NEK5, short for NIMA Related Kinase 5, is a member of the Never-in-mitosis kinase family. It is involved in regulating centrosome integrity, cell cycle progression, and has been associated with various biological processes such as mitochondrial functions, DNA damage response, and myogenesis [3,4,5,6]. In terms of associated pathways, it may be involved in pathways related to cell proliferation, migration, and metastasis [1,2]. Genetic models are valuable for studying its functions.

In breast cancer, silencing NEK5 can significantly suppress cell proliferation both in vivo and in vitro, inhibit migration and invasion, and it was shown to up-regulate Cyclin A2 and down-regulate Cyclin D1, D3, and E1 [1]. In breast cancer cells, NEK5 activation alters cell morphology and promotes cell migration independent of cell proliferation, and its overexpression or knockdown affects metastatic potential in a cell-type-specific manner [2]. In mouse oocytes, Nek5 depletion impairs meiotic G2/M transition and pre-implantation embryonic development [3]. Also, NEK5-silenced cells are more sensitive to etoposide-induced DNA damage, and NEK5 interacts with topoisomerase IIβ [4]. Moreover, NEK5 interacts with LonP1 in mitochondria, and its kinase activity is essential for mitochondrial functions and mtDNA maintenance [5].

In conclusion, NEK5 plays crucial roles in multiple biological processes. Its functions in cell cycle regulation, DNA damage response, and mitochondrial homeostasis are well-demonstrated through various studies. In disease areas, especially breast cancer, research on NEK5 using loss-of-function models has revealed its potential as a therapeutic target, highlighting its significance in understanding disease mechanisms and developing new treatments.