Cse1l, also known as Cellular Apoptosis Susceptibility (CAS), is a multiple-functional protein. It is involved in processes like apoptosis, cell survival, chromosome assembly, nucleocytoplasmic transport, microvesicle formation, and cancer metastasis. It functions in the mitotic spindle checkpoint and is associated with the RAS/RAF/MAPK/ERK signaling pathways [3,4,5].

Cse1l knockdown studies have shown its significance in multiple disease conditions. In lung cancer, siRNA-mediated knockdown of Cse1l impaired cell proliferation, invasion, migration and induced apoptosis, suggesting its role in tumor progression through the MET/STAT3/PD-L1 signaling [1]. In seminoma, Cse1l knockdown in TCam-2 cells attenuated cell proliferative capacity and led to cell cycle arrest in the G0/G1 phase, indicating its importance in maintaining cell proliferation and division [2]. In acute myeloid leukemia, shRNA-mediated knockdown of Cse1l promoted apoptosis, enhanced the sensitivity of cells to cytarabine, and reduced the expression of p-JKA2 and p-STAT3 proteins [6].

In conclusion, Cse1l plays essential roles in maintaining normal cell functions such as proliferation and cell cycle regulation. Through loss-of-function studies in different cell lines relevant to various cancers like lung cancer, seminoma, and acute myeloid leukemia, it has become evident that Cse1l is a potential therapeutic target. These findings contribute to understanding the oncogenic processes in these disease areas and may lead to new treatment strategies.