Li Ying, Huang Xiaohua, Wang Congcong, Li Yuzhong, Luan Mingchun, Ma Keli
Department of Clinical Laboratory, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116023, P.R. China.
Department of Biochemistry and Molecular Biology, Dalian Medical University, Dalian, Liaoning 116044, P.R. China.
Mol Med Rep. 2015 Apr;11(4):2959-66. doi: 10.3892/mmr.2014.3087. Epub 2014 Dec 12.
The ganglioside GM3 exerts its different effects via various growth factor receptors. The present study investigated and comparatively analyzed the opposing effects exerted by GM3 on the migration of mouse hepatocellular carcinoma Hepa1‑6 cells via epidermal growth factor receptor (EGFR) and hepatocyte growth factor receptor (HGFR/cMet). The results demonstrated that GM3 inhibited EGF‑stimulated motility, but promoted HGF‑stimulated motility of the Hepa1‑6 cells via phosphatidylinositol 3‑kinase/Akt‑mediated migration signaling. It is well established that the main cytokines modulating cell proliferation, invasion and metastasis are different in different types of tumor. This difference may, at least in part, explain why GM3 exerted its actions in a tumor‑type specific manner.
神经节苷脂GM3通过多种生长因子受体发挥其不同作用。本研究调查并比较分析了GM3通过表皮生长因子受体(EGFR)和肝细胞生长因子受体(HGFR/cMet)对小鼠肝癌Hepa1-6细胞迁移产生的相反作用。结果表明,GM3抑制表皮生长因子(EGF)刺激的运动性,但通过磷脂酰肌醇3激酶/蛋白激酶B(PI3K/Akt)介导的迁移信号促进HGF刺激的Hepa1-6细胞运动性。众所周知,调节细胞增殖、侵袭和转移的主要细胞因子在不同类型肿瘤中有所不同。这种差异可能至少部分解释了GM3为何以肿瘤类型特异性方式发挥作用。