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Article Open Access

Effects of cullin 4B on the proliferation and invasion of human gastric cancer cells

  • Authors:
    • Feng He
    • Xiu‑Mei Cheng
    • Wen‑Long Gu
  • View Affiliations / Copyright

    Affiliations: Department of Medical Oncology, The Affiliated Jianhu Hospital of Nantong University, Jianhu People's Hospital, Yancheng, Jiangsu 224700, P.R. China, Department of Basic Medicine, Jiangsu Vocational College of Medicine, Yancheng, Jiangsu 224000, P.R. China
    Copyright: © He et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 4973-4980
    |
    Published online on: January 26, 2018
       https://doi.org/10.3892/mmr.2018.8509
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Abstract

The major aim of the present study was to explore the effects of cullin 4B (CUL4B) on the proliferation and invasion of human gastric cancer cells. Gastric tumor tissues and paired adjacent non‑tumor tissues were obtained from 21 gastric cancer patients, and gastric cancer cell lines (AGS, MGC‑803, KATO‑III, MKN‑45, SGC‑7901, BGC‑823 and MKN‑74) were cultured. BGC‑823 cells were transfected with CUL4B small interfering (si)RNA or control siRNA. Reverse transcription‑quantitative polymerase chain reaction analysis was performed to detect the mRNA expression of CUL4B. Western blot analysis was performed to measure the protein levels of Wnt, β‑catenin, glutathione synthase kinase (GSK)‑3β, caspase‑3 and cyclin E. MTT and Transwell assays were performed to examine cell proliferation and invasion following CUL4B knockdown. In addition, the effect of CUL4B knockdown on the cell cycle and apoptosis of BGC‑823 cells was evaluated by flow cytometric analysis. The results indicated that compared with the adjacent non‑tumor tissues and a normal gastric epithelial cell line, gastric cancer tissues and cell lines exhibited significantly higher expression of CUL4B. Knockdown of CUL4B in gastric cancer cells suppressed cell proliferation, caused G1 arrest and inhibited cell invasion. Silencing of CUL4B also resulted in decreased Wnt and β‑catenin expression, but increased expression of GSK‑3β, caspase‑3 and cyclin E. These results indirectly demonstrate that CUL4B enhances the proliferation and invasion abilities of gastric cancer cells by upregulating the constituent factors Wnt and β‑catenin, as well as by negatively regulating the mRNA and protein expression of GSK‑3β, caspase‑3 and cyclin E. The potential mechanism of CUL4B highlighted in the present study may be helpful for the treatment of patients with gastric cancer.
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Copy and paste a formatted citation
Spandidos Publications style
He F, Cheng XM and Gu WL: Effects of cullin 4B on the proliferation and invasion of human gastric cancer cells. Mol Med Rep 17: 4973-4980, 2018.
APA
He, F., Cheng, X., & Gu, W. (2018). Effects of cullin 4B on the proliferation and invasion of human gastric cancer cells. Molecular Medicine Reports, 17, 4973-4980. https://doi.org/10.3892/mmr.2018.8509
MLA
He, F., Cheng, X., Gu, W."Effects of cullin 4B on the proliferation and invasion of human gastric cancer cells". Molecular Medicine Reports 17.4 (2018): 4973-4980.
Chicago
He, F., Cheng, X., Gu, W."Effects of cullin 4B on the proliferation and invasion of human gastric cancer cells". Molecular Medicine Reports 17, no. 4 (2018): 4973-4980. https://doi.org/10.3892/mmr.2018.8509
Copy and paste a formatted citation
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Spandidos Publications style
He F, Cheng XM and Gu WL: Effects of cullin 4B on the proliferation and invasion of human gastric cancer cells. Mol Med Rep 17: 4973-4980, 2018.
APA
He, F., Cheng, X., & Gu, W. (2018). Effects of cullin 4B on the proliferation and invasion of human gastric cancer cells. Molecular Medicine Reports, 17, 4973-4980. https://doi.org/10.3892/mmr.2018.8509
MLA
He, F., Cheng, X., Gu, W."Effects of cullin 4B on the proliferation and invasion of human gastric cancer cells". Molecular Medicine Reports 17.4 (2018): 4973-4980.
Chicago
He, F., Cheng, X., Gu, W."Effects of cullin 4B on the proliferation and invasion of human gastric cancer cells". Molecular Medicine Reports 17, no. 4 (2018): 4973-4980. https://doi.org/10.3892/mmr.2018.8509
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