ArticleCancer cell international2026
ACSF2 Functions as a regulatory switch for PARP inhibitor sensitivity in platinum-sensitive and homologous recombination-proficient high-grade serous ovarian cancer.
Article in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPoly(ADP-ribose) polymerase (PARP) inhibitor resistance represents a major clinical challenge in both homologous recombination deficiency-positive (HRD
objectiveThis study aimed to investigate whether ACSF2 modulates PARP inhibitor resistance by regulating p53-binding protein 1 (53BP1) nuclear foci formation and to determine if ACSF2 influences histone H4 Lysine 20 di-methylation (H4K20me2)-mediated 53BP1 recruitment via KMT5B in HRD
methodsUsing machine learning, ACSF2 was identified as a key resistance gene to PARP inhibitor. This discovery was based on an integrated analysis of six platinum-sensitive recurrent ovarian cancer (OC) cell lines (HRD
resultsACSF2 was provisionally identified as key mediator of PARP inhibitor resistance, with high expression correlating with poorer median overall survival in patients (42.00 vs. 49.60 months, P < 0.05). Similarly, ACSF2 acted as a key regulator of Niraparib sensitivity. Overexpression of ACSF2 increased the IC
conclusionACSF2 promotes Niraparib resistance in HRD
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