Ask about this productRelated genes to: ERCC6L antibody
- Gene:
- ERCC6L NIH gene
- Name:
- ERCC excision repair 6 like, spindle assembly checkpoint helicase
- Previous symbol:
- -
- Synonyms:
- FLJ20105, PICH, RAD26L
- Chromosome:
- Xq13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2007-08-02
- Date modifiied:
- 2016-05-23
Related products to: ERCC6L antibody
Related articles to: ERCC6L antibody
- Excision repair cross-complementation group 6-like (ERCC6L), also known as PICH, is a centromere-associated SNF2 family ATPase that functions as a DNA helicase essential for mitotic chromosome segregation. Emerging evidence has established its significant oncogenic role across a broad spectrum of human malignancies. This review synthesizes current knowledge on the expression landscape, oncogenic functions, molecular mechanisms, and clinical significance of ERCC6L in cancer. Pan-cancer analyses consistently demonstrate that ERCC6L is frequently overexpressed in most tumor types compared to normal tissues, driven by mechanisms such as DNA amplification and promoter hypomethylation. This upregulation strongly correlates with aggressive clinicopathological features, including advanced tumor stage, metastasis, and poor patient prognosis across cancers like breast cancer, hepatocellular carcinoma, lung adenocarcinoma, and gastric cancer. Functionally, ERCC6L acts as a potent driver of malignant phenotypes by promoting uncontrolled proliferation through cell cycle acceleration, exerting anti-apoptotic effects, and enhancing invasion and metastasis via epithelial-mesenchymal transition. Mechanistically, ERCC6L operates at the nexus of multiple cancer pathways. It interacts with key mitotic regulators including PLK1, FOXM1, and KIF4A to govern cell cycle progression, activates pro-survival signaling cascades such as PI3K/AKT and NF-κB, and drives metastasis via PJA2-mediated p53 ubiquitination in lung adenocarcinoma. Furthermore, ERCC6L promotes metabolic reprogramming by stabilizing HIF-1α or transactivating PLK1 to drive aerobic glycolysis, and modulates DNA damage response, linking it to radio- and chemoresistance. Emerging evidence also connects ERCC6L to an immunosuppressive tumor microenvironment, with associations including Th2 cell infiltration, macrophage polarization, and reduced immune infiltration in HRD-high tumors, suggesting potential as a predictive biomarker for immunotherapy. The consistent association with aggressive tumor behavior positions ERCC6L as a valuable prognostic biomarker and a promising therapeutic target. Preclinical studies demonstrate that ERCC6L inhibition suppresses tumor growth and enhances treatment efficacy; however, current evidence is limited to and xenograft models, and substantial further validation is required before clinical translation. - Source: PubMed
Publication date: 2026/07/01
Jiang LingyuZhou HuaihaiHe JingQin JunqiHuang JianweiWei JiapingZhou YifanZhong Yonglong - Lung adenocarcinoma (LUAD) is prone to metastasis and exhibits a poor prognosis. The DNA repair-related protein ERCC6L is implicated in tumorigenesis, but its role in LUAD invasion and metastasis remains unclear. The expression, function, and underlying mechanisms of ERCC6L were investigated using bioinformatics analysis, cellular assays, and animal experiments. ERCC6L was significantly upregulated in LUAD tissues and cell lines, and its high expression was associated with poor overall and recurrence-free survival. Functional experiments demonstrated that ERCC6L overexpression promoted the migration, invasion, and epithelial-mesenchymal transition (EMT) of LUAD cells. Mechanistically, ERCC6L activated the E3 ubiquitin ligase PJA2, which mediated K48-linked polyubiquitination and subsequent degradation of p53, thereby attenuating its tumor-suppressive function. In vivo studies confirmed that ERCC6L knockout suppressed tumor growth, metastasis, and EMT progression by regulating the PJA2/p53 signaling axis. ERCC6L promotes migration, invasion, and EMT in LUAD by facilitating PJA2-mediated ubiquitination and degradation of p53. The ERCC6L/PJA2/p53 axis represents a potential novel therapeutic target for inhibiting metastasis in LUAD. - Source: PubMed
Publication date: 2026/04/30
Jiang LingyuZhou HuaihaiLiang ShengjingWen ZhaokeQin JunqiLei ZhenniuLi RonglingMa YunzhiPeng ShucongZhou YifanZhong Yonglong - Somatic cell reprogramming to induced pluripotent stem cells (iPSCs) holds great promise for revolutionizing tissue repair and regenerative medicine. However, achieving high reprogramming efficiency remains challenging due to various endogenous or exogenous barriers. One major obstacle is DNA replication stress arising from rapid cell proliferation during iPSC reprogramming, which results in genomic instability and markedly reduced reprogramming efficiency. The Plk1-interacting checkpoint helicase [PICH; also known as DNA excision repair protein ERCC-6-like (ERCC6L)], a member of the SNF2 ATPase family, is pivotal in maintaining genomic stability by promoting sister chromatid disjunction upon replication stress. Our previous work revealed that PICH is essential for maintaining the genomic stability of embryonic hematopoietic stem cells, but whether and how PICH participates in iPSC reprogramming remains elusive. We show that PICH deficiency induces genomic instability and drastically reduces the efficiency of iPSC generation. Overexpression of Pich improves iPSC reprogramming efficiency by alleviating replication stress. Furthermore, PICH cooperates with telomere-associated protein RIF1, another protein required for sister chromatid disjunction, to maintain genomic stability in iPSCs, thereby enhancing reprogramming efficiency. Taken together, these results reveal a previously unknown role of PICH in facilitating the reprogramming of iPSCs via maintaining genomic stability under replication stress, and provide a new strategy for improving iPSC reprogramming efficiency. - Source: PubMed
Publication date: 2026/04/14
Zhang FengjiaoJi ChaoranJi FangZhang ChaoLiao HongweiShao ZhehuaJia FangGeng XinweiYing Songmin - To elucidate the oncogenic role and mechanistic basis of ERCC6L in cutaneous melanoma, focusing on its impact on tumor metabolism and progression. - Source: PubMed
Publication date: 2026/01/19
Zhang MengdiZhou ShengboHan BingGe Yining - The impact of biological sex on treatment response and prognosis in lung cancer remains poorly understood. This study investigates the relationship between sex-linked genes, DNA repair, senescence, and survival in male and female patients with lung cancer. - Source: PubMed
Publication date: 2025/09/20
Kinsella APrina-Mello AMarignol L