Epstein–Barr virus-encoded small RNA induces insulin-like growth factor 1 and supports growth of nasopharyngeal carcinoma-derived cell lines

Iwakiri, Dai; Sheen, Tzung‐Shiahn; Chen, Jen-Yan; Huang, Dolly P.; Takada, Kenzo

doi:10.1038/sj.onc.1208357

Cited by 109 publications

(77 citation statements)

References 11 publications

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“…The growth stimulatory properties of EBER have been demonstrated in several reports (Komano et al, 1999;Ruf et al, 2000;Yamamoto et al, 2000;Yajima et al, 2005). Previously, we have shown that EBER induces the expression of various cellular cytokines, interleukin 10 (IL-10) in B lymphocytes (Kitagawa et al, 2000), insulin-like growth factor 1 (IGF-1) in epithelial cells (Iwakiri et al, 2003(Iwakiri et al, , 2005 and IL-9 in T lymphocytes (Yang et al, 2004), each of which acts as an autocrine growth factor. However, the mechanisms by which EBER induces these cytokines have remained unresolved.…”

Section: Introductionmentioning

confidence: 99%

“…EBER contributes to malignant phenotype in BL cells (Komano et al, 1999) and induces several cytokines in various cell types. In EBV-infected epithelial cells, EBER induces IGF-1 (Iwakiri et al, 2003(Iwakiri et al, , 2005 whereas in EBV-infected T cells, EBER induces IL-9 (Yang et al, 2004). EBER is also critical in the efficient EBV-induced growth transformation of B lymphocytes (Yajima et al, 2005).…”

Section: Il-10 Induction By Rig-i-mediated Irf-3 Signaling M Samanta mentioning

confidence: 99%

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Epstein–Barr virus-encoded small RNA induces IL-10 through RIG-I-mediated IRF-3 signaling

2008

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Section: Introductionmentioning

confidence: 99%

Section: Il-10 Induction By Rig-i-mediated Irf-3 Signaling M Samanta mentioning

confidence: 99%

Epstein–Barr virus-encoded small RNA induces IL-10 through RIG-I-mediated IRF-3 signaling

2008

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“…It has been demonstrated that EBERs play a role in EBV-mediated oncogenesis in EBV latently-infected cells. First, EBERs affect membrane signaling by initiating the production of various interleukins (ILs) that are involved in cell growth, such as IL-6, IL-9, or insulin-like growth factor-1 (Ho et al, 1999;Kitagawa et al, 2000;Iwakiri et al, 2003;Iwakiri et al, 2005). They also play a role in regulation of apoptosis by binding the RNA-dependent protein kinase (PKR), subsequently inhibiting PKRmediated apoptosis in the EBV infected cells (Komano et al, 1999;Yamamoto et al, 2000).…”

Section: Treatment Strategies For the Patients With Ebv-associated Chlmentioning

confidence: 99%

“…Nt (Ho et al, 1999;Komano et al, 1999;Kitagawa et al, 2000;Yamamoto et al., 2000;Iwakiri et al, 2003;Iwakiri et al, 2005;Samanta et al, 2006;Samanta et al, 2008;Iwakiri et al, 2009;Iwakiri and Takada, 2010 Immunization with LMP1 gene or polyepitope expression vectors Taylor et al, 2004;Smith et al, 2006;Pan et al, 2009;Lutzky et al, 2010;Chia et al, Immunization with LMP2A gene or polyepitope expression vectors (Taylor et al, 2004;Smith et al, 2006;Pan et al, 2009;Lutzky et al, 2010;Chia et al, 2011) LMP2B Modulation of innate immune response nt TLR: Toll-like receptor, RIG: retinoic acid-inducible gene, PKR: RNA-dependent protein kinase, Nt: not tested, CTL: cytotoxic T lymphocyte, DC: dendritic cells.…”

Section: Inhibition Of Apoptosis (Pkr)mentioning

confidence: 99%

Epstein-Barr Virus-Associated Classical Hodgkin Lymphoma and Its Therapeutic Strategies

Lee¹

2011

Biomolecules and Therapeutics

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Lymphoma is a type of cancer involving cells of the immune system, and has two major categories: Hodgkin lymphoma (HL) and all other lymphomas (non-HL). Although the two types may display the same symptoms, they are readily distinguishable via microscopic examination, and differ in the way they develop, spread and are treated. HL is a unique clinicopathological disorder characterized by the rare presence of malignant cells (usually accounting for 0.1% to 10% of the cells in the total tumor mass) in a background of a nonneoplastic cellular microenvironment comprising T-and Blymphocytes and other cell types (Weiss et al., 1999). In the United States, about 8,500 new cases of HL were expected to be diagnosed in 2010, and the overall incidence is increasing each year (Maggioncalda et al., 2011).Although the pathogenesis of HL is still largely unknown, the association of HL with Epstein-Barr virus (EBV) infection has been demonstrated in many reports. For examples, HL patients show elevated antibody titers to EBV antigens (Levine et al., 1971), and the risk of developing HL is increased up to three-fold in population that have experienced infectious mononucleosis caused by primary EBV infection (Gutensohn Over the past few decades, our understanding of the epidemiology and immunopathogenesis of Hodgkin lymphoma (HL) has made enormous advances. Consequently, the treatment of HL has changed signifi cantly, rendering this disease of the most curable human cancers. To date, about 80% of patients achieve long-term disease-free survival. However, therapeutic challenges still remain, particularly regarding the salvage strategies for relapsed and refractory disease, which need further identifi cation of better prognostic markers and novel therapeutic schemes. Although the precise molecular mechanism by which Epstein-Barr virus (EBV) contributes to the generation of malignant cells present in HL still remains unknown, current increasing data on the role of EBV in the pathobiology of HL have encouraged people to start developing novel and specifi c therapeutic strategies for EBVassociated HL. This review will provide an overview of therapeutic approaches for acute EBV infection and the classical form of HL (cHL), especially focusing on EBV-associated HL cases. and Cole, 1980), and EBV DNA/RNA can be detected in HL tissues (Brink et al., 1997), suggesting that as a primary event in the development of this disease, EBV infection may play a very crucial role in the pathogenesis of HL. AbstractAccording to a population-based cohort study, the frequency of EBV associated HL among total HL cases varies from 30 to 50% (in certain cases even higher; >90% in developing and underdeveloped countries, and >95% in HIV associated cases), and most of them appear in classical Hodgkin lymphoma (cHL), the major type of HL (Herbst et al., 1991;Pallesen et al., 1991;Ambinder et al., 1993;Leoncini et al., 1996). Since EBV is an oncogenic virus that is able to subvert cellular processes supporting growth and survival, the approach to unravel the f...

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“…With these inspiring achievements, some scholars were intrigued by the autocrine growth of several tumor cells and successfully discovered the link between cytokine induction and EBERs in B and T lymphocyte, gastric carcinoma and nasopharyngeal carcinoma in the following decade. More recently, our knowledge has been deepened by unveiling the TLR3 and RIG-I signaling pathways induced by EBERs, which are responsible for the autocrine growth of lymphomas and some EBV associated pathogenesis (Iwakiri et al, 2005;Samanta et al, 2008). However, the accurate role of EBERs in the pathogenesis of NPC is still obscure.…”

Section: Introductionmentioning

confidence: 99%

Pathologic Significance of EBV Encoded RNA in NPC

Li¹,

Yang²,

Sun³

2012

Carcinogenesis, Diagnosis, and Molecular Targeted Treatment for Nasopharyngeal Carcinoma

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Epstein–Barr virus-encoded small RNA induces insulin-like growth factor 1 and supports growth of nasopharyngeal carcinoma-derived cell lines

Cited by 109 publications

References 11 publications

Epstein–Barr virus-encoded small RNA induces IL-10 through RIG-I-mediated IRF-3 signaling

Epstein–Barr virus-encoded small RNA induces IL-10 through RIG-I-mediated IRF-3 signaling

Epstein-Barr Virus-Associated Classical Hodgkin Lymphoma and Its Therapeutic Strategies

Pathologic Significance of EBV Encoded RNA in NPC

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