Cenpe-KO Mouse

Cenpe, also known as centromere protein E, is a microtubule plus-end-directed kinetochore protein belonging to the centromere protein (CENP) family. It plays a crucial role in mitosis, participating in processes related to the cell cycle. Mutations in Cenpe can lead to primary microcephaly syndrome [1,4].

In various diseases, Cenpe has been found to be involved. In non-WNT/non-SHH medulloblastoma, it is highly expressed and serves as an independent prognostic factor, and its knockdown inhibits cell proliferation by activating the p53 signaling pathway and blocking the cell cycle [1]. In pulmonary hypertension, Cenpe deficiency significantly inhibits the development of pulmonary vascular remodeling and right ventricular hypertrophy, and knocking out Cenpe inhibits the proliferation and induces apoptosis of primary pulmonary artery smooth muscle cells [2]. In cervical cancer, its up-regulation promotes cancer progression through IL-6-mediated PI3K-Akt and MAPK signaling pathways, and it shows high diagnostic accuracy [3]. In medulloblastoma cells, CENPE knockdown induces mitotic defects, apoptosis, and endogenous DNA damage accumulation [4]. In glioblastoma, CENPE promotes proliferation by directly binding to WEE1 and regulating cell cycle transitions [5]. In chemoresistant acute myeloid leukemia, knockdown of CENPE suppresses cell proliferation and reverses chemoresistance, and Lin28A is found to be correlated with CENPE expression [6]. In esophageal adenocarcinoma, high CENPE expression is associated with unfavorable overall survival, and its expression is related to DNA methylation status [7]. In chromophobe renal cell carcinoma, CENPE is a potential prognostic biomarker and is enriched in proliferation-related pathways [8]. In non-small cell lung cancer, high CENPE expression is related to poor prognosis [9]. In lung adenocarcinoma, CENPE promotes cell proliferation and is directly regulated by FOXM1 [10].

In conclusion, Cenpe is essential for normal cellular processes, especially those related to the cell cycle. Its dysregulation is associated with multiple diseases, and studies using loss-of-function models, such as knockdown experiments, have revealed its role in promoting tumor cell proliferation, affecting cell cycle regulation, and being involved in various signaling pathways in different cancers and other disease conditions.