BCL-3 promotes the tumor growth of hepatocellular carcinoma by regulating cell proliferation and the cell cycle through cyclin D1

Corrigendum in: /10.3892/or.2022.8456

  • Authors:
    • Kangsheng Tu
    • Zhikui Liu
    • Bowen Yao
    • Yumo Xue
    • Meng Xu
    • Changwei Dou
    • Guozhi Yin
    • Jun Wang
  • View Affiliations

  • Published online on: February 11, 2016     https://doi.org/10.3892/or.2016.4616
  • Pages: 2382-2390
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Abstract

Previous studies have demonstrated the aberrant expression and oncogenic role of B-cell CLL/lymphoma-3 (BCL-3) in human malignancies. However, the clinical significance of BCL-3 and its biological function in human hepatocellular carcinoma (HCC) remain unknown. In the present study, the expression levels of BCL-3 protein and mRNA in 90 pairs of HCC and matched non-tumor tissues were analyzed using immunohistochemistry and reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). We found that the expression levels of BCL-3 protein and mRNA in HCC tissues were significantly higher than those in the matched tumor-adjacent tissues. In addition, positive expression of BCL-3 was associated with adverse clinicopathological characteristics of the HCC patients including hepatitis B virus (HBV) infection, tumor size, cirrhosis and advanced tumor-node-metastasis (TNM) stage. Moreover, HCC patients with positive expression of BCL-3 had significantly decreased 5-year overall survival and recurrence-free survival. Importantly, BCL-3 expression was an independent prognostic factor for indicating the survival of the HCC patients. Functionally, BCL-3 knockdown markedly inhibited cell viability, proliferation and cell cycle progression in HepG2 cells, while BCL-3 overexpression promoted these cellular processes in Huh7 cells. Accordingly, in vivo experiments indicated that BCL-3 knockdown prominently suppressed the tumor growth of HepG2 cells in nude mice. Mechanistically, we revealed that the expression of cyclin D1 was decreased after BCL-3 knockdown in the HepG2 cells and was increased after BCL-3 overexpression in the Huh7 cells. Cyclin D1 silencing was found to abrogate the functional effects of BCL-3 on cellular processes in Huh7 cells. Taken together, our data suggest that BCL-3 may serve as a promising biomarker and an effective therapeutic target of HCC.
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April-2016
Volume 35 Issue 4

Print ISSN: 1021-335X
Online ISSN:1791-2431

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Spandidos Publications style
Tu K, Liu Z, Yao B, Xue Y, Xu M, Dou C, Yin G and Wang J: BCL-3 promotes the tumor growth of hepatocellular carcinoma by regulating cell proliferation and the cell cycle through cyclin D1 Corrigendum in /10.3892/or.2022.8456. Oncol Rep 35: 2382-2390, 2016
APA
Tu, K., Liu, Z., Yao, B., Xue, Y., Xu, M., Dou, C. ... Wang, J. (2016). BCL-3 promotes the tumor growth of hepatocellular carcinoma by regulating cell proliferation and the cell cycle through cyclin D1 Corrigendum in /10.3892/or.2022.8456. Oncology Reports, 35, 2382-2390. https://doi.org/10.3892/or.2016.4616
MLA
Tu, K., Liu, Z., Yao, B., Xue, Y., Xu, M., Dou, C., Yin, G., Wang, J."BCL-3 promotes the tumor growth of hepatocellular carcinoma by regulating cell proliferation and the cell cycle through cyclin D1 Corrigendum in /10.3892/or.2022.8456". Oncology Reports 35.4 (2016): 2382-2390.
Chicago
Tu, K., Liu, Z., Yao, B., Xue, Y., Xu, M., Dou, C., Yin, G., Wang, J."BCL-3 promotes the tumor growth of hepatocellular carcinoma by regulating cell proliferation and the cell cycle through cyclin D1 Corrigendum in /10.3892/or.2022.8456". Oncology Reports 35, no. 4 (2016): 2382-2390. https://doi.org/10.3892/or.2016.4616