Two epithelial tumor cell lines (HNE-1 and HONE-1) latently infected with Epstein-Barr virus that were derived from nasopharyngeal carcinomas.

Abstract

Two epithelial tumor cell lines were established from biopsy specimens of nasopharyngeal carcinomas (NPC). The specimens were taken from poorly differentiated squamous cell carcinomas ofthe nasopharynx. The tissues were prepared for cell culture and eventually two continuous epithelial cell lines were obtained and designated HONE-1 and HNE-1. Light and electron microscopic examination of these two cell lines demonstrated cells with an epithelial morphology including the presence of desmosomes. The HNE-1 cell line has been passaged more than 100 times and the HONE-1 cell line has been passaged more than 90 times. It was found that early-passage uncloned HNE-1 cells (passage 23) could be superinfected with the B95-8 and NPC-EBV isolates as demonstrated by the induction of Epstein-Barr virus (EBV)-specific early antigen(s) in a small percentage of the cells; HONE-1 cells could also be superinfected with EBV. Southern blot analysis detected EBV DNA in samples from uncloned HNE-1 cells at passages 12, 17, 21, 27, and 35. However, by passage 45, EBV DNA could no longer be detected in HNE-1 cells by Southern blot analysis. The EBV genome was detected in parental HONE-1 cells at subculture 9 and in clone 40 cells up to passage 40 thus far. When HNE-1 cells were examined for the expression of the EBV-encoded nuclear antigen (EBNA) at passage 12, only about 10% of the cells were found to be positive. The percentage of EBNA-positive HNE-1 cells decreased as the cells were passaged. A similar loss of EBNA was observed in uncloned HONE-1 cells, but not in HONE-1 clone 40 cells. In clone 40, which has been passaged 40 times thus far, 85-90% of the cells are still EBNA-positive. The data suggest that EBV genome-positive HNE-1 and HONE-1 cells were lost as the cells were cultivated in vitro and that cloning the cells at an early passage level may be critical in maintaining EBV genome-positive epithelial NPC cells. These EBV genomepositive epithelial NPC cell lines will be useful for studying the association of EBV and NPC.

The major 8p22 tumor suppressor DLC1 is frequently silenced by methylation in both endemic and sporadic nasopharyngeal, esophageal, and cervical carcinomas, and inhibits tumor cell colony formation

“…Cell lines, tumor and normal tissue samples Cell lines used were: 12 NPC (C666-1, CNE-1, CNE-2, HK1, HNE1, HNE2, HNE3, HONE1, TW-01, BM1, 5-8F and 6-10B) (Glaser et al, 1989;Qiu et al, 2004;Ying et al, 2005), 15 esophageal (EC1, EC18, EC109, HKESC1, HKESC2, SLMT-1, KYSE30, KYSE70, KYSE140, KYSE150, KYSE180, KYSE270, KYSE410, KYSE510 and KYSE520) (Tang et al, 2001;Ying et al, 2006), nine breast (MCF7, ZR-75-1, MB-231; T47D, MB-468, MB-435, SKBR3, BT549, and YCC-B2) (Kim et al, 2005;Ying et al, 2005) and eight cervical carcinoma (HeLa,Caski,C33A,SiHa,808,866,879 and 915) (Steenbergen et al, 2004;Ying et al, 2006). NP69, an SV40 Tantigen-immortalized nasopharyngeal epithelial cell line with many features of normal nasopharyngeal epithelial cells was used as a 'normal' control for NPC (Tsao et al, 2002).…”

MicroRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN

“…Among the cell lines that were employed in this study, HONE1 and C666 cells are poorly differentiated and are EBV positive. 33,34 HK1 is well differentiated and EBV negative. 35 Our results showed that anti-miR-200c transfection decreased cell growth, invasion, and migration, while miR-200c overexpression accelerates these processes.…”

Impact of G2 checkpoint defect on centromeric instability

“…The new aberrations (Supplementary Table S2 Cyclin B1 knockdown reinforces G 2 checkpoint function and reduces centromeric instability in cancer cells We next tested the impact of G 2 checkpoint defect on centromeric instability in cancer cells. Three cancer cell lines of different cell types: HeLa (cervical cancer), SLMT-1 (esophageal cancer) (Tang et al, 2001) and HNE-1 (nasopharyngeal cancer) (Glaser et al, 1989) were examined. Although cancer cells are known to retain some degree of G 2 checkpoint function, we anticipated that the G 2 checkpoint in cancer cells may not be as stringent as in normal cells.…”