H19 in normal development and neoplasia

Looijenga, Leendert H. J.; Verkerk, Annemieke J.M.H.; Groot, Nathan de; Hochberg, Abraham; Oosterhuis, J. Wolter

doi:10.1002/(sici)1098-2795(199703)46:3<419::aid-mrd22>3.0.co;2-s

Cited by 43 publications

(16 citation statements)

References 202 publications

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“…Similar results were obtained upon injection of cells of different human bladder carcinoma derived cell lines into nude mice [12]. All these observations led us to the conclusion that the H19 gene is not a tumor suppressor gene as has been previously claimed [10, 13].…”

Section: Introductionsupporting

confidence: 86%

The effect of retinoic acid on the activation of the human H19 promoter by a 3′ downstream region

et al. 1998

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The human H19 is paternally imprinted (maternally expressed). It is transcribed by RNA pol II, but has no protein product. Its function is unknown. We showed that the transcription of the human H19 gene is under the simultaneous control of both a 5P upstream (promoter) region and a 3P downstream region in cell lines derived from human choriocarcinomas. Moreover, the activation of the H19 promoter by retinoic acid in cells derived from human testicular germ cell tumors is dependent upon the 3P downstream region. The possibility that the action of retinoic acid on the H19 promoter is an indirect one and involves a member of the AP2 transcription factor family is discussed.z 1998 Federation of European Biochemical Societies.

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Section: Introductionsupporting

confidence: 86%

The effect of retinoic acid on the activation of the human H19 promoter by a 3′ downstream region

et al. 1998

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“…Furthermore, some lncRNAs have been reported to serve as precursors for small RNA species in addition to their well described functions as macro ncRNAs [23,60]. Of particular interest, H19, an imprinted RNA that is overexpressed in many tumors and displays oncogenic functions [61,62], has been found to host a miRNA [63]. It can therefore be considered as an example of a pri-miRNA that at the same time acts as an oncogenic lncRNA.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of primary microRNA 221/222 in acute myeloid leukemia

et al. 2013

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BackgroundAcute myeloid leukemia (AML) is a hematopoietic malignancy with a dismal outcome in the majority of cases. A detailed understanding of the genetic alterations and gene expression changes that contribute to its pathogenesis is important to improve prognostication, disease monitoring, and therapy. In this context, leukemia-associated misexpression of microRNAs (miRNAs) has been studied, but no coherent picture has emerged yet, thus warranting further investigations.MethodsThe expression of 636 human miRNAs was compared between samples from 52 patients with AML and 13 healthy individuals by highly specific locked nucleic acid (LNA) based microarray technology. The levels of individual mature miRNAs and of primary miRNAs (pri-miRs) were determined by quantitative reverse transcriptase (qRT) PCR. Transfections and infections of human cell lines were performed using standard procedures.Results64 miRNAs were significantly differentially expressed between AML and controls. Further studies on the clustered miRNAs 221 and 222, already known to act as oncogenes in other tumor types, revealed a deficiency of human myeloid cell lines to process vector derived precursor transcripts. Moreover, endogenous pri-miR-221/222 was overexpressed to a substantially higher extent than its mature products in most primary AML samples, indicating that its transcription was enhanced, but processing was rate limiting, in these cells. Comparison of samples from the times of diagnosis, remission, and relapse of AML demonstrated that pri-miR-221/222 levels faithfully reflected the stage of disease.ConclusionsExpression of some miRNAs is strongly regulated at the posttranscriptional level in AML. Pri-miR-221/222 represents a novel molecular marker and putative oncogene in this disease.

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“…In humans, H19 is expressed in childhood tumors such as Wilms' tumor and embryonal rhabdomyosarcoma, and also in adult cancers such as hepatoblastoma, lung cancer, choriocarcinoma, glioma, and esophageal cancer [6,22,23]. Considerable literature that covers different aspects of H19 imprinting is available in the mouse and human [24–28], but the nature and role of H19 imprinting in neoplasia in the rat has not been extensively investigated.…”

Section: Discussionmentioning

confidence: 99%

Biallelic expression of the H19 gene during spontaneous hepatocarcinogenesis in the albumin SV40 T antigen transgenic rat

Manoharan

Babcock

Willi

et al. 2003

Molecular Carcinogenesis

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Previous studies in this laboratory have demonstrated that the earliest cytogenetic alteration in the development of hepatic neoplasms in a transgenic strain of rats bearing the albumin Simian virus 40 T antigen (Alb SV40 T Ag) construct was a duplication of the chromosome 1q4.1-1q4.2 band. In this region, in the rat genome a cluster of linked imprinted genes occurs. One of these imprinted genes, H19, which is expressed in fetal liver but not in adult liver, was found to be expressed in virtually all neoplasms investigated. A single-nucleotide polymorphic marker in the H19 coding sequence was identified in two rat strains and utilized for the investigation of H19 imprinting. Our results reveal monoallelic expression of the maternal gene in fetal liver, but biallelic expression of the H19 gene in liver neoplasms, thus demonstrating the basis for the deregulation of the imprinted gene expression during hepatocarcinogenesis. These results suggest that the loss of genomic imprinting of the H19 gene found in the liver neoplasms of the Alb SV40 T Ag rat may result not from allelic loss, but from adverse changes in the epigenetic imprints present in the 5'-upstream region of the H19 promoter of the parental alleles.

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H19 in normal development and neoplasia

Cited by 43 publications

References 202 publications

The effect of retinoic acid on the activation of the human H19 promoter by a 3′ downstream region

The effect of retinoic acid on the activation of the human H19 promoter by a 3′ downstream region

Overexpression of primary microRNA 221/222 in acute myeloid leukemia

Biallelic expression of the H19 gene during spontaneous hepatocarcinogenesis in the albumin SV40 T antigen transgenic rat

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