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PubMed1992

The 10 S BC-1 ribonucleoprotein particle contains identifier sequence-binding proteins that interact with an array of GCAAG/CTTGC motifs between split promoter sequences for RNA polymerase III.

BC-1 RNA is a brain-specific small RNA transcript of identifier sequences present in the somas and dendrites of neurons. We recently reported that the RNA is complexed with a protein(s) to form a 10 S ribonucleoprotein particle (Kobayashi, S., Goto, S., and Anzai, K. (1991) J. Biol. Chem. 266, 4726-4730). We demonstrate here that this 10 S BC-1 ribonucleoprotein particle contains a DNA-binding protein(s) (Bp-1 protein) capable of interacting with a region between split promoter sequences for RNA polymerase III within the identifier sequences. The region has short inverted repeats: a perfect octanucleotide repeat (GCGCTTGCCTAGCAAGCGC) and an imperfect heptanucleotide repeat (GCCTAGCAAGCGCAAGGC), each of which contains a GCAAG/CTTGC motif. We also demonstrate that the binding of this protein either to the array of pentamer motifs or to BC-1 RNA is mutually exclusive. The molecular masses of photo-cross-linking adducts of Bp-1 protein to a 32P-labeled GCAAG/CTTGC motif-specific probe were estimated to be about 31 and 36 kDa, indicating that two species of Bp-1 proteins may be present in the brain.

Animals↗
PubMed2003

Novel paternity testing by distinguishing parental alleles at a VNTR locus in the differentially methylated region upstream of the human H19 gene.

Conventional PCR-based genotyping is useful for forensic testing but cannot be used to determine parental origins of alleles in DNA specimens. Here we describe a novel method of combined conventional genotyping and PIA typing (parentally imprinted allele typing) at a minisatellite region upstream from the H19 locus. The PIA typing uses two sets of primers and DNA digested with methylation-sensitive Hha I enzyme. The first amplification produces only the methylated fragment of paternal H19 allele, and the second detects polymorphism in the minisatellite. Hence, this distinguishes paternal and maternal alleles by difference in the DNA methylation. Furthermore, the polymorphism in this polymorphic locus was examined using 199 unrelated Japanese and 171 unrelated Germans, their polymorphism information content being 0.671 and 0.705, respectively. Feasibility of this typing is demonstrated for six families, and the usefulness is shown by application to paternity testing.

Alleles↗
PubMed2003

[Estimation of telomerase transcriptive activity in the umbilical cord and the mother's venous blood cells].

Stem cells possess the ability of the partition and differentiation into other cells, practically lifelong of the organism. The potential of the self-extraction of these cells practically unrestricted and results probably from the telomerase gene activity, especially subunit hTERT. To the analysis of 11 samples of the umbilical cord and mothers blood received immediately after the childbirth in which one compared the expression of telomerase genes hTERT, TP1, hTR. Four cases ascertained the expression subunit hTERT in the umbilical cord blood at the lack its transcripts in the venous blood of mothers. In one case we found 10-times higher concentration of subunit hTERT in the umbilical cord blood than in the venous blood of the mother. 6 cases did not demonstrate the expression of the hTERT nor in the umbilical cord blood nor in the venous blood of mothers. The transcriptive activity TP1 and hTR did not show differences among investigated groups. Received results put the question or the transcriptive activity subunit hTERT in the umbilical cord blood is a results of the presence of stem cells.

Adult↗
PubMed2004

Polymorphism of trinucleotide repeats in non-translated regions of SCA8 and SCA12 genes: allele distribution in a Polish control group.

Spinocerebellar ataxias are a group of neurodegenerative disorders caused by dynamic mutations of microsatellite repeats. Two novel forms of SCAs have been described recently: SCA8, with expansions of CTA/CTG repeats in 3'UTR of the SCA8 gene, and SCA12, caused by expansion of the CAG tract in 5'UTR of the SCA12/PP2R2B gene. Analysis of CTA/CTG and CAG polymorphism in those two genes was performed in a Polish control group consisting of 100 individuals without any neurological signs. The distribution and ranges of the number of non-pathogenic repeats were similar to those observed in other populations described previously. Expansion of CTA/CTG repeats in the SCA8 locus was found in 2 of 100 controls and in 5 probands among 150 pedigrees affected with unidentified ataxias. As such expanded alleles were also observed in their healthy relatives, the pathogenic role of expansions in the SCA8 gene remains uncertain.

3' Untranslated Regions↗
PubMed2004

[Clinical features and diagnosis of spinocerebellar ataxia].

In the past decade, a great progress has been made in understanding genetic basis of the spinocerebellar ataxia. Based upon the genotypes, more then 20 subgroups of autosomal dominant spinocerebellar ataxia have been identified with different gene mutations. Neither the pathomechanism nor the function of these genes is fully understood. In these disorders the main clinical sign is ataxia. Other symptoms may be present as well, but no specific clinical feature is known for differentiating subgroups. Specific diagnosis can be made by genetic tests. In this review we summarize the clinical features and genetic backgrounds of the most common spinocerebellar ataxias.

Ataxin-7↗
PubMed2004

Role of occludin, a tight junction protein, in blastocoel formation, and in the paracellular permeability and differentiation of trophectoderm in preimplantation mouse embryos.

Tight junctions (TJ) are critical for blastocoel formation in mammalian embryos. The present study aimed to examine the role of tight junctions in the differentiation of the trophectoderm (TE), and in the pluripotency of blastomeres, as well as in the formation and integrity of the blastocoel. We examined the effect of occludin antibody on blastocoel formation, blastocyst permeability, and expression of H19 and Oct-4, markers of TE differentiation and blastomere pluripotency, respectively. Eight-cell mouse embryos and morulae were cultured in the presence or absence of occludin antibody for 31 h. Occludin antibody inhibited blastocoel formation and increased permeability of the TE of nascent and expanding blastocysts to FITC-dextran (4 kDa), a permeability tracer. At the same time Oct-4 expression increased while expression of H19 became barely detectable. These observations indicate that occludin is involved in establishing the blastocoel, as well as in maintaining its impermeability, and that the development of tight junction is critical for TE formation in mouse embryos.

Animals↗
PubMed2004

Effect of all-trans retinoic acid on telomerase activity in ovarian cancer cells.

Vitamin A is an essential nutrient important for growth, vision, embryonic development, immune response and reproduction. Various retinoids have been shown to be effective chemotherapeutic and chemopreventive agents for a number of human cancers. Telomeres are nucleoprotein structures found at the end of chromosomes. During cellular division, the telomeres in normal cells shorten progressively and thus, function as a "molecular clock". Telomerase is a ribonucleoprotein complex that extends and maintains telomeres. Activation of telomerase is required for cells to overcome proliferative crisis. Telomerase activation is observed in 90% of human cancers, but not in normal somatic cells. We examined the role of telomerase in mediating the growth suppression of ovarian carcinoma cells by all-trans-retinoic acid (ATRA). Using a number of cell lines with varying levels of growth sensitivity to ATRA, we found that cells that exhibit ATRA-dependant suppression of growth also contained significantly reduced telomerase activity. We also observed a reduction in expression of the telomerase components, hTERT and hTR in ATRA treated ovarian carcinoma cells. Our results suggest that one mechanism by which ATRA acid inhibits cancer cell growth is by suppressing telomerase activity, thereby pushing cells to proliferative crisis.

Antineoplastic Agents↗
PubMed2004

Allele-specific methylation analysis on upstream promoter region of H19 by methylation-specific PCR with confronting two-pair primers.

H19 and IGF2 genes are imprinted genes and expressed differently depending on whether they are carried by a chromosome of maternal or paternal origin; H19 is expressed only from the maternal allele and IGF2 only from the paternally inherited allele. The upstream promoter region of H19 has the imprinting-control region (ICR) or CTCF binding sites, where the methylation status of this region is critical to the regulation of imprinting of the H19/IGF2 locus located in chromosome 11p15. There are various reports on imprinting disorders in this region. In colorectal cancer aberrant biallelic methylation of CTCF binding site has been reported, and aberrant hypomethylation of this region in bladder cancer. Thus, certain human neoplasms have either hyper- or hypo-methylation in the ICR. Hence it is still difficult to analyze allele-specific methylation disorder of the region, or differentially methylated regions (DMR), locate upstream of H19. Here we report a new method, which could distinguish paternal epigenetic or maternal epigenetic pattern by a single PCR assay, to combine methylation-specific PCR and PCR with confronting two-pair primers (MSP-CTPP). Using this method, we investigated the region close to H19 ICR in 161 colorectal cancer and 65 gastric cancer cases.

Aged↗
PubMed2004

Genomic imprinting in mammals.

In contrast to the biallelic expression of most genes, expression of imprinted genes is monoallelic and depends on the sex of the transmitting parents. In humans it has been implicated in some developmental failures, neurodevelopmental and neurobehavioral disorders (such as Prader-Willi/Angelman, Silver-Russel or Beckwith-Wiedemann syndromes). The aim of this review is to present the phenomenon of parental imprinting as well as its molecular mechanism in various mammals. Several maternal and paternal imprinted genes and gene clusters are described.

Animals↗
PubMed2004

Loss of IGF2 imprinting: mechanisms and consequences.

Although the leading dogma for the origin of the diversity in cancer cell subpopulations is based on a stepwise selection and accumulation of genetic changes that allow uncontrollable malignant growth, there is an emerging understanding that the variability of heritable phenotypes in cancer and cancer-prone cells may also involve epigenetic mechanisms. This is exemplified by the unscheduled activation of the normally repressed maternal IGF2 allele in a wide range of human cancers. The notion that this so-called loss of imprinting (LOI) provides a proliferative advantage by increasing the levels of the IGF-2 ligand available to its receptors is supported by the overgrowth symptoms of neonatal mice, which has been genetically manipulated to express Igf2 biallelically. Although the mechanisms underlying IGF2 LOI in human cancer remains unknown, it is likely to directly or indirectly involve the H19 imprinting control region (ICR). This stretch of 2 kb sequence just upstream of the H19 promoter functions to block enhancer-Igf2 promoter communications by means of a DNA methylation-sensitive chromatin insulator. We discuss here the possibility that pathological mechanisms leading to IGF2 LOI use different strategies with the neutralization of the H19 ICR insulator function as a common denominator.

Animals↗
PubMed2005

Down-regulation of the IGF-2/H19 locus during normal and malignant hematopoiesis is independent of the imprinting pattern.

H19 and IGF-2 are two growth regulatory genes located on chromosome 11p15 implicated in tumorigenesis. Both genes are imprinted and regulated reciprocally under many circumstances. In order to elucidate the contribution of H19 and IGF-2 to leukemogenesis, the mRNA expression level of both genes were quantitated in bone marrow biopsies and peripheral blood samples from normal (n=98), chronic myelomonocytic leukemia (CMML, n=43), chronic myelogenous leukemia (CML, n=40) and, acute myelogenous leukemia (AML, n=32) cases. A concomitant reduction of H19 and IGF-2 expression was observed in all leukemic samples compared to the healthy controls. This down-regulation was not accompanied by changes in methylation of the differentially methylated region (DMR). Whereas the H19 gene showed strict monoallelic expression in all informative normal (n=31) and leukemic (n=54) samples, the imprinting pattern of the IGF2 gene was found to be heterogeneous. No correlations between imprinting status (mono- versus biallelic expression), quantitative mRNA expression levels and course of disease were found for the IGF-2 gene. The data suggest a disturbed regulation of the IGF-2/H19 locus in myeloid leukemias which is not caused by loss of imprinting.

Alleles↗
PubMedDate not supplied

Imbalance in expression levels of insulin-like growth factor 2 and H19 transcripts linked to progression of hepatocellular carcinoma.

BACKGROUND: The imprinted genes insulin-like growth factor 2 (IGF2) and H19 play important roles in various malignancies including hepatocellular carcinoma (HCC). MATERIALS AND METHODS: We used DNA microarray and patient follow-up data to examine the relationship between expression of IGF2 and H19 and HCC. RESULTS: We found that imbalances in levels of IGF2 and H19 transcripts were correlated with advanced tumor stage and poor outcome in HCC patients. CONCLUSION: In addition to their known epigenetic or genetic abnormality in malignancies, these findings suggest that altered transcription of these two imprinted genes contributes to progression of HCC.

Aged↗
PubMed2006

Expression of human telomerase reverse transcriptase, Survivin, DD3 and PCGEM1 messenger RNA in archival prostate carcinoma tissue.

INTRODUCTION: The wide spectrum of biological behavior displayed by prostate cancer (PCa) warrants investigation of potential PCa-specific biomarkers that could identify more aggressive tumor types and therefore provide prognostic value. Upregulation of expression of human telomerase reverse transcriptase (hTERT), Survivin, DD3 and PCGEM1 mRNAs in PCa lesions has recently been described. The purpose of this study was to evaluate the clinical value of detection of over-expression of these biomarkers in the diagnosis and prognosis of PCa. MATERIAL AND METHODS: Archival formalin-fixed, paraffin-embedded (FFPE) prostatectomy tissue from 26 patients with PCa (Gleason score 3-9, mean 7) and 14 patients with benign prostatic hyperplasia (BPH) were analyzed by reverse transcription polymerase chain reaction (RT-PCR) for semiquantitative transcript levels of hTERT, Survivin, DD3 and PCGEM1. In addition, 25 matched normal (MN) tissue samples were examined. The expression of biomarker mRNA relative to b2-microglobulin mRNA was determined using AlphaImager 2200 data analysis software. RESULTS: The biomarkers had sensitivities ranging from 91% to 100%. Clinical specificities evaluated with the BPH tissue were the following: hTERT mRNA (93%), DD3 mRNA (57%), Survivin (29%) and PCGEM1 (14%). Biomarker expressions were up to 13.5-fold higher in PCa tissue as compared to MN tissue. None of the tumor biomarkers showed a positive correlation with pathological stage and Gleason score. CONCLUSIONS: The results of this study indicate potential utility of the hTERT mRNA and DD3 mRNA as diagnostic but not prognostic biomarkers for PCa.

Antigens, Neoplasm↗
PubMed1995

H19 expression and tumorigenicity of choriocarcinoma derived cell lines.

Certain embryonal tumors demonstrate a loss of heterozygosity at the parentally imprinted region of chromosome 11p15.5. It has been hypothesized that this implicates a tumor suppressor gene at this locus. The human H19 gene maps to 11p15.5, is expressed in fetal tissues including the placenta and is paternally imprinted. Here we show that the abundance of H19 transcripts in cells of two choriocarcinoma derived cell lines (JAr and JEG-3) differs greatly. While JAr cells express high levels of H19 RNA, the expression of H19 in JEG-3 cells is much lower than that of normal trophoblasts. Cells of these two cell lines were subcutaneously injected into nude mice with subsequent tumor formation. A fivefold increase in the H19 RNA level was measured in tumors derived from JEG-3 cell lines as compared to these cells before injection. However this increase in H19 RNA did not alter the clonogenicity in soft agar nor the growth rate of the cells derived from these tumors as compared to the original JEG-3 cells. Nevertheless, the cells retaining the elevated level of H19 transcripts were more tumorigenic than the original cells. We propose that there is a selection of cells expressing high levels of H19 from the total JEG-3 cell population during the microevolution of tumor formation. These observations, together with our previous publications on H19 expression in human cancers, do not support the notion of a tumor suppressor role for the H19 gene.

Animals↗
PubMed1995

Maintenance of normal imprinting of H19 and IGF2 genes in neuroblastoma.

H19 and insulin-like growth factor II (IGF2) are among a few genes which have been confirmed to be imprinted in normal human embryonal tissues. This results in monoallelic expression of maternal H19 and paternal IGF2. Loss of imprinting of these genes producing biallelic expression has been observed in Wilm's tumor and embryonal rhabdomyosarcoma, suggesting that an epigenetic change of DNA, in addition to a genetic change in oncogene(s) and/or tumor suppressor gene(s), may be involved in the development of these childhood cancers. Neuroblastoma, which is an embryonal tumor originating from neural crest-derived cells, occasionally occurs in individuals with the Beckwith-Wiedemann syndrome; Wilm's tumor and embryonal rhabdomyosarcoma occur even more frequently in the Beckwith-Wiedemann syndrome; and paternal uniparental disomy of H19 and IGF2 loci (chromosome 11p15) is present in the Beckwith-Wiedemann syndrome. Furthermore, neuroblastoma cell lines express IGF2, and autocrine/paracrine effects of IGF2 have been demonstrated in these cells. Thus, we examined for imprinting of both H19 and IGF2 in primary untreated neuroblastomas using the RsaI and ApaI polymorphisms within these genes, respectively. Seven of 15 tumors were informative for H19 and for IGF2, and all of these cases showed monoallelic expression of both of these genes. These results indicate that loss of imprinting of H19 and IGF2 does not occur in neuroblastomas.

Base Sequence↗
PubMed1993

Transport of BC1 RNA in hypothalamo-neurohypophyseal axons.

Ample evidence indicates that in nerve cells, several individual proteins are locally synthesized in postsynaptic domains in dendrites. By contrast, axonal terminals, at least in mammals, are generally thought to lack protein synthetic capacity. However, axonal nerve endings of the hypothalamo-neurohypophyseal tract have recently been shown to contain mRNAs encoding vasopressin, oxytocin, dynorphin, and neurofilament. In this report, we identify BC1 RNA, a small RNA polymerase III transcript that is specifically expressed in neurons, in hypothalamo-neurohypophyseal axons. BC1 RNA has previously been shown to be located in somatic and dendritic domains of various types of neurons in the rat nervous system. Here we present evidence to show that BC 1 RNA, like several neuropeptide mRNAs, is axonally transported from magnocellular hypothalamic neurons to neurosecretory nerve endings in the posterior pituitary. BC1 RNA, which has been reported to be a component of a ribonucleoprotein particle, is thus colocalized with dendritic mRNAs in dendritic domains and with axonal mRNAs in axonal domains, respectively. Such colocalization is indicative of functional interactions of BC1 RNA with those mRNAs that are targeted to extrasomatic domains of nerve cells.

Animals↗