DNA Oncogenic Virus-Induced Oxidative Stress, Genomic Damage, and Aberrant Epigenetic Alterations

Kgatle, Mankgopo; Spearman, Wendy; Kalla, Asgar Ali; Hairwadzi, Henry

doi:10.1155/2017/3179421

Cited by 36 publications

(30 citation statements)

References 162 publications

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“…Besides, during HPV infections ROS can be also produced by activated neutrophils and macrophages associated to the local immune response. Altogether, alterations in infected cell metabolism and the non-effective chronic inflammatory response may contribute to cell transformation [ 98 – 101 ].…”

Section: Progression Of Female Cancersmentioning

confidence: 99%

Oxidative stress in female cancers

et al. 2018

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Breast, cervical and ovarian cancers are highly prevalent in women worldwide. Environmental, hormonal and viral-related factors are especially relevant in the development of these tumors. These factors are strongly related to oxidative stress (OS) through the generation of reactive oxygen species (ROS). The OS is caused by an imbalance in the redox status of the organism and is literally defined as “an imbalance between ROS generation and its detoxification by biological system leading to impairment of damage repair by cell/tissue”. The multistep progression of cancer suggests that OS is involved in cancer initiation, promotion and progression. In this review, we described the role of OS and the interplay with environmental, host and viral factors related to breast, cervical and ovarian cancers initiation, promotion and progression. In addition, the role of the natural antioxidant compound curcumin and other compounds for breast, cervical and ovarian cancers prevention/treatment is discussed.

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Section: Progression Of Female Cancersmentioning

confidence: 99%

Oxidative stress in female cancers

et al. 2018

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“…DNA damage is directly linked to a large range of human diseases, including aging and cancer [ 14 – 16 ], and usually has severe effects on the cell—triggering cell-cycle arrest, cell death or tumorigenesis. Reactive oxygen species (ROS), which can be produced by diverse conditions of stress such as chronic viral infection and cancer hypoxia [ 17 , 18 ], are one of the major causes of DNA damage [ 19 ]. Most cancers, if not all, harbor deficient DNA repair mechanisms, resulting in increased genomic instability and less capacity to respond to DNA damages; therefore they heavily rely on alternative DNA repair mechanisms for survival [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

LIMD1 is induced by and required for LMP1 signaling, and protects EBV-transformed cells from DNA damage-induced cell death

et al. 2017

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LIMD1 (LIM domain-containing protein 1) is considered as a tumor suppressor, being deregulated in many cancers to include hematological malignancies; however, very little is known about the underlying mechanisms of its deregulation and its roles in carcinogenesis. Epstein-Barr Virus (EBV) is associated with a panel of malignancies of lymphocytic and epithelial origin. Using high throughput expression profiling, we have previously identified LIMD1 as a common marker associated with the oncogenic transcription factor IRF4 in EBV-related lymphomas and other hematological malignancies. In this study, we have identified potential conserved IRF4- and NFκB-binding motifs in the LIMD1 gene promoter, and both are demonstrated functional by promoter-reporter assays. We further show that LIMD1 is partially upregulated by EBV latent membrane protein 1 (LMP1) via IRF4 and NFκB in EBV latency. As to its role in the setting of EBV latent infection, we show that LIMD1 interacts with TRAF6, a crucial mediator of LMP1 signal transduction. Importantly, LIMD1 depletion impairs LMP1 signaling and functions, potentiates ionomycin-induced DNA damage and apoptosis, and inhibits p62-mediated selective autophagy. Taken together, these results show that LIMD1 is upregulated in EBV latency and plays an oncogenic role rather than that of a tumor suppressor. Our findings have identified LIMD1 as a novel player in EBV latency and oncogenesis, and open a novel research avenue, in which LIMD1 and p62 play crucial roles in linking DNA damage response (DDR), apoptosis, and autophagy and their potential interplay during viral oncogenesis.

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“…It should be noted that some oncogenic viruses, such as hepatitis B and C viruses, and EBV, increase the level of cellular ROS due to mitochondrial dysfunction and response to protein misfolding. Such viral-induced oxidative stress triggers not only metabolic changes, but also activation of NF-κB, which promotes oncogenesis in liver tissues and blood [ 89 ]. Non-oncogenic viruses, such as hepatitis delta virus, which co-infects host cells together with the hepatitis B virus, enhance ROS production and activate NF-κB and STAT3 pathways.…”

Section: The Nf-κb Signaling Pathway As An Antagonist Of Apoptotic Dementioning

confidence: 99%

Viral Infections: Negative Regulators of Apoptosis and Oncogenic Factors

Zamaraev¹,

Zhivotovsky²,

Kopeina³

2020

Biochemistry Moscow

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The disruption of apoptotic cell death process is closely associated with the etiology of various diseases, including cancer. Permanent viral infections can cause different types of cancers. Oncogenic viruses manipulate both external and internal apoptosis pathways, and inhibit the activity of proapoptotic proteins and signaling pathways, which facilitates carcinogenesis. Ineffective immune surveillance or immune response suppression can induce uncontrolled virus propagation and host cell proliferation. In this review, we discuss current data that provide insights into mechanisms of apoptotic death suppression by viruses and their role in oncogenesis.

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DNA Oncogenic Virus-Induced Oxidative Stress, Genomic Damage, and Aberrant Epigenetic Alterations

Cited by 36 publications

References 162 publications

Oxidative stress in female cancers

Oxidative stress in female cancers

LIMD1 is induced by and required for LMP1 signaling, and protects EBV-transformed cells from DNA damage-induced cell death

Viral Infections: Negative Regulators of Apoptosis and Oncogenic Factors

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