细胞识别分子 L1 通过调节细胞表面糖基化来调节细胞存活和迁移。
Cell Recognition Molecule L1 Regulates Cell Surface Glycosylation to Modulate Cell Survival and Migration.
机构信息
Department of Colorectal Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, China.
Dalian Medical University, Dalian, Liaoning 116044, China.
出版信息
Int J Med Sci. 2017 Sep 30;14(12):1276-1283. doi: 10.7150/ijms.20479. eCollection 2017.
Cell recognition molecule L1 (L1) plays an important role in cancer cell differentiation, proliferation, migration and survival, but its mechanism remains unclear. Our previous study has demonstrated that L1 enhanced cell survival and migration in neural cells by regulating cell surface glycosylation. In the present study, we show that L1 affected cell migration and survival in CHO (Chinese hamster ovary) cell line by modulation of sialylation and fucosylation at the cell surface via the PI3K (phosphoinositide 3-kinase) and Erk (extracellularsignal-regulated kinase) signaling pathways. Flow cytometry analysis indicated that L1 modulated cell surface sialylation and fucosylation in CHO cells. Activated L1 upregulated the protein expressions of ST6Gal1 (β-galactoside α-2,6-sialyltransferase 1) and FUT9 (Fucosyltransferase 9) in CHO cells. Furthermore, activated L1 promoted CHO cells migration and survival as shown by transwell assay and MTT assay. Inhibitors of sialylation and fucosylation blocked L1-induced cell migration and survival, while decreasing FUT9 and ST6Gal1 expressions via the PI3K-dependent and Erk-dependent signaling pathways. : L1 modulated cell migration and survival by regulation of cell surface sialylation and fucosylation via the PI3K-dependent and Erk-dependent signaling pathways.
细胞识别分子 L1（L1）在癌细胞的分化、增殖、迁移和存活中发挥着重要作用，但它的作用机制尚不清楚。我们之前的研究表明，L1 通过调节细胞表面糖基化来增强神经细胞的细胞存活和迁移。在本研究中，我们通过 PI3K（磷酸肌醇 3-激酶）和 Erk（细胞外信号调节激酶）信号通路，发现 L1 通过调节细胞表面的唾液酸化和岩藻糖化来影响 CHO（中国仓鼠卵巢）细胞系中的细胞迁移和存活。流式细胞术分析表明，L1 调节 CHO 细胞表面的唾液酸化和岩藻糖化。激活的 L1 上调了 CHO 细胞中 ST6Gal1（β-半乳糖苷α-2,6-唾液酸转移酶 1）和 FUT9（岩藻糖基转移酶 9）的蛋白表达。此外，如 Transwell 分析和 MTT 分析所示，激活的 L1 促进了 CHO 细胞的迁移和存活。唾液酸化和岩藻糖化的抑制剂通过 PI3K 依赖性和 Erk 依赖性信号通路阻断了 L1 诱导的细胞迁移和存活，同时降低了 FUT9 和 ST6Gal1 的表达。结论：L1 通过 PI3K 依赖性和 Erk 依赖性信号通路调节细胞表面的唾液酸化和岩藻糖化来调节细胞迁移和存活。
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