Mcm5, or minichromosome maintenance complex component 5, is a DNA licensing factor involved in cell proliferation [3]. It is also associated with cell cycle regulation, playing a well-known role in DNA replication [5]. In addition, it has been implicated in multiple signaling pathways, which are crucial for various biological processes such as organogenesis and tumor metastasis [3,5]. Genetic models, especially knockout models, can be valuable for further exploring its functions.

Mcm5 has been extensively studied in cancer research. In lung adenocarcinoma (LUAD), the m6A reader IGF2BP3 recognizes m6A-modified Mcm5 mRNAs, prolonging their stability, upregulating Mcm5 protein. This in turn competitively inhibits SIRT1-mediated deacetylation of Notch1 intracellular domain, promoting partial EMT and metastasis [1]. In colorectal cancer, DDX21, a highly expressed RNA binding protein, phase-separates and binds to the Mcm5 gene locus, and MCM5 is a key downstream target for CRC metastasis [2]. In glioblastoma, increased MCM5 expression promotes cell proliferation and resistance to TMZ [3]. In acute myeloid leukemia, elevated MCM5 levels predict a worse prognosis, and it promotes AML progression by accelerating the cell cycle and DNA replication [4]. In colon adenocarcinoma, MCM5 is an oncogene that promotes disease progression via cell cycle control [6]. In renal cell carcinoma, MCM5 overexpression is associated with a malignant status and poor prognosis, and it plays an important role in cell proliferation [7].

In conclusion, Mcm5 is essential for cell proliferation and DNA replication. Through model-based research, especially in cancer-related studies, it has been shown to be a crucial factor in the progression and prognosis of multiple cancers, including LUAD, colorectal cancer, glioblastoma, AML, colon adenocarcinoma, and renal cell carcinoma. Understanding Mcm5 functions provides potential therapeutic targets for these diseases.