NEK6, a NIMA-related serine/threonine protein kinase, is essential for mitosis progression, including mitotic spindle formation, metaphase-to-anaphase transition, and centrosome separation. It also has a role in DNA repair and can induce apoptosis when inhibited. It is involved in multiple pathways such as those related to cell cycle, and is of great biological importance in various cellular processes [1].

Knock-out of NEK6 in DU-145 prostate cancer cells decreases clonogenic capacity, proliferation, cell viability, and mitochondrial activity. It increases intracellular ROS levels, decreases antioxidant defenses, increases JNK phosphorylation and DNA damage markers, and induces cell death by apoptosis, making cells more sensitive to cisplatin. Also, in ovarian cancer, inhibiting NEK6 leads to decreased de novo purine synthesis and diminished chemoresistance. In osteosarcoma, down-regulation of NEK6 by siRNAs or miR-26a-5p inhibits cell proliferation, migration, and invasion while promoting apoptosis [3,2,4].

In conclusion, NEK6 is crucial for mitosis and DNA repair. Model-based research, especially gene knockout in cancer cell lines, reveals its significant roles in cancer-related processes such as chemoresistance, redox balance, and cell survival in prostate, ovarian, and osteosarcoma cancers. Understanding NEK6 may provide new strategies for cancer therapy.