ArticleCell death & disease2018
HBV infection potentiates resistance to S-phase arrest-inducing chemotherapeutics by inhibiting CHK2 pathway in diffuse large B-cell lymphoma.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Chidamide: Exploration of maintenance therapy for patients with DLBCL with HBV infection.iScience · 2026Article
- Mechanisms of first-line treatment resistance in diffuse large B-cell lymphoma.Frontiers in immunology · 2026Review
- Biomedical informatics analysis has revealed a novel hub gene of the HBx in the pathogenesis and progression of DLBCL.iScience · 2025Article
- Clinical Risk Stratification and Modifiable Risk Factors for Hepatitis B Virus-Related Follicular Lymphoma.ImmunoTargets and therapy · 2025Article
- HBx induces chemoresistance in diffuse large B cell lymphoma by inhibiting intrinsic apoptosis via the NF-κB/XIAP pathway.Molecular therapy. Nucleic acids · 2024Article
- LncRNA MALAT1 promotes Erastin-induced ferroptosis in the HBV-infected diffuse large B-cell lymphoma.Cell death & disease · 2024Article
- Real-world clinical features and survival outcomes in diffuse large B-cell lymphoma patients with hepatitis B virus infection.Infectious agents and cancer · 2024Article
- From Crypts to Cancer: A Holistic Perspective on Colorectal Carcinogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- The Possible Role of Pathogens and Chronic Immune Stimulation in the Development of Diffuse Large B-Cell Lymphoma.Biomedicines · 2024Review
- Case report: CAR-T therapy demonstrated safety and efficacy in relapsed/refractory diffuse large B-cell lymphoma patients complicated with hepatitis B-related cirrhosis.Frontiers in oncology · 2024Article
- Hepatitis B surface antigen positivity is associated with poor short- and long-term outcomes in patients with diffuse large B-cell lymphoma who received CHOP or R-CHOP.Frontiers in immunology · 2024Article
- HBV-associated DLBCL of poor prognosis: advance in pathogenesis, immunity and therapy.Frontiers in immunology · 2023Review
- The Role of HBx Protein in Diseases Beyond the Liver.Infection and drug resistance · 2023Review
- Inhibition of Autophagy Promotes the Elimination of Liver Cancer Stem Cells by CD133 Aptamer-Targeted Delivery of Doxorubicin.Biomolecules · 2022Article
- lncNBAT1/APOBEC3A is a mediator of HBX-induced chemoresistance in diffuse large B cell lymphoma cells.Molecular therapy. Nucleic acids · 2022Article
- Bombyx mori Nucleopolyhedrovirus (BmNPV) Induces G2/M Arrest to Promote Viral Multiplication by DepletingInsects · 2021Article
- The inhibition of ABCB1/MDR1 or ABCG2/BCRP enables doxorubicin to eliminate liver cancer stem cells.Scientific reports · 2021Article
- Impact of Hepatitis B Virus Genetic Variation, Integration, and Lymphotropism in Antiviral Treatment and Oncogenesis.Microorganisms · 2020Review
- Hepatitis B Surface Antigen Positivity Is an Independent Unfavorable Prognostic Factor in Diffuse Large B-Cell Lymphoma in the Rituximab Era.The oncologist · 2020Article
- Ataxia-Telangiectasia Mutated is located in cardiac mitochondria and impacts oxidative phosphorylation.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A considerable number of diffuse large B-cell lymphoma (DLBCL) patients are infected with hepatitis B virus (HBV), which is correlated with their poor outcomes. However, the role of HBV infection in DLBCL treatment failure remains poorly understood. Here, our data demonstrated that HBV infection was closely associated with poorer clinical prognosis independent of its hepatic dysfunction in germinal center B-cell type (GCB type) DLBCL patients. Interestingly, we found that DLBCL cells expressing hepatitis B virus X protein (HBX) did not exhibit enhanced cell growth but did show reduced sensitivity to methotrexate (MTX) and cytarabine (Ara-C), which induced S-phase arrest. Mechanism studies showed that HBX specifically inhibited the phosphorylation of checkpoint kinase 2 (CHK2, a key DNA damage response protein). CHK2 depletion similarly conferred resistance to the S-phase arrest-inducing chemotherapeutics, consistent with HBX overexpression in DLBCL cells. Moreover, overexpression of wild-type CHK2 rather than its unphosphorylated mutant (T68A) significantly restored the reduced chemosensitivity in HBX-expressing cells, suggesting that HBV infection conferred resistance to chemotherapeutics that induced S-phase arrest by specifically inhibiting the activation of CHK2 response signaling in DLBCL.
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