Lack of DMBT1 expression in oesophageal, gastric and colon cancers

Mori, Masaki; Shiraishi, Takeshi; Tanaka, Shinji; Yamagata, Motoyuki; Mafune, Ken–ichi; Tanaka, Yoïchi; Ueo, Hiroaki; Barnard, Graham F.; Sugimachi, Keizō

doi:10.1038/sj.bjc.6690035

Cited by 89 publications

(82 citation statements)

References 7 publications

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“…It is a glycoprotein containing multiple scavenger receptor cysteine-rich (SRCR) domains separated by SRCR-interspersed domains (SID) (Mollenhauer et al, 1997. Somatic alterations in genome structure affecting the DMBT1 gene region and loss of DMBT1 gene expression have been observed in glioblastomas, medulloblastomas (Mollenhauer et al, 1997) and in non-CNS tumors such as lung cancers (Takeshita et al, 1999;Wu et al, 1999) and GI tumors (Mori et al, 1999). In malignant astrocytic tumors further studies confirmed either hemizygous or homozygous alterations (Fujisawa et al, 1999;Sasaki et al, 2001;Somerville et al, 1998;Steck et al, 1999).…”

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confidence: 80%

Rare mutations of the DMBT1 gene in human astrocytic gliomas

et al. 2002

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The Deleted in Malignant Brain Tumors 1 gene (DMBT1) has been proposed as a tumor suppressor gene candidate in human brain tumors, based on the observation of homozygous deletions affecting the DMBT1 region or part of the gene. In order to support this hypothesis, we performed a mutational analysis of the entire coding region of DMBT1, employing SSCP analysis and direct DNA sequencing in a series of 79 astrocytic gliomas. Five somatic mutations were detected. Two mutations, one of which resulted in an amino acid exchange, occurred in glioblastomas. One pilocytic astrocytoma carried two missense mutations and another pilocytic astrocytoma contained a somatic mutation, not affecting the presumed protein. In addition, 21 of the 27 single nucleotide polymorphisms identified in this study have not been recognized previously. The data indicate, that small mutations are not a frequent finding in gliomas.

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confidence: 80%

Rare mutations of the DMBT1 gene in human astrocytic gliomas

et al. 2002

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“…Lack of DMBT1 expression has also been reported in medulloblastoma and glioblastoma, 20 lung, 24 as well as esophageal, gastric and colon cancer. 25 The possible factors that cause lack of DMBT1 expression are still unclear. Somerville et al 22 suggested that homozygous loss at 74k STS, located at the N-terminal position of DMBT1, can be related with lack of DMBT1 expression because of its putative vicinity with the promoter.…”

Section: Discussionmentioning

confidence: 99%

“…4 Homozygous deletion has also been found in medulloblastoma, 20 oligodendroglioma, 23 lung cancer 24 and gastrointestinal cancer. 25 Although the function of this gene is not clear yet, the high frequency of deletions at the DMBT1 locus makes it to be one of the putative candidate tumor suppressor genes in chromosome 10.…”

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confidence: 99%

Homozygous deletion and expression of PTEN and DMBT1 in human primary neuroblastoma and cell lines

Muñoz

Lázcoz

Inda

et al. 2004

Intl Journal of Cancer

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Neuroblastoma is the most common pediatric solid tumor. Although many allelic imbalances have been described, a bona fide tumor suppressor gene for this disease has not been found yet. In our study, we analyzed 2 genes, PTEN and DMBT1, mapping 10q23.31 and 10q25.3-26.1, respectively, which have been found frequently altered in other kinds of neoplasms. We screened both genes for homozygous deletions in 45 primary neuroblastic tumors and 12 neuroblastoma cell lines. Expression of these genes in cell lines was assessed by RT-PCR analysis. We could detect 2 of 41 (5%) primary tumors harboring PTEN homozygous deletions. Three of 41 (7%) primary tumors and 2 of 12 cell lines presented homozygous losses at the g14 STS on the DMBT1 locus. All cell lines analyzed expressed PTEN, but lack of DMBT1 mRNA expression was detected in 2 of them. We tried to see whether epigenetic mechanisms, such as aberrant promoter hypermethylation, had any role in DMBT1 silencing. The 2 cell lines lacking DMBT1 expression were treated with 5-aza-2-deoxycytidine; DMBT1 expression was restored in only one of them (MC-IXC). From our work, we can conclude that PTEN and DMBT1 seem to contribute to the development of a small fraction of neuroblastomas, and that promoter hypermethylation might have a role in DMBT1 gene silencing.

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“…It was then proposed as a candidate tumor suppressor gene for lung and gastrointestinal tumors caused by homozygous deletions or by a lack of expression (Mori et al 1999, Wu et al 1999, Mollenhauer et al 2000. DMBT1 is involved in epithelial differentiation and mucosal innate immunity by binding to a large panel of pathogens including HIV (Mollenhauer et al 2000, Ligtenberg et al 2010, Madsen et al 2010, Al-Awqati 2011.…”

Section: Introductionmentioning

confidence: 99%

Deleted in malignant brain tumor 1 is secreted in the oviduct and involved in the mechanism of fertilization in equine and porcine species

Ambruosi¹,

Accogli²,

Douet³

et al. 2013

Reproduction

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Oviductal environment affects preparation of gametes for fertilization, fertilization itself, and subsequent embryonic development. The aim of this study was to evaluate the effect of oviductal fluid and the possible involvement of deleted in malignant brain tumor 1 (DMBT1) on IVF in porcine and equine species that represent divergent IVF models. We first performed IVF after pre-incubation of oocytes with or without oviductal fluid supplemented or not with antibodies directed against DMBT1. We showed that oviductal fluid induces an increase in the monospermic fertilization rate and that this effect is canceled by the addition of antibodies, in both porcine and equine species. Moreover, pre-incubation of oocytes with recombinant DMBT1 induces an increase in the monospermic fertilization rate in the pig, confirming an involvement of DMBT1 in the fertilization process. The presence of DMBT1 in the oviduct at different stages of the estrus cycle was shown by western blot and confirmed by immunohistochemical analysis of ampulla and isthmus regions. The presence of DMBT1 in cumulus-oocyte complexes was shown by western blot analysis, and the localization of DMBT1 in the zona pellucida and cytoplasm of equine and porcine oocytes was observed using immunofluorescence analysis and confocal microscopy. Moreover, we showed an interaction between DMBT1 and porcine spermatozoa using surface plasmon resonance studies. Finally, a bioinformatic and phylogenetic analysis allowed us to identify the DMBT1 protein as well as a DMBT1-like protein in several mammals. Our results strongly suggest an important role of DMBT1 in the process of fertilization.

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Lack of DMBT1 expression in oesophageal, gastric and colon cancers

Cited by 89 publications

References 7 publications

Rare mutations of the DMBT1 gene in human astrocytic gliomas

Rare mutations of the DMBT1 gene in human astrocytic gliomas

Homozygous deletion and expression of PTEN and DMBT1 in human primary neuroblastoma and cell lines

Deleted in malignant brain tumor 1 is secreted in the oviduct and involved in the mechanism of fertilization in equine and porcine species

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