Ankrd53, also known as ankyrin repeat domain 53, is involved in maintaining chromosome integrity and stability. It plays a role in spindle dynamics during mitosis, regulating microtubule-associated processes like MT stabilization/destabilization and polymerization/depolymerization, which are crucial for sister chromatid congression and segregation [1]. It is also associated with pathways such as the TGF-β signaling pathway [2].

In ANKRD53-depleted HeLa cells, mitotic progression was delayed, the number of unaligned chromosomes increased, spindle MT polymerization decreased, and the spindle assembly checkpoint was activated. ANKRD53 depletion also led to an increase in bi-nuclei and polylobed nuclei, indicating its role in cytokinesis [1]. In stomach adenocarcinoma (STAD), ANKRD53 was downregulated, and as an independent predictive biomarker, it was involved in immune-related aspects such as interacting with immune checkpoint molecules, immunological pathways, and immunotherapy, in addition to being associated with MSI, TMB, and neoantigens. scRNA-seq data showed its main expression in CD8+ T and dendritic cells [2].

In conclusion, Ankrd53 is essential for maintaining chromosome integrity and stability, especially during mitosis and cytokinesis. Its dysregulation is associated with diseases like stomach adenocarcinoma. Studies on ANKRD53-depleted cells have provided insights into its role in these biological processes and disease conditions, highlighting its potential as a biomarker and therapeutic target.