Display options
Cite
Guo HJ, Li HY, Chen ZH, et al. NAMPT promotes hepatitis B virus replication and liver cancer cell proliferation through the regulation of aerobic glycolysis. Oncol Lett. 2021;21(5):390doi: 10.3892/ol.2021.12651.
Guo, H. J., Li, H. Y., Chen, Z. H., Zhou, W. J., Li, J. J., Zhang, J. Y., Wang, J., Luo, X. Y., Zeng, T., Shi, Z., & Mo, C. F. (2021). NAMPT promotes hepatitis B virus replication and liver cancer cell proliferation through the regulation of aerobic glycolysis. Oncology letters, 21(5), 390. https://doi.org/10.3892/ol.2021.12651
Guo, Hui-Jie, et al. "NAMPT promotes hepatitis B virus replication and liver cancer cell proliferation through the regulation of aerobic glycolysis." Oncology letters vol. 21,5 (2021): 390. doi: https://doi.org/10.3892/ol.2021.12651
Guo HJ, Li HY, Chen ZH, Zhou WJ, Li JJ, Zhang JY, Wang J, Luo XY, Zeng T, Shi Z, Mo CF. NAMPT promotes hepatitis B virus replication and liver cancer cell proliferation through the regulation of aerobic glycolysis. Oncol Lett. 2021 May;21(5):390. doi: 10.3892/ol.2021.12651. Epub 2021 Mar 18. PMID: 33777213; PMCID: PMC7988713.
Copy Download .nbib Format: NLM
Share it on

Oncol Lett. 2021 May;21(5):390. doi: 10.3892/ol.2021.12651. Epub 2021 Mar 18.

NAMPT promotes hepatitis B virus replication and liver cancer cell proliferation through the regulation of aerobic glycolysis.

Oncology letters

Hui-Jie Guo, Hong-Yu Li, Zi-Hao Chen, Wen-Jing Zhou, Jia-Jie Li, Jia-Yi Zhang, Jing Wang, Xing-Yan Luo, Ting Zeng, Zhao Shi, Chun-Fen Mo

Affiliations

  1. Department of Immunology, School of Basic Medical Sciences, Chengdu Medical College, Chengdu, Sichuan 610500, P.R. China.
  2. Department of Anatomy, Histology and Embryology, Development and Regeneration Key Laboratory of Sichuan Province, Chengdu Medical College, Chengdu, Sichuan 610500, P.R. China.

PMID: 33777213 PMCID: PMC7988713 DOI: 10.3892/ol.2021.12651

Abstract

Nicotinamide phosphoribosyltransferase (NAMPT) is a critical rate-limiting enzyme involved in NAD synthesis that has been shown to contribute to the progression of liver cancer. However, the potential role and mechanism of NAMPT in hepatitis B virus (HBV)-associated liver cancer remain unclear. The present study assessed the expression of NAMPT in HBV-positive and -negative liver cancer cells, and investigated whether HBV-induced NAMPT expression is dependent on HBV X protein (HBx). In addition, the role of NAMPT in HBV replication and transcription, and in HBV-mediated liver cancer cell growth was explored. The effects of NAMPT on the glycolytic pathway were also evaluated. Reverse transcription-quantitative PCR and western blotting results revealed that NAMPT expression levels were significantly higher in HBV-positive liver cancer cells than in HBV-negative liver cancer cells, and this effect was HBx-dependent. Moreover, the activation of NAMPT was demonstrated to be required for HBV replication and transcription. The NAMPT inhibitor FK866 repressed cell survival and promoted cell death in HBV-expressing liver cancer cells, and these effects were attenuated by nicotinamide mononucleotide. Furthermore, the inhibition of NAMPT was associated with decreased glucose uptake, decreased lactate production and decreased ATP levels in HBV-expressing liver cancer cells, indicating that NAMPT may promote the aerobic glycolysis. Collectively, these findings reveal a positive feedback loop in which HBV enhances NAMPT expression and the activation of NAMPT promotes HBV replication and HBV-mediated malignant cell growth in liver cancer. The present study highlights the important role of NAMPT in the regulation of aerobic glycolysis in HBV-mediated liver cancer, and suggests that NAMPT may be a promising treatment target for patients with HBV-associated liver cancer.

Copyright: © Guo et al.

Keywords: NAMPT; aerobic glycolysis; hepatitis B virus; liver cancer

Conflict of interest statement

The authors declare that they have no competing interests.

References

  1. Cancer Lett. 2017 Aug 1;400:194-202 - PubMed
  2. Sci Rep. 2015 Dec 10;5:18175 - PubMed
  3. Cancer Lett. 2019 Mar 1;444:60-69 - PubMed
  4. Oncotarget. 2015 Nov 10;6(35):38107-26 - PubMed
  5. Front Pharmacol. 2019 Oct 25;10:1270 - PubMed
  6. Cold Spring Harb Perspect Med. 2015 Feb 02;5(2):a021444 - PubMed
  7. J Hepatol. 2019 May;70(5):904-917 - PubMed
  8. Mol Carcinog. 2019 Apr;58(4):524-532 - PubMed
  9. Pharmacol Ther. 2015 Jul;151:16-31 - PubMed
  10. CA Cancer J Clin. 2014 Jan-Feb;64(1):9-29 - PubMed
  11. Oncotarget. 2017 Jun 29;8(49):85054-85067 - PubMed
  12. Front Oncol. 2018 Dec 12;8:622 - PubMed
  13. Cell. 2011 Mar 4;144(5):646-74 - PubMed
  14. J Virol. 2014 Mar;88(5):2442-51 - PubMed
  15. Br J Cancer. 2020 Sep;123(7):1154-1163 - PubMed
  16. Gastroenterology. 2012 Jul;143(1):199-212.e4 - PubMed
  17. Nat Rev Endocrinol. 2015 Sep;11(9):535-46 - PubMed
  18. J Neurosci Res. 2005 Jan 1-15;79(1-2):216-23 - PubMed
  19. Antioxid Redox Signal. 2018 Jan 20;28(3):251-272 - PubMed
  20. J Hepatol. 2016 Apr;64(1 Suppl):S84-S101 - PubMed
  21. Curr Opin Virol. 2018 Jun;30:1-8 - PubMed
  22. Sci Rep. 2015 Feb 12;5:8421 - PubMed
  23. Clin Microbiol Infect. 2015 Nov;21(11):969-74 - PubMed
  24. World J Gastroenterol. 2020 Mar 7;26(9):883-903 - PubMed
  25. Biochem Soc Trans. 2020 Jun 30;48(3):733-744 - PubMed
  26. Nat Med. 2015 Jun;21(6):591-600 - PubMed
  27. Clin Cancer Res. 2014 Sep 15;20(18):4861-72 - PubMed
  28. Oncotarget. 2017 Oct 6;8(56):96027-96034 - PubMed
  29. Methods. 2001 Dec;25(4):402-8 - PubMed
  30. Gastroenterology. 2007 Jun;132(7):2557-76 - PubMed
  31. Gastroenterology. 2018 Sep;155(3):799-814.e13 - PubMed
  32. J Pathol. 2015 Jan;235(2):355-67 - PubMed
  33. Int J Med Sci. 2020 Jul 9;17(12):1783-1794 - PubMed
  34. Ageing Res Rev. 2018 Nov;47:1-17 - PubMed
  35. Int J Cancer. 2018 Dec 15;143(12):3120-3130 - PubMed
  36. Mol Cell Oncol. 2015 Jun 10;3(1):e1052180 - PubMed

Publication Types