatory roles in cancer biology, ZNF207 has emerged as a promising target for precision oncology. Further elucidation of its molecular mechanisms may facilitate the development of early diagnostic strategies and targeted therapeutic interventions.