Chodl, or chondrolectin, is a gene encoding a type I transmembrane protein with a C-type lectin carbohydrate recognition domain in its extracellular portion. It is predominantly expressed in muscle cells, such as skeletal muscle, and is also present in testis, brain, and lung in adult mice [4]. Chodl plays roles in processes like motor axon extension, synaptogenesis, and may be involved in pathways related to cell-cell interactions [5]. Gene knockout models can be valuable for studying its functions.

In cancer research, Chodl shows different patterns. In colorectal cancer, its promoter hypermethylation inactivates Chodl, promoting carcinogenesis, and high Chodl expression predicts improved survival [1]. In hepatocellular carcinoma, its expression is decreased, but 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 reduces cell migration and invasion abilities [3]. In lung cancer, high CHODL protein expression is associated with shorter survival, and targeting it could be an anticancer strategy [6].

In zebrafish, Chodl-deficient models show anatomical and functional defects of the neuromuscular synapse, with motor axon growth and branching impaired, indicating its role in synaptogenesis [5].

In conclusion, Chodl is essential for processes like synaptogenesis in neuromuscular junctions. In cancer, it has complex roles where its expression and methylation status can impact tumorigenesis, metastasis, and patient prognosis. Gene knockout models in zebrafish and potentially mouse models in the future can further clarify its functions in these disease areas.