Open Access

BCL6B suppresses proliferation and migration of colorectal carcinoma cells through inhibition of the PI3K/AKT signaling pathway

  • Authors:
    • Yue Gu
    • Aifang Li
    • Hui Sun
    • Xueru Li
    • He Zha
    • Jiali Zhao
    • Jiaqing Xie
    • Zongyue Zeng
    • Lan Zhou
  • View Affiliations

  • Published online on: February 1, 2018     https://doi.org/10.3892/ijmm.2018.3451
  • Pages: 2660-2668
  • Copyright: © Gu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

B‑cell CLL/lymphoma 6 member B (BCL6B), a BCL6‑homologous gene, has been reported to be a tumor suppressor that is silenced in a variety of human cancers, including colorectal cancer (CRC). Although it was recently demonstrated that reduced expression of BCL6B is associated with tumor stage and lymph node metastasis in CRC, little is known on whether BCL6B contributes to CRC development, or the related underlying mechanism. The aim of the present study was to detect BCL6B expression in CRC cells, and determine the molecular mechanisms underlying the role of BCL6B in CRC development by investigating cell proliferation and migration in vitro. As a result, BCL6B expression was found to be notably repressed in CRC cells compared with normal intestinal epithelial cells by reverse transcription‑polymerase chain reaction and western blot analysis. CRC cell proliferation was significantly inhibited by BCL6B upregulation, as indicated by MTT and colony‑forming assays. Cell apoptosis was markedly induced, as indicated by flow cytometry, and BCL6B‑transfected CRC cells exhibited decreased migration ability. Additionally, BCL6B overexpression diminished the phosphorylation level of AKT in CRC cells. These effects of BCL6B were empowered by treatment with the specific phosphoinositide 3 kinase (PI3K)/AKT inhibitor LY294002. Furthermore, overexpression of BCL6B resulted in upregulation of E‑cadherin and downregulation of cyclin D1 and matrix metalloproteinase‑9, which were strongly enhanced by LY294002. In conclusion, the findings of the present study demonstrated that BCL6B suppressed the proliferation and migration of CRC cells indirectly, via inhibition of PI3K.
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May-2018
Volume 41 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Gu Y, Li A, Sun H, Li X, Zha H, Zhao J, Xie J, Zeng Z and Zhou L: BCL6B suppresses proliferation and migration of colorectal carcinoma cells through inhibition of the PI3K/AKT signaling pathway. Int J Mol Med 41: 2660-2668, 2018
APA
Gu, Y., Li, A., Sun, H., Li, X., Zha, H., Zhao, J. ... Zhou, L. (2018). BCL6B suppresses proliferation and migration of colorectal carcinoma cells through inhibition of the PI3K/AKT signaling pathway. International Journal of Molecular Medicine, 41, 2660-2668. https://doi.org/10.3892/ijmm.2018.3451
MLA
Gu, Y., Li, A., Sun, H., Li, X., Zha, H., Zhao, J., Xie, J., Zeng, Z., Zhou, L."BCL6B suppresses proliferation and migration of colorectal carcinoma cells through inhibition of the PI3K/AKT signaling pathway". International Journal of Molecular Medicine 41.5 (2018): 2660-2668.
Chicago
Gu, Y., Li, A., Sun, H., Li, X., Zha, H., Zhao, J., Xie, J., Zeng, Z., Zhou, L."BCL6B suppresses proliferation and migration of colorectal carcinoma cells through inhibition of the PI3K/AKT signaling pathway". International Journal of Molecular Medicine 41, no. 5 (2018): 2660-2668. https://doi.org/10.3892/ijmm.2018.3451