Chst11, short for carbohydrate sulfotransferase 11, is a Golgi membrane protein that catalyzes the transfer of sulfate to position 4 of the N-acetylgalactosamine residues of chondroitin. Chondroitin sulfate, whose sulfation is regulated by Chst11, is a key proteoglycan in cartilage, playing an important role in the growth plate development of cartilage [6]. It may also be involved in integrin signaling based on some analyses [2].

Chst11-deficient mice exhibit severe chondrodysplasia, congenital arthritis, and neonatal lethality, highlighting its crucial role in skeletal morphogenesis [6]. In human diseases, high expression of Chst11 is associated with poor prognosis in various cancers. For example, in glioblastoma, its overexpression promotes cell mobility and modulating chondroitin 4-sulfate on cells, and targeting Chst11-derived chondroitin 4-sulfate can attenuate cell invasiveness and improve survival of orthotopic glioma cell transplant mice [1]. In lung cancer, its expression contributes to tumor malignancy [2]. In pancreatic cancer, high expression correlates with poor prognosis and tumor immune infiltration [3]. In clear cell renal cell carcinoma, it promotes cell proliferation, migration, and invasion [7]. Also, in breast cancer, its expression is higher in basal-like and Her2-amplified cell lines and is associated with tumor progression, and its expression is controlled by DNA methylation [4]. In hepatocellular carcinoma cells, decreased or forced expression of Chst11 can alter metastatic potential and drug sensitivity, probably via the mitogen-activated protein kinase (MAPK) signal pathway [5].

In conclusion, Chst11 is essential for skeletal morphogenesis as demonstrated by mouse models. In disease research, its role in various cancers, such as promoting tumor progression and influencing prognosis, has been revealed through functional studies. Understanding Chst11's function provides potential targets for treating these diseases.