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

Bo,Jian; Wang,Xiaojuan; Li,Jie; Wang,Wenqing; Zhang,Jinqian

doi:10.3892/ol.2017.6114

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
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Affiliations: Department of Hematology, Chinese People's Liberation Army General Hospital, Beijing 100853, P.R. China, Department of Hematology, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China, Department of Pathology, Chinese People's Liberation Army General Hospital, Beijing 100853, P.R. China, Department of Pathology, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China, Department of Laboratory Medicine, The Second People's Hospital of Guangdong, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China
Published online on: May 3, 2017 https://doi.org/10.3892/ol.2017.6114
Pages: 433-440

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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.

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1	Kew MC: Epidemiology of chronic hepatitis B virus infection, hepatocellular carcinoma and hepatitis B virus-induced hepatocellular carcinoma. Pathol Biol (Paris). 58:273–277. 2010. View Article : Google Scholar : PubMed/NCBI
2	Mizuguchi Y, Takizawa T and Uchida E: Host cellular microRNA involvement in the control of hepatitis B virus gene expression and replication. World J Hepatol. 7:696–702. 2015. View Article : Google Scholar : PubMed/NCBI
3	Marcucci F, Spada E, Mele A, Caserta CA and Pulsoni A: The association of hepatitis B virus infection with B-cell non-Hodgkin lymphoma-a review. Am J Blood Res. 2:18–28. 2012.PubMed/NCBI
4	Ciesek S, Helfritz FA, Lehmann U, Becker T, Strassburg CP, Neipp M, Ciner A, Fytili P, Tillmann HL, Manns MP and Wedemeyer H: Persistence of occult hepatitis B after removal of the hepatitis B virus-infected liver. J Infect Dis. 197:355–360. 2008. View Article : Google Scholar : PubMed/NCBI
5	Yoffe B, Burns DK, Bhatt HS and Combes B: Extrahepatic hepatitis B virus DNA sequences in patients with acute hepatitis B infection. Hepatology. 12:187–192. 1990. View Article : Google Scholar : PubMed/NCBI
6	Marcucci F and Mele A: Hepatitis viruses and non-Hodgkin lymphoma: Epidemiology, mechanisms of tumorigenesis, and therapeutic opportunities. Blood. 117:1782–1789. 2011. View Article : Google Scholar
7	Engels EA, Cho ER and Jee SH: Hepatitis B virus infection and risk of non-Hodgkin lymphoma in South Korea: A cohort study. Lancet Oncol. 11:827–834. 2010. View Article : Google Scholar : PubMed/NCBI
8	Yi HZ, Chen JJ, Cen H, Yan W and Tan XH: Association between infection of hepatitis B virus and onset risk of B-cell non-Hodgkin's lymphoma: A systematic review and a meta-analysis. Med Oncol. 31:842014. View Article : Google Scholar : PubMed/NCBI
9	Galun E, Ilan Y, Livni N, Ketzinel M, Nahor O, Pizov G, Nagler A, Eid A, Rivkind A, Laster M, et al: Hepatitis B virus infection associated with hematopoietic tumors. Am J Pathol. 145:1001–1007. 1994.PubMed/NCBI
10	Kim JH, Bang YJ, Park BJ, Yoo T, Kim CW, Kim TY, Heo DS, Lee HS and Kim NK: Hepatitis B virus infection and B-cell non-Hodgkin's lymphoma in a hepatitis B endemic area: A case-control study. Jpn J Cancer Res. 93:471–477. 2002. View Article : Google Scholar : PubMed/NCBI
11	Marcucci F, Mele A, Spada E, Candido A, Bianco E, Pulsoni A, Chionne P, Madonna E, Cotichini R, Barbui A, et al: High prevalence of hepatitis B virus infection in B cell non-Hodgkin lymphoma. Haematologica. 91:554–557. 2006.PubMed/NCBI
12	Nath A, Agarwal R, Malhotra P and Varma S: Prevalence of hepatitis B virus infection in non-Hodgkin's lymphoma. A systematic review and meta-analysis. Intern Med J. 40:633–641. 2010. View Article : Google Scholar : PubMed/NCBI
13	Bréchot C, Thiers V, Kremsdorf D, Nalpas B, Pol S and Paterlini-Bréchot P: Persistent hepatitis B virus infection in subjects without hepatitis B surface antigen: Clinically significant or purely ‘occult’? Hepatology. 34:194–203. 2001. View Article : Google Scholar : PubMed/NCBI
14	Yuki N, Nagaoka T, Yamashiro M, Mochizuki K, Kaneko A, Yamamoto K, Omura M, Hikiji K and Kato M: Long-term histologic and virologic outcomes of acute self-limited hepatitis B. Hepatology. 37:1172–1179. 2003. View Article : Google Scholar : PubMed/NCBI
15	Rehermann B, Ferrari C, Pasquinelli C and Chisari FV: The hepatitis B virus persists for decades after patients' recovery from acute viral hepatitis despite active maintenance of a cytotoxic T-lymphocyte response. Nat Med. 2:1104–1108. 1996. View Article : Google Scholar : PubMed/NCBI
16	Chen MH, Hsiao LT, Chiou TJ, Liu JH, Gau JP, Teng HW, Wang WS, Chao TC, Yen CC and Chen PM: High prevalence of occult hepatitis B virus infection in patients with B-cell non-Hodgkin's lymphoma. Ann Hematol. 87:475–480. 2008. View Article : Google Scholar : PubMed/NCBI
17	Rossi D, Sala L, Minisini R, Fabris C, Falleti E, Cerri M, Burlone ME, Toniutto P, Gaidano G and Pirisi M: Occult hepatitis B virus infection of peripheral blood mononuclear cells among treatment-naive patients with chronic lymphocytic leukemia. Leuk Lymphoma. 50:604–611. 2009. View Article : Google Scholar : PubMed/NCBI
18	Wang F, Xu RH, Han B, Shi YX, Luo HY, Jiang WQ, Lin TY, Huang HQ, Xia ZJ and Guan ZZ: High incidence of hepatitis B virus infection in B-cell subtype non-Hodgkin lymphoma compared with other cancers. Cancer. 109:1360–1364. 2007. View Article : Google Scholar : PubMed/NCBI
19	Sie L, Loong S and Tan EK: Utility of lymphoblastoid cell lines. J Neurosci Res. 87:1953–1959. 2009. View Article : Google Scholar : PubMed/NCBI
20	Sugimoto M, Tahara H, Ide T and Furuichi Y: Steps involved in immortalization and tumorigenesis in human B-lymphoblastoid cell lines transformed by Epstein-Barr virus. Cancer Res. 64:3361–3364. 2004. View Article : Google Scholar : PubMed/NCBI
21	Hussain T and Mulherkar R: Lymphoblastoid cell lines: A continuous in vitro source of cells to study carcinogen sensitivity and DNA repair. Int J Mol Cell Med. 1:75–87. 2012.PubMed/NCBI
22	Georgakis GV, Li Y, Rassidakis GZ, Martinez-Valdez H, Medeiros LJ and Younes A: Inhibition of heat shock protein 90 function by 17-allylamino-17-demethoxy-geldanamycin in Hodgkin's lymphoma cells down-regulates Akt kinase, dephosphorylates extracellular signal-regulated kinase, and induces cell cycle arrest and cell death. Clin Cancer Res. 12:584–590. 2006. View Article : Google Scholar : PubMed/NCBI
23	Gui CY, Ngo L, Xu WS, Richon VM and Marks PA: Histone deacetylase (HDAC) inhibitor activation of p21WAF1 involves changes in promoter-associated proteins, including HDAC1. Proc Natl Acad Sci USA. 101:pp. 1241–1246. 2004; View Article : Google Scholar : PubMed/NCBI
24	Maggio E, van den Berg A, Diepstra A, Kluiver J, Visser L and Poppema S: Chemokines, cytokines and their receptors in Hodgkin's lymphoma cell lines and tissues. Ann Onc. 13 Suppl 1:52–56. 2002. View Article : Google Scholar
25	Côté CD, Rasmussen BA, Duca FA, Zadeh-Tahmasebi M, Baur JA, Daljeet M, Breen DM, Filippi BM and Lam TK: Resveratrol activates duodenal Sirt1 to reverse insulin resistance in rats through a neuronal network. Nat Med. 21:498–505. 2015. View Article : Google Scholar : PubMed/NCBI
26	Simms-Waldrip TR, Sunkersett G, Coughlin LA, Savani MR, Arana C, Kim J, Kim M, Zhan X, Greenberg DE, Xie Y, et al: Antibiotic-induced depletion of anti-inflammatory clostridia is associated with the development of graft-versus-host disease in pediatric stem cell transplantation patients. Biol Blood Marrow Transplant. 23:820–829. 2017. View Article : Google Scholar : PubMed/NCBI
27	Jain N, Oswal N, Chawla AS, Agrawal T, Biswas M, Vrati S, Rath S, George A, Bal V and Medigeshi GR: CD8 T cells protect adult naive mice from JEV-induced morbidity via lytic function. PLoS Negl Trop Dis. 11:e00053292017. View Article : Google Scholar : PubMed/NCBI
28	Feitelson MA and Duan LX: Hepatitis B virus × antigen in the pathogenesis of chronic infections and the development of hepatocellular carcinoma. Am J Pathol. 150:1141–1157. 1997.PubMed/NCBI
29	Natoli G, Avantaggiati ML, Chirillo P, Puri PL, Ianni A, Balsano C and Levrero M: Ras- and Raf-dependent activation of c-jun transcriptional activity by the hepatitis B virus transactivator pX. Oncogene. 9:2837–2843. 1994.PubMed/NCBI
30	Wang XW, Gibson MK, Vermeulen W, Yeh H, Forrester K, Stürzbecher HW, Hoeijmakers JH and Harris CC: Abrogation of p53-induced apoptosis by the hepatitis B virus X gene. Cancer Res. 55:6012–6016. 1995.PubMed/NCBI
31	Imai S, Armstrong CM, Kaeberlein M and Guarente L: Transcriptional silencing and longevity protein Sir2 is an NAD-dependent histone deacetylase. Nature. 403:795–800. 2000. View Article : Google Scholar : PubMed/NCBI
32	Smith JS, Brachmann CB, Celic I, Kenna MA, Muhammad S, Starai VJ, Avalos JL, Escalante-Semerena JC, Grubmeyer C, Wolberger C and Boeke JD: A phylogenetically conserved NAD+-dependent protein deacetylase activity in the Sir2 protein family. Proc Natl Acad Sci USA. 97:pp. 6658–6663. 2000; View Article : Google Scholar : PubMed/NCBI
33	Huang H and Tindall DJ: Dynamic FoxO transcription factors. J Cell Sci. 120:2479–2487. 2007. View Article : Google Scholar : PubMed/NCBI
34	Salminen A, Kauppinen A, Suuronen T and Kaarniranta K: SIRT1 longevity factor suppresses NF-kappaB-driven immune responses: Regulation of aging via NF-kappaB acetylation? Bioessays. 30:939–942. 2008. View Article : Google Scholar : PubMed/NCBI
35	van Leeuwen I and Lain S: Sirtuins and p53. Adv Cancer Res. 102:171–195. 2009. View Article : Google Scholar : PubMed/NCBI
36	Deng CX: SIRT1, is it a tumor promoter or tumor suppressor? Int J Biol Sci. 5:147–152. 2009. View Article : Google Scholar : PubMed/NCBI