BHRF1 exerts an antiapoptotic effect and cell cycle arrest via Bcl-2 in murine hybridomas

Milián, Ernest; Prats, Eva; Cairó, Jordi J.; Gòdia, Francesc; Vives, Joaquim

doi:10.1016/j.jbiotec.2015.06.379

Cited by 14 publications

(18 citation statements)

References 36 publications

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“…For example, early gene BCRF1 , also known as viral interleukin-10 (vIL-10) , encodes a homolog of IL-10 that functions as a paracrine growth factor in EBV-associated lymphomas 105. BHRF1 exhibits homology to the human oncoprotein Bcl-2 and delays cell death during EBV lytic replication 106,107. Chiu, et al demonstrated that BALF3, a homologue to terminase, is not only involved in the induction of host genomic instability, but also mediates the impact of EBV on NPC relapse 108.…”

Section: The Pathogenic Role Of Lytic Infection In Ebv-associated mentioning

confidence: 99%

Epstein-Barr virus lytic reactivation regulation and its pathogenic role in carcinogenesis

Li¹,

Liu²,

Hu³

et al. 2016

Int. J. Biol. Sci.

106

111

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Epstein-Barr virus (EBV) has been associated with several types of human cancers. In the host, EBV can establish two alternative modes of life cycle, known as latent or lytic and the switch from latency to the lytic cycle is known as EBV reactivation. Although EBV in cancer cells is found mostly in latency, a small number of lytically-infected cells promote carcinogenesis through the release of growth factors and oncogenic cytokines. This review focuses on the mechanisms by which EBV reactivation is controlled by cellular and viral factors, and discusses how EBV lytic infection contributes to human malignancies.

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Section: The Pathogenic Role Of Lytic Infection In Ebv-associated mentioning

confidence: 99%

Epstein-Barr virus lytic reactivation regulation and its pathogenic role in carcinogenesis

Li¹,

Liu²,

Hu³

et al. 2016

Int. J. Biol. Sci.

106

111

View full text Add to dashboard Cite

show abstract

“…Therefore, mechanism of EBV reactivation involves oxidative stress, inflammation (IL-6/IL-8/IL-13), angiogenesis, genomic instability and cell death. 51 , 61 – 64 In addition, EBV lytic proteins involve in carcinogenesis process, such as BGLF4 and BGLF5 which can promote genomic instability, BARF1 and BHRF1 which can exhibit homology to Bcl-2 and play an anti-apoptotic role. Notably, the lytic genes encode immune evasion proteins, including BNLF2a which inhibits the transporter of antigen processing, BILF1 which induces major histocompatibility complex (MHC) class I internalization and degradation.…”

Section: Ebv Reactivation and Oncogenesis In Npcmentioning

confidence: 99%

EBV based cancer prevention and therapy in nasopharyngeal carcinoma

Cao

2017

npj Precision Onc

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Epstein–Barr virus is an important cancer causing virus. Nasopharyngeal carcinoma is an infection-related cancer strongly driven by Epstein–Barr virus. In this cancer model, we identified the major host targets of latent membrane protein 1 which is a driving oncogene encoded by Epstein–Barr virus in latency infection. latent membrane protein 1 activates several oncogenic signaling axes causing multiple malignant phenotypes and therapeutic resistance. Also, Epstein–Barr virus up-regulates DNA methyltransferase 1 and mediates onco-epigenetic effects in the carcinogenesis. The collaborating pathways activated by latent membrane protein 1 constructs an oncogenic signaling network, which makes latent membrane protein 1 an important potential target for effective treatment or preventive intervention. In Epstein–Barr virus lytic phase, the plasma level of Epstein–Barr virus DNA is considered as a distinguishing marker for nasopharyngeal carcinoma in subjects from healthy high-risk populations and is also a novel prognostic marker in Epstein–Barr virus-positive nasopharyngeal carcinoma. Now the early detection and screening of the lytic proteins and Epstein–Barr virus DNA have been applied to clinical and high-risk population. The knowledge generated regarding Epstein–Barr virus can be used in Epstein–Barr virus based precision cancer prevention and therapy in the near future.

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“…The anti-apoptotic effects of BHRF1 are mainly due to its ability to bind to BH3-only pro-apoptotic Bcl-2 proteins and to inhibit the formation of Bax/Bak oligomers in the OMM (Cross et al, 2008 ; Flanagan and Letai, 2008 ; Kvansakul et al, 2010 ; Milian et al, 2015 ). BHRF1 binds to the BH3-only proteins Bim, Bak, Bid and PUMA (Kvansakul et al, 2010 ).…”

Section: Ebv and Kshvmentioning

confidence: 99%

Mitochondrial Proteins Coded by Human Tumor Viruses

et al. 2018

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Viruses must exploit the cellular biosynthetic machinery and evade cellular defense systems to complete their life cycles. Due to their crucial roles in cellular bioenergetics, apoptosis, innate immunity and redox balance, mitochondria are important functional targets of many viruses, including tumor viruses. The present review describes the interactions between mitochondria and proteins coded by the human tumor viruses human T-cell leukemia virus type 1, Epstein-Barr virus, Kaposi's sarcoma-associated herpesvirus, human hepatitis viruses B and C, and human papillomavirus, and highlights how these interactions contribute to viral replication, persistence and transformation.

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BHRF1 exerts an antiapoptotic effect and cell cycle arrest via Bcl-2 in murine hybridomas

Cited by 14 publications

References 36 publications

Epstein-Barr virus lytic reactivation regulation and its pathogenic role in carcinogenesis

Epstein-Barr virus lytic reactivation regulation and its pathogenic role in carcinogenesis

EBV based cancer prevention and therapy in nasopharyngeal carcinoma

Mitochondrial Proteins Coded by Human Tumor Viruses

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