Consecutive stimulation of HBsAg promotes the viability of the human B lymphoblastoid cell line IM‑9 through regulating the SIRT1‑NF‑κB pathway

Retraction in: /10.3892/ol.2023.13825

  • Authors:
    • Jian Bo
    • Xiaojuan Wang
    • Jie Li
    • Wenqing Wang
    • Jinqian Zhang
  • View Affiliations

  • Published online on: May 3, 2017     https://doi.org/10.3892/ol.2017.6114
  • Pages: 433-440
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Patients with chronic HBV infection have been reported to suffer a significantly increased risk of NHL, but the underlying mechanisms remain to be clearly explained. The aim of the present study was to clarify the relationship between chronic HBV infection and NHL development. Fluorescence‑activated cell sorting, Annexin V/7‑aminoactinomycin D staining and MTS assay were used to analyze the rate of apoptosis and cell viability. In addition, western blotting was used to detect protein expression. The effects of the activator of SIRT1, SRT1720, and the inhibitor of SIRT1, nicotinamide, were also analyzed. The expression levels cytokines and chemokines were determined by multiplex assay. Hepatitis B surface antigen (HBsAg) was demonstrated to increase the viability of the human peripheral B lymphoblastoid cell line, IM‑9, in a dose‑ and time‑dependent manner. HBsAg also decreased histone H3 acetylation and p21 expression at the molecular level. HBsAg upregulated the expression of anti‑apoptotic B‑cell lymphoma‑extra‑large and B-cell lymphoma 2 proteins, and inactivated the intrinsic apoptosis pathway by reducing BCL2 associated X, apoptosis regulator expression and increasing the expression of sirtuin 1 (SIRT1) and nuclear factor‑κB (NF‑κB). HBsAg also altered the levels of certain chemokines and cytokines, including interleukin (IL)‑4, ‑10 and ‑12, C‑X‑C motif chemokine 10 and C‑C motif chemokine ligand 5. Inhibition of SIRT1 suppressed the effects induced by HBsAg. The anti‑apoptotic effect of HBsAg in IM‑9 cell lines occurred via the promotion of cell viability, inhibition of apoptosis, regulation of chemokines and cytokines, acetylation of histone H3 and alteration of SIRT1 and NF‑κB expression. In conclusion, chronic stimulation with HBsAg promoted the viability of the human B lymphoblastoid cell line, IM‑9, through regulation of the SIRT1‑NF‑κB pathway. This may be an underlying mechanism of HBV‑associated NHL.
View Figures
View References

Related Articles

Journal Cover

July-2017
Volume 14 Issue 1

Print ISSN: 1792-1074
Online ISSN:1792-1082

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Bo J, Wang X, Li J, Wang W and Zhang J: Consecutive stimulation of HBsAg promotes the viability of the human B lymphoblastoid cell line IM‑9 through regulating the SIRT1‑NF‑κB pathway Retraction in /10.3892/ol.2023.13825. Oncol Lett 14: 433-440, 2017
APA
Bo, J., Wang, X., Li, J., Wang, W., & Zhang, J. (2017). Consecutive stimulation of HBsAg promotes the viability of the human B lymphoblastoid cell line IM‑9 through regulating the SIRT1‑NF‑κB pathway Retraction in /10.3892/ol.2023.13825. Oncology Letters, 14, 433-440. https://doi.org/10.3892/ol.2017.6114
MLA
Bo, J., Wang, X., Li, J., Wang, W., Zhang, J."Consecutive stimulation of HBsAg promotes the viability of the human B lymphoblastoid cell line IM‑9 through regulating the SIRT1‑NF‑κB pathway Retraction in /10.3892/ol.2023.13825". Oncology Letters 14.1 (2017): 433-440.
Chicago
Bo, J., Wang, X., Li, J., Wang, W., Zhang, J."Consecutive stimulation of HBsAg promotes the viability of the human B lymphoblastoid cell line IM‑9 through regulating the SIRT1‑NF‑κB pathway Retraction in /10.3892/ol.2023.13825". Oncology Letters 14, no. 1 (2017): 433-440. https://doi.org/10.3892/ol.2017.6114