Crtac1, also known as cartilage acidic protein 1, is a glycosylated calcium-binding extracellular matrix protein. It has roles in the development, function, and repair of the nervous system. Structurally, it consists of a three-domain fold with a compact β-propeller-TTR combination, stabilized by potassium ions [6].

In non-small cell lung cancer (NSCLC), overexpression of Crtac1 increases the chemosensitivity to cisplatin. It promotes NFAT transcriptional activation by increasing intracellular Ca2+ levels, inducing STUB1 expression, accelerating Akt1 protein degradation, and enhancing cisplatin-induced apoptosis [1]. In urothelial carcinoma, low Crtac1 expression is associated with aggressive characteristics and poor prognosis, while exogenous expression suppresses cell proliferation, invasion, and angiogenesis [5]. In bladder cancer, Crtac1 inhibits cell proliferation, migration, invasion, and epithelial-mesenchymal transition by downregulating Yin Yang 1 to inactivate the TGF-β pathway [7]. In spinal ligament degeneration, CRTAC1+ chondrocyte-like cells are involved in the pathogenesis, interacting with SPP1+ macrophages [2]. In atherosclerosis, CRTAC1 is identified as a marker of atherosclerosis progression [4]. In lung adenocarcinoma, lower Crtac1 expression is associated with poor prognosis, and upregulation inhibits cell proliferation, invasion, and migration [3].

In conclusion, Crtac1 plays crucial roles in multiple disease processes such as cancer and degenerative diseases. Its function in modulating chemosensitivity in NSCLC, influencing tumor aggressiveness in urothelial and bladder cancers, contributing to spinal ligament degeneration, and being a marker in atherosclerosis and lung adenocarcinoma, reveals its significance in understanding disease mechanisms. Studies on Crtac1, especially through in vivo models, provide valuable insights into potential therapeutic strategies for these diseases.