GINS1, a subunit of the GINS complex, functions in eukaryotic DNA replication along with the MCM2-7 complex and Cdc45 [3]. It is involved in regulating DNA replication in the initiation and elongation phases, which is crucial for cell cycle modulation and thus has overall significance in cellular proliferation [2,4].

GINS1 has been found to be overexpressed in several cancers. In diffuse large B-cell lymphoma (DLBCL), FOXP1 transcriptionally activates GINS1 expression, and the FOXP1-GINS1 axis promotes DLBCL proliferation and doxorubicin resistance [1]. In hepatocellular carcinoma (HCC), GINS1 promotes ZEB1-mediated epithelial-mesenchymal transition and tumor metastasis via β-catenin signaling [2]. In glioma, GINS1 promotes cell proliferation and migration through USP15-mediated deubiquitination of TOP2A [3]. In bladder cancer, GINS1 promotes the initiation and progression by activating the AKT/mTOR/c-Myc signaling pathway [4]. High GINS1 expression is also associated with poor prognosis in gastric cancer, sarcoma, and HCC, and it can induce sorafenib resistance in HCC by promoting cancer stem properties [5,6,7]. In lung adenocarcinoma, GINS1 facilitates development via Wnt/β-catenin activation [8].

In conclusion, GINS1 plays a significant role in DNA replication and cell cycle-related processes. Its overexpression in various cancers, as revealed through in vivo and functional studies, suggests its potential as a prognostic biomarker and therapeutic target in multiple cancer types. The understanding of GINS1's functions in these disease conditions has been enhanced through research on its expression and regulatory mechanisms in different cancer models [1-10].