Nasopharyngeal carcinoma cell line (C666-1) consistently harbouring Epstein-Barr virus

Cheung, Siu Tim; Huang, Dolly P.; Hui, Angela B.; Lo, Kwok Wai; Ko, Chuen Wai; Tsang, Yuen Shan; Wong, Nathalie; Whitney, Bruce M.; Lee, Joseph C. K.

doi:10.1002/(sici)1097-0215(19990924)83:1<121::aid-ijc21>3.0.co;2-f

Cited by 361 publications

(341 citation statements)

References 15 publications

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“…The EBV-positive C666-1 NPC cell line 34 was maintained in RPMI 1640 supplemented with 10% fetal bovine serum, 100 mg/l penicillin, and 100 mg/l streptomycin (RPMI-10) at 371C 5% CO 2 . C15 and C17 NP xenograft tumors were passaged in vivo, as described previously.…”

Section: Methodsmentioning

confidence: 99%

Targeted depletion of BMI1 sensitizes tumor cells to P53-mediated apoptosis in response to radiation therapy

et al. 2009

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Overexpression of BMI1 correlates with cancer development, progression, and therapy failure; however, the underlying molecular mechanisms remain to be fully elucidated. Using the C666-1 nasopharyngeal cancer (NPC) model, the role of BMI1 in mediating response of NPC cells to radiation therapy (RT) was investigated. The results showed a novel radioresistance function for BMI1 in NPC, wherein BMI1 depletion sensitized NPC cells to RT. Cell cycle analysis and transmission electron microscopy (TEM) showed apoptosis as the major mode of cell death, and the mitochondria as a primary targeted cellular organelle. Genomewide microarray and pathway analyses revealed that the P53 pathway is a critical mediator of this process. Cotransfection with siP53 rescued C666-1 cells from cytotoxicity upon BMI1 depletion and RT, thereby corroborating the role for P53. Pretreatment with the antioxidant, Trolox, inhibited apoptosis, indicating that production of reactive oxygen species (ROS) is also mediating cytotoxicity. In vivo, BMI1 depletion combined with RT abrogated tumor-forming capacity in SCID mice, showing the relevance of this process in a more complex tumor environment. Hence, we show a novel role for BMI1 in conferring radioresistance in cancer cells through the downregulation of p53-mediated apoptosis. These results suggest a potential strategy of BMI1 depletion combined with RT for tumors wherein BMI1 appears to be driving disease progression.

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Section: Methodsmentioning

confidence: 99%

Targeted depletion of BMI1 sensitizes tumor cells to P53-mediated apoptosis in response to radiation therapy

et al. 2009

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“…51321). The NPC cells C666-1 18 were simultaneously plated and transfected with 60 nM siRNA and 0.5 ll/cm 2 of Lipofectamine 2,000 (Invitrogen), diluted in OptiMEM I medium (Invitrogen). Using flow cytometry with a GAPDH-FAM siRNA (Ambion, No.…”

Section: Immunohistochemistrymentioning

confidence: 99%

Multiple dysregulated pathways in nasopharyngeal carcinoma revealed by gene expression profiling

Shi¹,

Bastianutto²,

Li³

et al. 2006

Intl Journal of Cancer

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Gene expression profiling was conducted using primary human nasopharyngeal carcinoma (NPC) biopsy samples to improve the understanding of the molecular pathways defining NPC and to identify novel potential therapeutic targets. RNA samples were extracted from 36 patients suspected to have NPC and hybridized onto the Affymetrix U133A chip. NPC was diagnosed in 19 patients, 11 had lymphoid hyperplasia (LH), and 6 were “normal” biopsies. Clinical stages for these NPC patients ranged from I–IV, including one M1. All NPC patients (except the M1) were treated with curative intent, which included radiotherapy alone (4 patients), or combined with chemotherapy (14 patients). Unsupervised clustering demonstrated a distinct NPC expression pattern, compared to normal biopsies. Subsequent Significance Analysis of Microarrays (SAM) derived from 14 NPC and 6 normal samples discovered 1,089 differentially regulated genes. Pathway analyses revealed novel insights into the mechanisms leading to NPC, whereby upregulation of NFκB2 and survivin play central roles in increasing resistance to apoptosis, and changes in integrin and WNT/β‐catenin signaling leading to uncontrolled proliferation. The role of survivin in resisting apoptosis in NPC was confirmed by RNA interference. Our data provide novel insights into the development and progression of NPC, and suggest survivin as a novel therapeutic target for NPC. © 2006 Wiley‐Liss, Inc.

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“…It is positively stained for cytokeratin, an epithelial marker. In addition, it expresses EBV nuclear antigen (EBNA), latent membrane proteins 1(LMP1) and LMP2 transcripts and thus resembles the EBV latency II pattern (Cheung et al, 1999). The LPM 1 and LMP 2A activate the phosphatidylinositol 3 0 -OH kinase (PI3-K)/protein kinase B (Akt) pathway, which is deregulated in various human malignancies.…”

Section: Introductionmentioning

confidence: 99%

Metformin Induces G1 Cell Cycle Arrest and Inhibits Cell Proliferation in Nasopharyngeal Carcinoma Cells

Zhao

Wen

Jia

et al. 2011

The Anatomical Record

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It has been reported that metformin, a biguanide derivative widely used in type II diabetic patients, has antitumor activities in some cancers by activation of AMP-activated protein kinase (AMPK). But its role in nasopharyngeal carcinoma (NPC) is not known. Here, we reported for the first time that 1-50 mM of metformin in a dose-and time-dependent manner suppressed cell proliferation and colony formation in NPC cell line, C666-1. Further studies revealed that the protein level of cyclin D1 decreased and the percentage of the cells in G0/G1 phase increased by 5 mM metformin treatment. Metformin also induced the phosphorylation of AMPK (T172) in a time-dependent manner. Mammalian target of rapamycin complex 1 (mTORC1), which is negatively regulated by AMPK and plays a central role in cell growth and proliferation, was inhibited by metformin, as manifested by dephosphorylation of its downstream targets 40S ribosomal S6 kinase 1 (S6K1) (T389), the eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1 (4E-BP1) (T37/46) and S6 (S235/236) in C666-1 cells. In a summary, metformin prevents proliferation of C666-1 cells by down-regulating cyclin D1 level and inducing G1 cell cycle arrest. AMPK-mediated inhibition of mTORC1 signaling may be involved in this process. Anat Rec, 294:1337Rec, 294: -1343Rec, 294: , 2011. V V C 2011 Wiley-Liss, Inc.

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Nasopharyngeal carcinoma cell line (C666-1) consistently harbouring Epstein-Barr virus

Cited by 361 publications

References 15 publications

Targeted depletion of BMI1 sensitizes tumor cells to P53-mediated apoptosis in response to radiation therapy

Targeted depletion of BMI1 sensitizes tumor cells to P53-mediated apoptosis in response to radiation therapy

Multiple dysregulated pathways in nasopharyngeal carcinoma revealed by gene expression profiling

Metformin Induces G1 Cell Cycle Arrest and Inhibits Cell Proliferation in Nasopharyngeal Carcinoma Cells

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