ERCC excision repair 6 like, spindle assembly checkpoint helicase (ERCC6L)

ERCC excision repair 6 like, spindle assembly checkpoint helicase (ERCC6L) is an ATP-dependent DNA helicase and member of the SNF2/SWI family, involved in the faithful segregation of sister chromatids during mitosis by resolving ultrafine DNA bridges (UFBs) that can form between chromatids[1][2][5]. The protein is largely excluded from the nucleus during interphase and associates with chromatin after nuclear envelope breakdown[1][5]. ERCC6L interacts with proteins such as PLK1 and components of the BTRR complex, facilitating chromosome decatenation and ensuring genomic stability[2]. It is overexpressed in multiple human cancers, with high levels correlating with tumor progression and poor clinical outcomes, displaying roles in cell cycle regulation, DNA repair, invasion, and epithelial–mesenchymal transition[3][4]. Loss or dysfunction of ERCC6L leads to increased DNA damage, defective mitosis, and reliance on compensatory DNA repair pathways, as observed in synthetic lethal screens with RAD52 deficiency[2]. Currently, ERCC6L is an emerging biomarker and potential therapeutic target for cancer, though direct pharmacological inhibitors are not yet established in clinical practice[3][4][5].

Other names

ERCC6LPICHRAD26LDNA excision repair protein ERCC-6-likeATP-dependent helicase ERCC6-likePLK1-interacting checkpoint helicaseTumor antigen BJ-HCC-15excision repair cross-complementation group 6 likeexcision repair cross-complementing rodent repair deficiency complementation group 6-likeFLJ20105

Not directly targeted by drugs (as of current knowledge), but acts through ATP-dependent helicase activity essential for mitotic genome maintenance[2] Potential synthetic lethality with RAD52 deficiency[2]