Insulin-like growth factor-I induces epithelial to mesenchymal transition via GSK-3β and ZEB2 in the BGC-823 gastric cancer cell line.
Insulin-like growth factor-I induces epithelial to mesenchymal transition via GSK-3β and ZEB2 in the BGC-823 gastric cancer cell line.
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DOI：
10.3892/ol.2014.2687
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发表时间：
2015-01
期刊：
影响因子：
2.9
通讯作者：
Qu X
中科院分区：
文献类型：
--
作者：
Li H;Xu L;Zhao L;Ma Y;Zhu Z;Liu Y;Qu X
转移是胃癌患者死亡的最常见原因。胰岛素样生长因子-I（IGF-I）可诱导上皮细胞向间质细胞转化（EMT），EMT与多种肿瘤的转移有关，但IGF-I诱导胃癌EMT的分子机制尚不清楚。本研究旨在探讨诱导BGC-823胃癌细胞EMT的作用。IGF-I通过上调ZEB 2转录因子的水平诱导EMT，这依赖于PI 3 K/Akt信号通路。此外，糖原合成酶激酶3β（Glycogen synthase kinase 3β，GSK-3β）作为PI 3 K/Akt的细胞内下游效应子，通过抑制ZEB 2的表达和随后对IGF-I诱导的EMT的抑制来维持上皮细胞表型，提示潜在的PI 3 K/Akt-GSK-3β-ZEB 2信号通路参与IGF-I诱导的胃癌BGC-823细胞EMT。总之，本研究的结果表明IGF-I通过激活PI 3 K/Akt-GSK-3β-ZEB 2信号通路诱导胃癌BGC-823细胞中的EMT。因此，本研究可能为胃癌转移机制提供更多有用的信息。
Metastasis is the most common cause of mortality in patients with gastric cancer. Epithelial-to-mesenchymal transition (EMT), which may be stimulated by insulin-like growth factor-I (IGF-I) is involved in the metastasis of numerous tumors; however, the molecular mechanism by which IGF-I may induce tumor cell EMT remains to be elucidated in gastric cancer. The present study aimed to investigate the induction of EMT in BGC-823 gastric cancer cells. It was identified that IGF-I induced EMT by upregulating the levels of ZEB2 transcription factor, and this was dependent on the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway in these cells. In addition, glycogen synthase kinase 3β (GSK-3β), an intracellular downstream effector of PI3K/Akt, sustained the epithelial phenotype by repressing ZEB2 expression and the subsequent inhibition of EMT induced by IGF-I, suggesting the involvement of a potential PI3K/Akt-GSK-3β-ZEB2 signaling pathway in IGF-I-induced EMT in gastric cancer BGC-823 cells. Overall, the results of the present study suggest that IGF-I induced EMT by the activation of a PI3K/Akt-GSK-3β-ZEB2 signaling pathway in gastric cancer BGC-823 cells. Therefore, this study may provide more useful information regarding the mechanism of gastric cancer metastasis.
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