需要适当的染色体分离以确保染色体稳定性。着丝粒 (CEN) 是 CENP-A 定义的独特染色质结构域，负责在有丝分裂过程中募集动粒 (KT)，最终调节微管纺锤体附着和有丝分裂检查点功能。许多 CEN/KT 基因的上调在癌症中很常见。在这里，我们发现虽然 FOXM1 与 MYBL2 一起占据了许多 CEN/KT 基因的启动子，但仅 FOXM1 过表达不足以驱动 FOXM1 相关的转录程序。 CENP-F 是典型的外着丝粒成分；然而，它与 FOXM1 一起共同调节 G2/M 转录和正确的染色体分离。 CENP-F 的缺失会导致 G2/M 基因的染色质可及性改变，并减少 FOXM1-MBB 复合物的形成。我们证明协调的 CENP-FFOXM1 转录调控是一种癌症特异性功能。我们观察到一小部分 CEN/KT 基因，包括 CENP-C，它们不受 FOXM1 调节。 CENP-A 过表达背景下 CENP-C 的上调导致染色体错误分离和细胞死亡增加，表明 CENP-C 逃避 FOXM1 调节是一种癌症生存机制。我们共同证明 FOXM1 和 CENP-F 协调调节 G2/M 基因，并且这种协调特定于基因子集，以维持染色体不稳定水平和随后的细胞存活。

Proper chromosome segregation is required to ensure chromosomal stability. The centromere (CEN) is a unique chromatin domain defined by CENP-A and is responsible for recruiting the kinetochore (KT) during mitosis, ultimately regulating microtubule spindle attachment and mitotic checkpoint function. Upregulation of many CEN/KT genes is commonly observed in cancer. Here, we show that although FOXM1 occupies promoters of many CEN/KT genes with MYBL2, FOXM1 overexpression alone is insufficient to drive the FOXM1-correlated transcriptional program. CENP-F is canonically an outer kinetochore component; however, it functions with FOXM1 to coregulate G2/M transcription and proper chromosome segregation. Loss of CENP-F results in altered chromatin accessibility at G2/M genes and reduced FOXM1-MBB complex formation. We show that coordinated CENP-FFOXM1 transcriptional regulation is a cancer-specific function. We observe a small subset of CEN/KT genes including CENP-C, that are not regulated by FOXM1. Upregulation of CENP-C in the context of CENP-A overexpression leads to increased chromosome missegregation and cell death suggesting that escape of CENP-C from FOXM1 regulation is a cancer survival mechanism. Together, we show that FOXM1 and CENP-F coordinately regulate G2/M genes, and this coordination is specific to a subset of genes to allow for maintenance of chromosome instability levels and subsequent cell survival.