Characterization of DNA rearrangements of N‐myc gene amplification in three neuroblastoma cell lines by pulsed‐field gel electrophoresis

Katô, Hiroshi; Okamura, Koji; Kurosawa, Yoshikazu; Kishikawa, Teruaki; Hashimoto, Keiichiro

doi:10.1016/0014-5793(89)80790-2

Cited by 19 publications

(12 citation statements)

References 24 publications

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“…The reason for this is not clear, but it is possible that apoptosis pathways in neuroblastoma might be impaired. Our results showed that SH-SY5Y that has no MYCN gene amplification 28 was sensitive to ASK1-induces apoptosis, whereas IMR-32 that has amplification 29,30 did not show any response at all. We were not able to detect any activation of p38 MAPK in IMR-32 cells although the same kinase could be activated by osmotic shock given by sorbitol.…”

Section: K709rmentioning

confidence: 59%

ASK1 resistant neuroblastoma is deficient in activation of p38 kinase

et al. 2001

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Apoptosis Signal-regulating Kinase 1 (ASK1) is known to either induce apoptosis or differentiation in various cell lines of neuronal origin. We analyzed the effect of the constitutively active mutant of ASK1 (ASK1-DN) in an adenoviral vector in four neuroblastoma cell lines, two murine, C1300 and NXS2, and two human, SH-SY5Y and IMR-32. Already after 24 h upon infection, C1300 and SH-SY5Y cells arrested in growth when judged by [ 3 H]thymidine incorporation, and the majority of the cells demonstrated apoptotic appearance, which was confirmed by DNA-laddering in gel electrophoresis. In contrast, NXS2 and IMR-32 cell lines remained unaffected. Immunoblotting revealed strongly phosphorylated p38 MAPK accompanied by weakly phosphorylated JNK in C1300 and SH-SY5Y, whereas none of these kinases were activated by adenoviruses expressing the kinase negative ASK1 mutant or b-galactosidase. There was no expressionofphosphorylatedkinasesinIMR-32cells, butNXS2 showed a faint band of phosphorylated p38 MAPK. Addition of thep38MAPKspecificinhibitor,SB203580,protectedC1300and SH-SY5Y cells from apoptosis induced by ASK1-DN. The antineoplastic agent, paclitaxel, activates ASK1 and JNK, and promotes the in vitro assembly of stable microtubules. Addition of10 nMpaclitaxelsensitisedtheNXS2celllinetoASK1-induced cell death. Our results indicate that ASK1 induces apoptosis in neuroblastoma cells mainly via the p38 MAPK pathway, and resistant neuroblastoma cells can be sensitised to ASK1 by paclitaxel.

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Section: K709rmentioning

confidence: 59%

ASK1 resistant neuroblastoma is deficient in activation of p38 kinase

et al. 2001

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“…Circular DNAs harboring MYC were also present (Von Hoff et al, 1988). Other studies have shown that the size and sequence of amplified regions differ between the neuroblastoma tumors and cell lines (Montgomery et al, 1983;Shiloh et al, 1985Shiloh et al, , 1986Shiloh et al, , 1987Amler and Schwab, 1989;Kato et al, 1989). These results led us to consider MYCN amplification in two different contexts: one is rearrangement in the initial stage of amplification, and the other is rearrangement during subsequent stages.…”

Section: Discussionmentioning

confidence: 95%

“…There have been several studies aimed at understanding the structural organization of amplified regions Montgomery et al, 1983;Shiloh et al, 1985Shiloh et al, , 1986Shiloh et al, , 1987Kinder et al, 1986;Zehnbauer et al, 1988;Amler and Schwab, 1989;Kato et al, 1989; Akiyama and Nishi, 1991;Nishi et al, 1992), whereas others have tried to discover the mechanism operative during the early events of amplification (Von Hoff et al, 1988;IIunt et al, 1900).…”

Section: Introductionmentioning

confidence: 99%

Structural organization of MYCN amplicons of neuroblastoma tumors, xenografts, and cell lines characterized by the sequences encompassing the MYCN amplicons in a human neuroblastoma cell line

Akiyama

Kanda

Yamada

et al. 1993

Genes Chromosomes & Cancer

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We characterized differences in the structural organization of the MYCN amplicons of a number of neuroblastomas by analyzing 8 contigs spanning 330 kb cloned from the MYCN amplicon of a neuroblastoma cell line. Some regions were amplified in almost all specimens, the conserved regions (CRs), and others were differentially amplified in some subsets, the non-conserved regions (NCRs). CRs constituted only 20% of the 330 kb region, with the remainder being NCRs. The regions that inevitably co-segregate with the MYCN gene make up the core, whereas flanking regions are retained at random. If a histogram of the frequency with which the amplified NCR sequences from one specimen match those of the cell line MC-NB-I shows a random distribution, the NCRs would co-segregate with MYCN as a result of random events. However, both the tumors and cell lines/xenografts showed a distribution with two distinct peaks; one from a group containing a small number of sequences with a fairly high degree of homology to the NCRs of MC-NB-I, and the other from a group containing a large number of sequences with little homology. These results indicate that the flanking segments are preferentially co-segregated with MYCN by a non-random mechanism.

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“…Immunoblotting confirmed that CREB is expressed in SHSY5Y and BE2 cells, and N-myc is overexpressed in IMR32, BE2 and C1300 cells (not shown). 16 …”

Section: Mash1-enhancer Active In Neuroblastomamentioning

confidence: 99%

A novel MASH1 enhancer with N-myc and CREB-binding sites is active in neuroblastoma

et al. 2006

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Neuroblastoma is one of the most common solid tumors in childhood. With the aim of developing a targeting vector for neuroblastoma, we cloned and characterized an enhancer in the 5 0 -flanking regions of the MASH1 gene by a random-trap method from a 36 kb cosmid DNA. The enhancer-containing clone was identified by the expression of GFP when transfected into neuroblastoma cell lines. The enhancer-luciferase activity is higher in neuroblastoma cell lines, IMR32, BE2 and SH-SY5Y, compared with those in non-neuroblastoma cell lines, U1242 glioma, N417 small cell lung cancer and EOMA hemangioma. The core enhancer was determined within a 0.2 kb fragment, yielding three-to fourfold higher activity than that of the MASH1 promoter alone in IMR32 and BE2. This area possesses GATA-and CREB-binding sites, as well as the E-box. EMSA on this area demonstrated that CREB/ATF could bind the DNA. Chromatin immunoprecipitation assay revealed that N-myc, CREB, and co-activators CBP and PCAF, but not HDAC1, are bound to the core enhancer at the same time as the co-activators and N-myc bind to the promoter. This supports the idea that the commonly overexpressed genes HASH1 and N-myc are regulated in concert, confirming their importance as prognostic markers or targets for therapy.

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Characterization of DNA rearrangements of N‐myc gene amplification in three neuroblastoma cell lines by pulsed‐field gel electrophoresis

Cited by 19 publications

References 24 publications

ASK1 resistant neuroblastoma is deficient in activation of p38 kinase

ASK1 resistant neuroblastoma is deficient in activation of p38 kinase

Structural organization of MYCN amplicons of neuroblastoma tumors, xenografts, and cell lines characterized by the sequences encompassing the MYCN amplicons in a human neuroblastoma cell line

A novel MASH1 enhancer with N-myc and CREB-binding sites is active in neuroblastoma

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