Identification and characterization of a 500-kb homozygously deleted region at 1p36.2-p36.3 in a neuroblastoma cell line

Ohira, Miki; Kageyama, Hajime; Mihara, Motohiro; Furuta, Shigeyuki; Machida, Takeshi; Shishikura, Tomotane; Takayasu, Hajime; Islam, Ashraful; Nakamura, Yohko; Takahashi, Masato; Tomioka, Nobumoto; Sato, Shigeru; Kaneko, Yasuhiko; Toyoda, Atsushi; Hattori, Masahira; Sakaki, Yoshiyuki; Ohki, Masafumi; Horii, Akira; Soeda, Eiichi; Inazawa, Johji; Seki, Naohiko; Kuma, Hidekazu; Nozawa, Iwao; Nakagawara, Akira

doi:10.1038/sj.onc.1203786

Cited by 76 publications

(74 citation statements)

References 39 publications

(38 reference statements)

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“…HeLa cells were used as a positive control (Liu et al, 1997). As reported (Ohira et al, 2000), DFF45 was undetectable in NB-1 and NB-C201 cells, whereas variable levels of DFF45 were detected in the remaining cells (Figure 2a, top panel). Previous results indicated that DFF45 is expressed as two transcripts of 3.8 and 2.4 kb in length .…”

supporting

confidence: 58%

“…As described by Ohira et al (2000), we failed to detect any mutations within DFF45 in NBLs. Similar results were reported by Yang et al (2001).…”

supporting

confidence: 51%

“…Extensive loss of heterozygosity (LOH) analysis narrowed the overlapping deleted region of 1p in NBL, suggesting that there could be at least three NBL suppressor loci (Schleiermacher et al, 1994;Takeda et al, 1994;Amler et al, 1995;Cheng et al, 1995;Martinsson et al, 1995;White et al, 1995). We found that NBL cell lines, NB-1 and NB-C201, carry a homozygous deletion at 1p36.2, and identified six genes within this region including DFF45/ICAD, PGD, CORT, UFD2a, KIF1B-b and PEX14 (Ohira et al, 2000). Among them, we have demonstrated that UFD2a promotes the proteasome-dependent degradation of p73 (Hosoda et al, 2005).…”

mentioning

confidence: 54%

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DFF45/ICAD restores cisplatin-induced nuclear fragmentation but not DNA cleavage in DFF45-deficient neuroblastoma cells

et al. 2007

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We have previously defined a homozygously deleted region at chromosome 1p36.2-p36.3 in human neuroblastoma cell lines, NB-1 and NB-C201, and identified six genes including DFF45/ICAD within this region. In this study, we found that NB-C201 cells are much more resistant to various genotoxic stresses such as cisplatin (CDDP) than CHP134 and SH-SY5Y cells that do not have the homozygous deletion. To examine a role(s) of DFF45 in the regulation of apoptosis in response to CDDP, we have established stably DFF45-expressing NB-C201 cell clones (DFF45-1 and DFF45-3) and a control cell clone (NB-C201-C) using a retrovirus-mediated gene transfer. In contrast to NB-C201-C cells, DFF45-3 cells displayed apoptotic nuclear fragmentation in response to CDDP. Although CDDP-induced proteolytic cleavage of procaspase-3 and DFF45 in DFF45-3 cells, we could not detect a typical apoptotic DNA fragmentation. Additionally, deletion analysis revealed that C-terminal region of DFF45 is required for inducing nuclear fragmentation. Unexpectedly, (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays demonstrated that DFF45 has undetectable effect on CDDP sensitivity of NB-C201 cells. Taken together, our present results suggest that DFF45/DFF40 system may be sufficient for CDDP-induced nuclear fragmentation but not DNA cleavage.

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supporting

confidence: 58%

“…As described by Ohira et al (2000), we failed to detect any mutations within DFF45 in NBLs. Similar results were reported by Yang et al (2001).…”

supporting

confidence: 51%

mentioning

confidence: 54%

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DFF45/ICAD restores cisplatin-induced nuclear fragmentation but not DNA cleavage in DFF45-deficient neuroblastoma cells

et al. 2007

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“…DFFA is in fact localized in the 1p-deleted SRO (smallest region of overlap) at 1p36.2-3 defined by our group, and according to Ohira et al (2000) within a homozygously deleted region in a neuroblastoma cell line. CASP9 is localized at 1p36.21, approximately 4 Mb proximal to our SRO-region, but still in the region commonly deleted by neuroblastoma tumours.…”

mentioning

confidence: 85%

“…Fifteen of the 16 BACs included in this study reside in this region. According to distances in the UCSC brow- Analyses of CASP9 and DFFA in human neuroblastomaser the SRO-region is approximately 3.5 Mb, and it partially overlaps the 500 kb homozygously deleted region defined by Ohira et al (2000). Four of the 16 BACs (318-F24, 513-I12, 347-P23 and 387-I22) reside in the overlapping region ( Figure 1C,D).…”

Section: Genetics and Genomicsmentioning

confidence: 99%

Analyses of apoptotic regulators CASP9 and DFFA at 1P36.2, reveal rare allele variants in human neuroblastoma tumours

et al. 2002

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The genes encoding Caspase-9 and DFF45 have both recently been mapped to chromosome region 1p36.2, that is a region alleged to involve one or several tumour suppressor genes in neuroblastoma tumours. This study presents an update contig of the 'Smallest Region of Overlap of deletions' in Scandinavian neuroblastoma tumours and suggests that DFF45 is localized in the region. The genomic organization of the human DFF45 gene, deduced by in-silico comparisons of DNA sequences, is described for the first time in this paper. In the present study 44 primary tumours were screened for mutation by analysis of the genomic sequences of the genes. In two out of the 44 tumours this detected in the DFFA gene one rare allele variant that caused a non-polar to a polar amino acid exchange in a preserved hydrophobic patch of DFF45. One case was hemizygous due to deletion of the more common allele of this polymorphism. Out of 194 normal control alleles only one was found to carry this variant allele, so in respect of it, no healthy control individual out of 97 was homozygous. Moreover, our RT -PCR expression studies showed that DFF45 is preferably expressed in low-stage neuroblastoma tumours and to a lesser degree in high-stage neuroblastomas. We conclude that although coding mutations of Caspase-9 and DFF45 are infrequent in neuroblastoma tumours, our discovery of a rare allele in two neuroblastoma cases should be taken to warrant further studies of the role of DFF45 in neuroblastoma genetics.

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Insulin and solid‐phase synthesis, 1964–1970

Marglin¹

2008

Biopolymers

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A chemical synthesis of insulin was undertaken by solid phase principles during the period 1964–70. © 2007 Wiley Periodicals, Inc. Biopolymers (Pept Sci) 90: 200–202, 2008.This article was originally published online as an accepted preprint. The “Published Online” date corresponds to the preprint version. You can request a copy of the preprint by emailing the Biopolymers editorial office at biopolymers@wiley.com

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Identification and characterization of a 500-kb homozygously deleted region at 1p36.2-p36.3 in a neuroblastoma cell line

Cited by 76 publications

References 39 publications

DFF45/ICAD restores cisplatin-induced nuclear fragmentation but not DNA cleavage in DFF45-deficient neuroblastoma cells

DFF45/ICAD restores cisplatin-induced nuclear fragmentation but not DNA cleavage in DFF45-deficient neuroblastoma cells

Analyses of apoptotic regulators CASP9 and DFFA at 1P36.2, reveal rare allele variants in human neuroblastoma tumours

Insulin and solid‐phase synthesis, 1964–1970

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