GINS4 (GINS Complex Subunit 4)

The α5-nAChR/GINS4 axis was further validated in both mouse xenograft models and human LUAD tissue samples. Collectively, the results indicate the existence of a novel α5-nAChR/GINS4 signaling pathway contributing to nicotine-associated LUAD progression.

Finally, in a preterm rat model, we demonstrate that GINS4 induced BPD-like pathological alterations in lung tissues, characterized by alveolar septal simplification and thickening. Collectively, this study identifies GINS4 as a potential novel therapeutic target for prevention and treatment of BPD.

GINS4 silencing suppressed proliferation and cycle while promoted ferroptosis in HCC cells by regulating PI3K/AKT signaling via binding to POLE2.

Hsa_circ_0008673 might promote BC progression via modulating miR-578/GINS4 pathway.

Further analyses demonstrated that both messenger RNA (mRNA) and protein expression profiles of GINS4 and ESR1 were significantly associated with UCEC development and progression in TCGA and GSE17025 cohorts. Based on the integrated bioinformatic analyses, our data indicated that GINS4 and ESR1 might serve as potential prognostic markers and targets for UCEC therapy.