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Article

Overexpression of Bmi‑1 promotes epithelial‑mesenchymal transition in CD133+Hep G2 cells

  • Authors:
    • Zefeng Zhang
    • Qiyi Wang
    • Xiaoling Bu
    • Chuangqiang Zhang
    • Hao Chen
    • Weihong Sha
    • Wanwei Liu
  • View Affiliations / Copyright

    Affiliations: Department of Gastroenterology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China, Department of Anesthesiology, The First People's Hospital of Foshan, Foshan, Guangdong 528000, P.R. China
  • Pages: 6156-6161
    |
    Published online on: August 24, 2017
       https://doi.org/10.3892/mmr.2017.7347
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Abstract

Cancer stem cells (CSCs) and epithelial‑mesenchymal transition (EMT) are critical factors contributing to tumor metastasis and recurrence. The BMI1 proto‑oncogene (Bmi‑1) promotes the development and progression of hematologic malignancies and of several types of solid tumors. The aim of the present study was to explore the mechanism by which Bmi‑1 may promote invasion and migration of hepatocellular carcinoma Hep G2 cells. CD133 antigen is a transmembrane glycoprotein and regarded as a cancer stem cells marker in hepatocellular carcinoma. CD133+Hep G2 cells were enriched by magnetic‑activated cell sorting and exhibited greater viability compared with CD133‑Hep G2 cells, as measured by Cell Counting kit‑8 assay. Then, Bmi‑1 was overexpressed in CD133+Hep G2 cells by transfection with the Bmi‑1/pcDNA3.1(+) expression plasmid, and overexpression was confirmed by reverse‑transcription‑polymerase chain reaction and western blotting. Overexpression of Bmi‑1in CD133+Hep G2 cells resulted in the downregulation of E‑cadherin and upregulation of Vimentin at the protein level. The invasion and migration abilities of CD133+Hep G2 cells were increased in the Bmi‑1/pcDNA3.1(+)‑transfected group, as measured by Transwell invasion and wound healing assays, respectively. In conclusion, Bmi‑1 promoted invasion and migration of CD133+Hep G2 cells most likely through inducing EMT. The present findings may offer a potential novel target for the development of hepatocellular carcinoma therapies.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang Z, Wang Q, Bu X, Zhang C, Chen H, Sha W and Liu W: Overexpression of Bmi‑1 promotes epithelial‑mesenchymal transition in CD133+Hep G2 cells. Mol Med Rep 16: 6156-6161, 2017.
APA
Zhang, Z., Wang, Q., Bu, X., Zhang, C., Chen, H., Sha, W., & Liu, W. (2017). Overexpression of Bmi‑1 promotes epithelial‑mesenchymal transition in CD133+Hep G2 cells. Molecular Medicine Reports, 16, 6156-6161. https://doi.org/10.3892/mmr.2017.7347
MLA
Zhang, Z., Wang, Q., Bu, X., Zhang, C., Chen, H., Sha, W., Liu, W."Overexpression of Bmi‑1 promotes epithelial‑mesenchymal transition in CD133+Hep G2 cells". Molecular Medicine Reports 16.5 (2017): 6156-6161.
Chicago
Zhang, Z., Wang, Q., Bu, X., Zhang, C., Chen, H., Sha, W., Liu, W."Overexpression of Bmi‑1 promotes epithelial‑mesenchymal transition in CD133+Hep G2 cells". Molecular Medicine Reports 16, no. 5 (2017): 6156-6161. https://doi.org/10.3892/mmr.2017.7347
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang Z, Wang Q, Bu X, Zhang C, Chen H, Sha W and Liu W: Overexpression of Bmi‑1 promotes epithelial‑mesenchymal transition in CD133+Hep G2 cells. Mol Med Rep 16: 6156-6161, 2017.
APA
Zhang, Z., Wang, Q., Bu, X., Zhang, C., Chen, H., Sha, W., & Liu, W. (2017). Overexpression of Bmi‑1 promotes epithelial‑mesenchymal transition in CD133+Hep G2 cells. Molecular Medicine Reports, 16, 6156-6161. https://doi.org/10.3892/mmr.2017.7347
MLA
Zhang, Z., Wang, Q., Bu, X., Zhang, C., Chen, H., Sha, W., Liu, W."Overexpression of Bmi‑1 promotes epithelial‑mesenchymal transition in CD133+Hep G2 cells". Molecular Medicine Reports 16.5 (2017): 6156-6161.
Chicago
Zhang, Z., Wang, Q., Bu, X., Zhang, C., Chen, H., Sha, W., Liu, W."Overexpression of Bmi‑1 promotes epithelial‑mesenchymal transition in CD133+Hep G2 cells". Molecular Medicine Reports 16, no. 5 (2017): 6156-6161. https://doi.org/10.3892/mmr.2017.7347
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