NCAPD2 drives ESCC progression by enhancing the chromatin accessibility of P53 and E2F related genes
Although alterations in chromatin condensation underlie the heterogeneity of cancer cells, the specific role of chromatin condensation and its impact on chromatin accessibility remains unclear. We conducted ATAC-seq and RNA-seq analyses on condensin key factor NCAPD2-deficient esophageal squamous cell carcinoma (ESCC) cells. Our findings reveal that the absence of NCAPD2 disrupts chromatin condensation, leading to enhanced accessibility of promoter regions associated with the p53 and E2F related genes in ESCC. This disruption results in abnormal gene expression, cell cycle arrest, and apoptosis, ultimately impeding ESCC progression. Furthermore, PPM1B can directly dephosphorylate NCAPD2, consequently impacting the expression of P53 and E2F related genes. Overall, our study identifies the role of NCAPD2 in modulating promoter region accessibility in ESCC and paves a new way for clinical interventions.