Chodl, also known as chondrolectin, is a gene encoding a type I transmembrane protein belonging to the C-type lectin family. It is predominantly expressed in muscle cells such as skeletal muscle, and is also found in tissues like testis, brain, and lung [5]. Chodl has been implicated in multiple biological processes. In the nervous system, it is involved in motor axon extension and neuromuscular junction formation [4].

In disease-related studies, Chodl shows differential expression patterns. In colorectal cancer, promoter hypermethylation of CHODL leads to its downregulation, promoting carcinogenesis, and is a poor prognostic factor for early-stage patients [1]. In hepatocellular carcinoma, CHODL expression is decreased in clinical samples and cell lines, yet overexpression in SMMC7721 cells increases cell migration and invasion [2]. In high-grade serous ovarian cancer, elevated CHODL expression is seen in metastasis tissues, and knockdown experiments show its role in reducing cell migration and invasion abilities [3]. In lung cancer, strong CHODL protein positivity is associated with shorter patient survival, and targeting CHODL might be a strategy for anticancer drug development [6].

In conclusion, Chodl plays essential roles in processes like neuromuscular junction formation. Its abnormal regulation is closely associated with multiple cancers, including colorectal, hepatocellular, ovarian, and lung cancers. Understanding Chodl through functional studies, especially those using gene knockout models as implied in some of these disease-related findings, can provide insights into disease mechanisms and potential therapeutic strategies.