A naturally derived gastric cancer cell line shows latency I Epstein–Barr virus infection closely resembling EBV-associated gastric cancer

Oh, Sang Taek; Seo, Jae Hyun; Moon, Uk Yeol; Kang, Kyoung‐Tak; Shin, Dong Jik; Yoon, Sungjoo Kim; Kim, Woo Ho; Park, Jae Gahb; Lee, Suk Kyeong

doi:10.1016/j.virol.2003.12.005

Cited by 80 publications

(78 citation statements)

References 18 publications

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“…EBV-positive GC presents histologically and pathologically different features from EBV-negative GC (Akiba et al, 2008;Lee et al, 2004). EBV-positive GC exerts modulated latency 1, expressing latent genes such as EBNA1, LMP2A, BamHI-A rightward frame 1 (BARF1), and EBV-encoded RNAs (EBERs) (Imai et al, 1994;Oh et al, 2004). EBV lytic genes such as BamHI-Z leftward and rightward reading frame 1 (BZLF1 and BRLF1, respectively) are also expressed in EBVpositive GC following anti-cancer drug treatment (Feng et al, 2002;Jung et al, 2007b).…”

Section: Introductionmentioning

confidence: 99%

Association between Epstein-Barr Virus Infection and Chemoresistance to Docetaxel in Gastric Carcinoma

Shin

Kim

Lee

2011

Molecules and Cells

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Epstein-Barr virus (EBV) is associated with human cancers such as nasopharyngeal carcinoma, Burkitt's lymphoma, Hodgkin's disease, and gastric carcinoma (GC). EBV is associated with about 10% of all GC cases globally. EBV-associated GC has distinct features from EBV-negative GC. However, it is still unclear if EBV infection has any effect on GC chemoresistance. Cell proliferation assay, cell cycle analysis, and active caspase Western blot revealed that the EBV-positive GC cell line (AGS-EBV) showed chemoresistance to docetaxel compared to the EBV-negative GC cell line (AGS). Docetaxel treatment increased expression of Bax similarly in AGS and AGS-EBV cell lines. However, Bcl-2 induction was markedly higher in AGS-EBV cells, after docetaxel treatment. Although docetaxel increased the expression of p53 to a similar extent in both cell lines, induction of p21 in AGS-EBV cells was lower than in AGS cells. Furthermore, expression of survivin was higher in AGS-EBV cells than in AGS cells following docetaxel treatment as well as at basal state. EBVlytic gene expression was induced by docetaxel treatment in AGS-EBV cells. The results suggest that EBV infection and lytic induction confers chemoresistance to GC, possibly by regulating cellular and EBV latent and lytic gene expression.

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Section: Introductionmentioning

confidence: 99%

Association between Epstein-Barr Virus Infection and Chemoresistance to Docetaxel in Gastric Carcinoma

Shin

Kim

Lee

2011

Molecules and Cells

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“…SNU-719 is a naturally derived EBV-infected GC cell line (24,25). AGS is an EBV-negative GC cell line (26) that was used to transduce the LMP2A gene from SNU-719 using a retroviral vector.…”

Section: Methodsmentioning

confidence: 99%

“…Previously, we reported that SNU-719 is a gastric carcinoma cell line that is naturally infected with EBV and that this cell line expresses EBNA-1, LMP2A and EBERs but not LMP1 similar to most EBVaGC cases (24). To examine the oncogenic potential of LMP2A in gastric epithelial cells, the LMP2A gene from SNU-719 was cloned and transduced into an EBV-negative gastric cancer cell line, AGS, using a retroviral vector and the growth ability of cell clones expressing LMP2A was analyzed.…”

Section: Introductionmentioning

confidence: 96%

Establishment and characterization of gastric carcinoma cell clones expressing LMP2A of Epstein-Barr virus

Seo

Jun²,

Kwon³

et al. 2009

Int J Mol Med

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Abstract. Although Epstein-Barr virus (EBV) has been detected in 5-15% of gastric carcinoma (GC) cases, the mechanism by which EBV contributes to its tumorigenesis remains unclear. Only a subset of EBV latent proteins such as EBV nuclear antigen-1 and latent membrane protein 2A (LMP2A) are expressed in EBV-associated GC (EBVaGC) cases. In this study, to elucidate the role of LMP2A in the tumorigenesis of EBVaGC, we established permanent cell lines expressing LMP2A. The LMP2A gene was cloned from a naturally EBV-infected EBVaGC cell line, SNU-719 and transduced into an EBV-negative GC cell line, AGS, using a retroviral vector. The sequence of SNU-719 LMP2A showed several conserved variations compared to that of the prototype EBV strain B95-8 LMP2A. Four of seven established cell clones expressed LMP2A protein at detectable levels. These cell clones did not show enhanced cell growth compared to control cells in normal or low serum-containing medium. Furthermore, LMP2A expression had no effect on colony forming ability of the cell clones in soft agar. Our results suggest that LMP2A alone has little effect on tumorigenesis of EBVaGC.

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“…23 In this study, we examined the effect of ionizing radiation on EBV genome expression in the SNU-719 cell line, a human gastric epithelial carcinoma cell line with natural EBV infection. 24 This cell line shows modified latency 1 EBV infection closely resembling EBVaGC and was reported to develop tumors when injected into nude mice and the developed tumor displayed similar characteristics with EBVaGC. 24,25 …”

mentioning

confidence: 90%

“…24 This cell line shows modified latency 1 EBV infection closely resembling EBVaGC and was reported to develop tumors when injected into nude mice and the developed tumor displayed similar characteristics with EBVaGC. 24,25 …”

mentioning

confidence: 90%

Radiation-induced Epstein–Barr virus reactivation in gastric cancer cells with latent EBV infection

et al. 2017

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Epstein–Barr virus, a ubiquitous human herpes virus with oncogenic activity, can be found in 6%–16% of gastric carcinomas worldwide. In Epstein–Barr virus–associated gastric carcinoma, only a few latent genes of the virus are expressed. Ionizing irradiation was shown to induce lytic Epstein–Barr virus infection in lymphoblastoid cell lines with latent Epstein–Barr virus infection. In this study, we examined the effect of ionizing radiation on the Epstein–Barr virus reactivation in a gastric epithelial cancer cell line (SNU-719, an Epstein–Barr virus–associated gastric carcinoma cell line). Irradiation with X-ray (dose = 5 and 10 Gy; dose rate = 0.5398 Gy/min) killed approximately 25% and 50% of cultured SNU-719 cells, respectively, in 48 h. Ionizing radiation increased the messenger RNA expression of immediate early Epstein–Barr virus lytic genes (BZLF1 and BRLF1), determined by real-time reverse transcription polymerase chain reaction, in a dose-dependent manner at 48 h and, to a slightly lesser extent, at 72 h after irradiation. Similar findings were observed for other Epstein–Barr virus lytic genes (BMRF1, BLLF1, and BcLF1). After radiation, the expression of transforming growth factor beta 1 messenger RNA increased and reached a peak in 12–24 h, and the high-level expression of the Epstein–Barr virus immediate early genes can convert latent Epstein–Barr virus infection into the lytic form and result in the release of infectious Epstein–Barr virus. To conclude, Ionizing radiation activates lytic Epstein–Barr virus gene expression in the SNU-719 cell line mainly through nuclear factor kappaB activation. We made a brief review of literature to explore underlying mechanism involved in transforming growth factor beta–induced Epstein–Barr virus reactivation. A possible involvement of nuclear factor kappaB was hypothesized.

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A naturally derived gastric cancer cell line shows latency I Epstein–Barr virus infection closely resembling EBV-associated gastric cancer

Cited by 80 publications

References 18 publications

Association between Epstein-Barr Virus Infection and Chemoresistance to Docetaxel in Gastric Carcinoma

Association between Epstein-Barr Virus Infection and Chemoresistance to Docetaxel in Gastric Carcinoma

Establishment and characterization of gastric carcinoma cell clones expressing LMP2A of Epstein-Barr virus

Radiation-induced Epstein–Barr virus reactivation in gastric cancer cells with latent EBV infection

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