“蜗牛”是一个被指示的转录抑制因子，在上皮-间充质转化（EMT）和转移中扮演关键角色。最近，许多基因可以通过稳定表达“蜗牛”在多个细胞系中诱导。然而，这些上调基因的生物学作用大多不清楚。本文报道了在多种乳腺癌细胞中诱导了编码关键GlcNAc硫酸化酶CHST2的基因。生物学上，CHST2减少导致抑制乳腺癌细胞的迁移和转移，而过表达CHST2则促进裸鼠的细胞迁移和肺转移。此外，MECA79抗原的表达水平升高，并用特定抗体阻断细胞表面的MECA79抗原可以覆盖CHST2上调介导的细胞迁移。此外，硫酸化抑制剂氯酸钠有效抑制了CHST2诱导的细胞迁移。总的来说，这些数据为乳腺癌进展和转移中的蜗牛/ CHST2 / MECA79轴的生物学提供了新的见解，以及诊断和治疗乳腺癌转移的潜在治疗策略。“©2023年作者（们）。”

Snail is a denoted transcriptional repressor that plays key roles in epithelial-mesenchymal transition (EMT) and metastasis. Lately, a plethora of genes can be induced by stable expression of Snail in multiple cell lines. However, the biological roles of these upregulated genes are largely elusive. Here, we report identification of a gene encoding the key GlcNAc sulfation enzyme CHST2 is induced by Snail in multiple breast cancer cells. Biologically, CHST2 depletion results in inhibition of breast cancer cell migration and metastasis, while overexpression of CHST2 promotes cell migration and lung metastasis in nude mice. In addition, the expression level of MECA79 antigen is elevated and blocking the cell surface MECA79 antigen with specific antibodies can override cell migration mediated by CHST2 upregulation. Moreover, the sulfation inhibitor sodium chlorate effectively inhibits the cell migration induced by CHST2. Collectively, these data provide novel insights into the biology of Snail/CHST2/MECA79 axis in breast cancer progression and metastasis as well as potential therapeutic strategy for the diagnosis and treatment of breast cancer metastasis.© 2023. The Author(s).