A fine-structure deletion map of human chromosome 11p: Analysis of J1 series hybrids

Gläser, Thomas; Housman, David E.; Lewis, William H.; Gerhard, Daniela S.; Jones, Carol

doi:10.1007/bf01534910

Cited by 123 publications

(42 citation statements)

References 94 publications

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“…Eight loci used in this analysis have been mapped previously (Glaser et al, 1989;Tanigami et al, 1992) into the region delimited by the 11p15 breakpoints of JI-7/43a and Jl-9 (i.e., between Dl1S12 and the gene cluster containing TH, INS, IGF2, CTSD, and HI9). Six additional loci have been located in this interval (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…As well as adding many new markers, the Not I map has refined the order of several genes and anonymous DNA markers within the J1-deletion hybrid intervals (Glaser et al, 1989). The ORD4, MUC2, and RNR genes were assigned to the most telomeric (JI-9) region originally shown to contain HRAS, INS, IGF, TH, CTSD, and R19.…”

Section: Discussionmentioning

confidence: 99%

“…RD, AG73, and A204 were purchased from the American Type Culture Collection (ATCC) (Rockville, MD). Ten hybrid cell lines from the Jl-deletion panel (}{ao et al, 1976) contain progressively smaller segments of llp15 (Glaser et al, 1989).…”

Section: Methodsmentioning

confidence: 99%

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An Ordered NotI Fragment Map of Human Chromosome Band 11p15

et al. 1994

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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An Ordered NotI Fragment Map of Human Chromosome Band 11p15

et al. 1994

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“…The H19 gene maps to human chromosome 11p15.5 (Glaser et al, 1989) and to the distal part of chromosome 7 in the mouse (Pachnis et al, 1984). In human and mouse, H19 is located in the vicinity of IGF-2 and the two genes are imprinted (Bartolomei et al, 1991;Zhang and Tycko, 1992).…”

Section: Introductionmentioning

confidence: 99%

Steroid hormones modulate H19 gene expression in both mammary gland and uterus

et al. 1999

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H19 is an imprinted and developmentally regulated gene whose product remains apparently untranslated. In a previous study on breast adenocarcinomas, we reported that overexpression of the H19 gene was signi®cantly correlated with the presence of steroid receptors, suggesting the putative role of hormones in H19 transcription. To determine the mode of steroid action, we have detected levels of H19 RNA synthesis during mammary gland development by in situ hybridization (ISH): two peaks of H19 transcription occur during puberty and pregnancy. Furthermore, we demonstrated by ISH that in the uterus H19 RNA synthesis is high during estrus and metestrus phases. To test steroid control of H19 transcription, ovariectomized and adrenalectomized mice were supplemented, 1 week after surgery, with 17-b-estradiol (E2, 20 mg/kg/day), progesterone (P, 1 mg/kg/day) or corticosterone (B, 0.3 mg/ kg/day) for 2 weeks. According to ISH data, E2 and to a lesser extent B stimulated H19 transcription in the uterus, whereas P inhibited it. To con®rm the in vivo results, in vitro experiments were performed using cultures of MCF-7 cells (a hormone-sensitive mammary cell line). E2 stimulated the endogenous H19 gene of this cell line and tamoxifen inhibited this e ect. Furthermore, we performed transient cotransfections in MCF-7, in HBL-100 (another hormone-sensitive mammary cell line) and in BT-20 (a hormone-insensitive mammary cell line) with various constructs of ERa (WT or mutated) and PR-A, in presence or absence of steroid hormones. We demonstrated that ERa up-regulated the H19 promoter in MCF-7 and in HBL-100, whereas PR-A did not have any e ect per se. Moreover, in MCF-7, PR-A antagonized clearly the ERa-mediated promoter enhancement, but in HBL-100 this counteracting e ect on the ERa up-regulation was not found. Interestingly, the same experiments performed in BT-20 cell line provided very similar results as those obtained in MCF-7 cells, with a clear down-regulation mediated by PR-A on the H19 promoter. All these in vitro data are in agreement with in vivo results. In addition, data obtained with ERa mutants indicate that H19 promoter activation is both ligand-dependent and ligand-independent. We have thus demonstrated that H19 gene expression is controlled by steroid hormones; furthermore, this gene is highly expressed in hormone-sensitive organs when the hormonal stimulation is accompanied with a morphological repair.

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“…The gene is mapped to human chromosome 11p15.5 and is transcribed by RNA polymerase II (Glaser et al, 1989). The transcript is then capped, spliced and transported to cytoplasm but not translated (Eddy, 2001).…”

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confidence: 99%

Riboregulator H19 induction of MDR1-associated drug resistance in human hepatocellular carcinoma cells

2007

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Acquisition of drug resistance is one of the main obstacles encountered in cancer chemotherapy. Overexpression of multi-drug resistance 1 (MDR1) gene and its protein product P-glycoprotein, accompanied with a decrease in doxorubicin accumulation level, was observed in doxorubicin-resistant R-HepG2 cells, a subline derived by selection of human hepatocellular carcinoma HepG2 cells with doxorubicin. In addition, Northern-blot analysis revealed an eight fold upregulation of the imprinted H19 mRNA in R-HepG2 cells. H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. Results from methylation-specific polymerase chain reaction analysis indicated that the MDR1 gene promoter was hypomethylated in R-HepG2 cells. Antisense H19 oligonucleotides transfection induced a marked increase in the percentage of MDR1 promoter methylation and decrease in MDR1 expression in R-HepG2 cells. Thus, the H19 gene is believed to induce P-glycoprotein expression and MDR1-associated drug resistance at least in liver cancer cells through regulation of MDR1 promoter methylation.

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A fine-structure deletion map of human chromosome 11p: Analysis of J1 series hybrids

Cited by 123 publications

References 94 publications

An Ordered NotI Fragment Map of Human Chromosome Band 11p15

An Ordered NotI Fragment Map of Human Chromosome Band 11p15

Steroid hormones modulate H19 gene expression in both mammary gland and uterus

Riboregulator H19 induction of MDR1-associated drug resistance in human hepatocellular carcinoma cells

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