Chsy1, chondroitin sulfate synthase 1, is a glycosyltransferase involved in the synthesis of chondroitin sulfate. It participates in multiple biological processes and is associated with pathways like BMP signaling, succinate metabolism, and PI3K/AKT/HIF1A [1,2]. Genetic models, such as gene knockout in mice, are valuable for studying its functions.

In CRC liver metastasis, Chsy1 promotes CD8+ T cell exhaustion via activation of the succinate metabolism pathway, facilitating metastasis [1]. In osteoarthritis, Chsy1 deficiency reduces extracellular matrix production and aggravates cartilage injury by upregulating BMP signaling [2]. In gastric cancer, knockdown of Chsy1 inhibits cell proliferation, colony formation, and migration, while promoting apoptosis [3]. In the intervertebral disc, sensory nerve denervation or CGRP knockdown reduces Chsy1 expression, disrupting extracellular matrix homeostasis [4]. In glioma, LINC01094 promotes progression by modulating the miR-224-5p/Chsy1 axis [5]. In peripheral nerve injury, silencing Chsy1 at the lesion site decreases versican accumulation and promotes axon growth [6]. In HCC, Chsy1 promotes aggressive phenotypes via activation of the hedgehog signaling pathway [7]. In colorectal cancer, Chsy1 promotes proliferation and suppresses apoptosis through regulation of the NFκB and/or caspase-3/7 signaling pathway [8]. In oral squamous cell carcinoma, circ_0005050 acts as an oncogenic factor through the miR-487a-3p/Chsy1 axis [9]. In clear cell renal cell carcinoma, LINC01094 promotes development via the miR-224-5p/Chsy1 axis [10].

In conclusion, Chsy1 is crucial in various biological processes and disease conditions. Gene knockout or knockdown models have revealed its role in cancer metastasis, cell proliferation, apoptosis, extracellular matrix regulation, and nerve regeneration. Understanding Chsy1's functions through these models provides potential therapeutic targets for diseases like cancer and osteoarthritis.