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Article

Insulin-like growth factor-I induces epithelial to mesenchymal transition via GSK-3β and ZEB2 in the BGC-823 gastric cancer cell line

  • Authors:
    • Heming Li
    • Ling Xu
    • Lei Zhao
    • Yanju Ma
    • Zhitu Zhu
    • Yunpeng Liu
    • Xiujuan Qu
  • View Affiliations / Copyright

    Affiliations: Department of Medical Oncology, The First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China, Department of Oncology, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, P.R. China
  • Pages: 143-148
    |
    Published online on: November 7, 2014
       https://doi.org/10.3892/ol.2014.2687
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Abstract

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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Copy and paste a formatted citation
Spandidos Publications style
Li H, Xu L, Zhao L, Ma Y, Zhu Z, Liu Y and Qu X: Insulin-like growth factor-I induces epithelial to mesenchymal transition via GSK-3β and ZEB2 in the BGC-823 gastric cancer cell line. Oncol Lett 9: 143-148, 2015.
APA
Li, H., Xu, L., Zhao, L., Ma, Y., Zhu, Z., Liu, Y., & Qu, X. (2015). Insulin-like growth factor-I induces epithelial to mesenchymal transition via GSK-3β and ZEB2 in the BGC-823 gastric cancer cell line. Oncology Letters, 9, 143-148. https://doi.org/10.3892/ol.2014.2687
MLA
Li, H., Xu, L., Zhao, L., Ma, Y., Zhu, Z., Liu, Y., Qu, X."Insulin-like growth factor-I induces epithelial to mesenchymal transition via GSK-3β and ZEB2 in the BGC-823 gastric cancer cell line". Oncology Letters 9.1 (2015): 143-148.
Chicago
Li, H., Xu, L., Zhao, L., Ma, Y., Zhu, Z., Liu, Y., Qu, X."Insulin-like growth factor-I induces epithelial to mesenchymal transition via GSK-3β and ZEB2 in the BGC-823 gastric cancer cell line". Oncology Letters 9, no. 1 (2015): 143-148. https://doi.org/10.3892/ol.2014.2687
Copy and paste a formatted citation
x
Spandidos Publications style
Li H, Xu L, Zhao L, Ma Y, Zhu Z, Liu Y and Qu X: Insulin-like growth factor-I induces epithelial to mesenchymal transition via GSK-3β and ZEB2 in the BGC-823 gastric cancer cell line. Oncol Lett 9: 143-148, 2015.
APA
Li, H., Xu, L., Zhao, L., Ma, Y., Zhu, Z., Liu, Y., & Qu, X. (2015). Insulin-like growth factor-I induces epithelial to mesenchymal transition via GSK-3β and ZEB2 in the BGC-823 gastric cancer cell line. Oncology Letters, 9, 143-148. https://doi.org/10.3892/ol.2014.2687
MLA
Li, H., Xu, L., Zhao, L., Ma, Y., Zhu, Z., Liu, Y., Qu, X."Insulin-like growth factor-I induces epithelial to mesenchymal transition via GSK-3β and ZEB2 in the BGC-823 gastric cancer cell line". Oncology Letters 9.1 (2015): 143-148.
Chicago
Li, H., Xu, L., Zhao, L., Ma, Y., Zhu, Z., Liu, Y., Qu, X."Insulin-like growth factor-I induces epithelial to mesenchymal transition via GSK-3β and ZEB2 in the BGC-823 gastric cancer cell line". Oncology Letters 9, no. 1 (2015): 143-148. https://doi.org/10.3892/ol.2014.2687
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