Dscc1, also known as DNA replication and sister chromatid cohesion 1, is involved in DNA replication, repair, and sister chromatid cohesion. It functions in a pathway related to these processes and is crucial for maintaining genomic stability [5]. Genetic models, like mouse mutant lines, are valuable for studying Dscc1's function.

In mouse mutant lines, null mutation of Dscc1 led to a significant increase in micronucleus (MN) formation, which are hallmarks of genomic instability. Mice with Dscc1 null mutation also displayed phenotypes characteristic of patients with cohesinopathy disorders, indicating Dscc1's role in maintaining genomic stability in vivo [1].

In human cells, loss of SIRT1 could rescue phenotypes associated with DSCC1 loss, paralleling the restoration of protein acetylation of SMC3 [1]. Additionally, in various cancer studies, DSCC1 was found to be overexpressed in cancers such as lung adenocarcinoma, gastric cancer, and breast cancer, promoting cancer cell proliferation, stemness, EMT, and metastatic potential, and its high expression was often correlated with poor prognosis [2,3,4,6].

In conclusion, Dscc1 is essential for maintaining genomic stability through its role in DNA-related processes. Mouse models with Dscc1 knockout have revealed its significance in conditions related to genomic instability, like cohesinopathy disorders. In cancer research, its overexpression in multiple cancer types suggests it could be a potential biomarker and therapeutic target for these malignancies.