TTK, also known as monopolar spindle 1 (hMps1), is a serine/threonine kinase. It is an integral part of the spindle assembly checkpoint signaling pathway, playing a crucial role in cell cycle regulation. Abnormal TTK expression has been associated with various biological processes and diseases [1,2,3,4,5,6,7,8].

In endometrial cancer, high TTK expression is linked to lower patient survival, and it can potentially serve as a biomarker for early detection. Repressing TTK expression in EC cells reduces cell proliferation, invasion, EMT, and chemoresistance [1].

In pancreatic ductal adenocarcinoma, H3K18la activates the transcription of TTK, and TTK forms a positive feedback loop with glycolysis, exacerbating oncogenesis [2].

In colorectal cancer, targeted depletion of TTK impairs cell proliferation, cell cycle progression, and organoid formation [3].

In liver cancer, TTK inhibitor sensitizes cells to radiation through regulating cell cycle in a p21-mediated manner [4].

In esophageal cancer, the ANXA2/TTK complex activates the Akt/mTOR signaling pathway, promoting cancer progression [5].

In glioblastoma, TTK promotes temozolomide resistance by inducing autophagy [6].

In vascular smooth muscle cells, TTK upregulation phosphorylates p120-catenin, and TTK inhibitor mitigates neointimal formation and atherosclerotic lesions [7].

In cisplatin-resistant ovarian cancer cells, down-regulation of TTK can recover cisplatin sensitivity [8].

In conclusion, TTK is a key regulator in multiple biological processes, especially in cell cycle-related events. Through gene-knockout or other loss-of-function experiments in various disease models, it has been shown to play significant roles in cancers such as endometrial, pancreatic, colorectal, liver, esophageal, glioblastoma, and ovarian cancer, as well as in atherosclerosis. Understanding TTK's function provides potential therapeutic targets for these diseases.