The interplay between EBV and KSHV viral products and NF-κB pathway in oncogenesis

Charostad, Javad; Nakhaie, Mohsen; Dehghani, Arezo; Faghihloo, Ebrahim

doi:10.1186/s13027-020-00317-4

Cited by 18 publications

(22 citation statements)

References 114 publications

(144 reference statements)

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“…EBV that causes B‐cell lymphoma and nasopharyngeal carcinoma encode LMP1 protein that functions as CD40 homolog to prevent apoptosis of EBV‐infected B‐cell by upregulating NF‐κB activation. 329 Kaposi's sarcoma‐associated herpesvirus that causes sarcoma and lymphoma encodes viral FLICE inhibitory protein (vFLIP) that hijacks both canonical and noncanonical NF‐κB pathways promoting cell survival and proliferation. 329 Besides direct transcribing cell proliferation‐related genes, NF‐κB also induces the expression of proinflammatory cytokines such as IL‐1β, IL‐6, and TNFα, which play a key role in the NF‐κB‐dependent tumor cell proliferation.…”

Section: Nf‐κb and Cancermentioning

confidence: 99%

NF‐κB signaling in inflammation and cancer

Zhang

et al. 2021

MedComm

188

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Since nuclear factor of κ‐light chain of enhancer‐activated B cells (NF‐κB) was discovered in 1986, extraordinary efforts have been made to understand the function and regulating mechanism of NF‐κB for 35 years, which lead to significant progress. Meanwhile, the molecular mechanisms regulating NF‐κB activation have also been illuminated, the cascades of signaling events leading to NF‐κB activity and key components of the NF‐κB pathway are also identified. It has been suggested NF‐κB plays an important role in human diseases, especially inflammation‐related diseases. These studies make the NF‐κB an attractive target for disease treatment. This review aims to summarize the knowledge of the family members of NF‐κB, as well as the basic mechanisms of NF‐κB signaling pathway activation. We will also review the effects of dysregulated NF‐κB on inflammation, tumorigenesis, and tumor microenvironment. The progression of the translational study and drug development targeting NF‐κB for inflammatory diseases and cancer treatment and the potential obstacles will be discussed. Further investigations on the precise functions of NF‐κB in the physiological and pathological settings and underlying mechanisms are in the urgent need to develop drugs targeting NF‐κB for inflammatory diseases and cancer treatment, with minimal side effects.

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Section: Nf‐κb and Cancermentioning

confidence: 99%

NF‐κB signaling in inflammation and cancer

Zhang

et al. 2021

MedComm

188

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“…Thus, these viruses can contribute to the oncogenic state either through chronic NF-κB-dependent inflammation or by the sustained activity of viral activators of NF-κB. Examples of virally encoded NF-κB activators include the LMP1 protein of Epstein–Barr virus (B cell lymphoma, nasopharyngeal carcinoma) [ 64 ], the vFLIP protein of Kaposi sarcoma herpesvirus (sarcoma, lymphoma) [ 64 ], the Tax protein of HTLV-1 (T cell leukemia) [ 65 ], the X protein of hepatitis B virus (liver cancer) [ 66 ], and the E6 and E7 proteins of some strains of the human papillomavirus (cervical cancer) [ 67 ].…”

Section: Cancer Cell-induced Activation Of Nf-κbmentioning

confidence: 99%

NF-κB and Human Cancer: What Have We Learned over the Past 35 Years?

Gilmore

2021

Biomedicines

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Transcription factor NF-κB has been extensively studied for its varied roles in cancer development since its initial characterization as a potent retroviral oncogene. It is now clear that NF-κB also plays a major role in a large variety of human cancers, including especially ones of immune cell origin. NF-κB is generally constitutively or aberrantly activated in human cancers where it is involved. These activations can occur due to mutations in the NF-κB transcription factors themselves, in upstream regulators of NF-κB, or in pathways that impact NF-κB. In addition, NF-κB can be activated by tumor-assisting processes such as inflammation, stromal effects, and genetic or epigenetic changes in chromatin. Aberrant NF-κB activity can affect many tumor-associated processes, including cell survival, cell cycle progression, inflammation, metastasis, angiogenesis, and regulatory T cell function. As such, inhibition of NF-κB has often been investigated as an anticancer strategy. Nevertheless, with a few exceptions, NF-κB inhibition has had limited success in human cancer treatment. This review covers general themes that have emerged regarding the biological roles and mechanisms by which NF-κB contributes to human cancers and new thoughts on how NF-κB may be targeted for cancer prognosis or therapy.

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“…RNA-cleaving deoxyribozymes (DNAzymes) (DZ1) are synthetic single-stranded DNA-based catalytic molecules engineered to bind and to cleave target mRNA at specific sites. DZ1 was used as a therapeutic agent in a range of preclinical cancer models; it has entered clinical trials in Europe, China, and Australia [ 61 ]. This review surveys regulatory insights into mechanisms of diseases and in the use of catalytic DNA in vitro and in vivo, including nanosensors, nanoflowers, and nanosponges, and the emerging role of adaptive immunity underlying DNAzyme inhibition of cancer growth.…”

Section: Therapeutics Treatments In Ebv- and -Kshv-infected Malignanciesmentioning

confidence: 99%

Nanotechnology Frontiers in γ-Herpesviruses Treatments

Granato

2021

IJMS

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Epstein–Barr Virus (EBV) and Kaposi’s sarcoma associated-herpesvirus (KSHV) are γ-herpesviruses that belong to the Herpesviridae family. EBV infections are linked to the onset and progression of several diseases, such as Burkitt lymphoma (BL), nasopharyngeal carcinoma (NPC), and lymphoproliferative malignancies arising in post-transplanted patients (PTDLs). KSHV, an etiologic agent of Kaposi’s sarcoma (KS), displays primary effusion lymphoma (PEL) and multicentric Castleman disease (MCD). Many therapeutics, such as bortezomib, CHOP cocktail medications, and natural compounds (e.g., quercetin or curcumin), are administrated to patients affected by γ-herpesvirus infections. These drugs induce apoptosis and autophagy, inhibiting the proliferative and cell cycle progression in these malignancies. In the last decade, many studies conducted by scientists and clinicians have indicated that nanotechnology and nanomedicine could improve the outcome of several treatments in γ-herpesvirus-associated diseases. Some drugs are entrapped in nanoparticles (NPs) expressed on the surface area of polyethylene glycol (PEG). These NPs move to specific tissues and exert their properties, releasing therapeutics in the cell target. To treat EBV- and KSHV-associated diseases, many studies have been performed in vivo and in vitro using virus-like particles (VPLs) engineered to maximize antigen and epitope presentations during immune response. NPs are designed to improve therapeutic delivery, avoiding dissolving the drugs in toxic solvents. They reduce the dose-limiting toxicity and reach specific tissue areas. Several attempts are ongoing to synthesize and produce EBV vaccines using nanosystems.

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The interplay between EBV and KSHV viral products and NF-κB pathway in oncogenesis

Cited by 18 publications

References 114 publications

NF‐κB signaling in inflammation and cancer

NF‐κB signaling in inflammation and cancer

NF-κB and Human Cancer: What Have We Learned over the Past 35 Years?

Nanotechnology Frontiers in γ-Herpesviruses Treatments

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