MicroRNA-34a functions as a potential tumor suppressor by inducing apoptosis in neuroblastoma cells

Neuroblastoma (NB) is one of the most common forms of cancer in children, accounting for 15% of pediatric cancer deaths. The clinical course of these tumors is highly variable and is dependent on such factors as age at presentation, stage, ploidy and genomic abnormalities. Hemizygous deletion of chr...

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Veröffentlicht in:Oncogene 2007-07, Vol.26 (34), p.5017-5022
Hauptverfasser: Welch, C, Chen, Y, Stallings, R L
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Stallings, R L
description Neuroblastoma (NB) is one of the most common forms of cancer in children, accounting for 15% of pediatric cancer deaths. The clinical course of these tumors is highly variable and is dependent on such factors as age at presentation, stage, ploidy and genomic abnormalities. Hemizygous deletion of chromosome 1p occurs in approximately 30% of advanced stage tumors, is associated with a poor prognosis, and likely leads to the loss of one or more tumor suppressor genes. We show here that microRNA (miRNA)-34a (1p36.23) is generally expressed at lower levels in unfavorable primary NB tumors and cell lines relative to normal adrenal tissue and that reintroduction of this miRNA into three different NB cell lines causes a dramatic reduction in cell proliferation through the induction of a caspase-dependent apoptotic pathway. As a potential mechanistic explanation for this observation, we demonstrate that miR-34a directly targets the messenger ribonucleic acid (mRNA) encoding E2F3 and significantly reduces the levels of E2F3 protein, a potent transcriptional inducer of cell-cycle progression. Furthermore, miR-34a expression increases during retinoic acid-induced differentiation of the SK-N-BE cell line, whereas E2F3 protein levels decrease. Thus, adding to the increasing role of miRNAs in cancer, miR-34a may act as a suppressor of NB tumorgenesis.
doi_str_mv 10.1038/sj.onc.1210293
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The clinical course of these tumors is highly variable and is dependent on such factors as age at presentation, stage, ploidy and genomic abnormalities. Hemizygous deletion of chromosome 1p occurs in approximately 30% of advanced stage tumors, is associated with a poor prognosis, and likely leads to the loss of one or more tumor suppressor genes. We show here that microRNA (miRNA)-34a (1p36.23) is generally expressed at lower levels in unfavorable primary NB tumors and cell lines relative to normal adrenal tissue and that reintroduction of this miRNA into three different NB cell lines causes a dramatic reduction in cell proliferation through the induction of a caspase-dependent apoptotic pathway. As a potential mechanistic explanation for this observation, we demonstrate that miR-34a directly targets the messenger ribonucleic acid (mRNA) encoding E2F3 and significantly reduces the levels of E2F3 protein, a potent transcriptional inducer of cell-cycle progression. Furthermore, miR-34a expression increases during retinoic acid-induced differentiation of the SK-N-BE cell line, whereas E2F3 protein levels decrease. Thus, adding to the increasing role of miRNAs in cancer, miR-34a may act as a suppressor of NB tumorgenesis.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1210293</identifier><identifier>PMID: 17297439</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Ageing, cell death ; Apoptosis ; Biological and medical sciences ; Cancer ; Caspase ; Cell Biology ; Cell differentiation ; Cell Line, Tumor ; Cell physiology ; Cell proliferation ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Child ; Chromosome 1 ; Chromosome Deletion ; Chromosomes, Human, Pair 1 ; E2F3 protein ; E2F3 Transcription Factor - genetics ; Fundamental and applied biological sciences. Psychology ; Gene deletion ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Genetic aspects ; Genetics ; Health aspects ; Human Genetics ; Humans ; Internal Medicine ; Medical sciences ; Medicine ; Medicine &amp; Public Health ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; MicroRNAs - physiology ; miRNA ; Molecular and cellular biology ; Neuroblastoma ; Neuroblastoma - genetics ; Neuroblastoma - metabolism ; Neuroblastoma - pathology ; Neuroblastoma cells ; Neurology ; Oncology ; Pediatrics ; Physiological aspects ; Ploidy ; Proteins ; Retinoic acid ; Ribonucleic acid ; Risk factors ; RNA ; short-communication ; Transcription ; Tumor suppressor genes ; Tumors ; Tumors of the nervous system. 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The clinical course of these tumors is highly variable and is dependent on such factors as age at presentation, stage, ploidy and genomic abnormalities. Hemizygous deletion of chromosome 1p occurs in approximately 30% of advanced stage tumors, is associated with a poor prognosis, and likely leads to the loss of one or more tumor suppressor genes. We show here that microRNA (miRNA)-34a (1p36.23) is generally expressed at lower levels in unfavorable primary NB tumors and cell lines relative to normal adrenal tissue and that reintroduction of this miRNA into three different NB cell lines causes a dramatic reduction in cell proliferation through the induction of a caspase-dependent apoptotic pathway. As a potential mechanistic explanation for this observation, we demonstrate that miR-34a directly targets the messenger ribonucleic acid (mRNA) encoding E2F3 and significantly reduces the levels of E2F3 protein, a potent transcriptional inducer of cell-cycle progression. 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The clinical course of these tumors is highly variable and is dependent on such factors as age at presentation, stage, ploidy and genomic abnormalities. Hemizygous deletion of chromosome 1p occurs in approximately 30% of advanced stage tumors, is associated with a poor prognosis, and likely leads to the loss of one or more tumor suppressor genes. We show here that microRNA (miRNA)-34a (1p36.23) is generally expressed at lower levels in unfavorable primary NB tumors and cell lines relative to normal adrenal tissue and that reintroduction of this miRNA into three different NB cell lines causes a dramatic reduction in cell proliferation through the induction of a caspase-dependent apoptotic pathway. As a potential mechanistic explanation for this observation, we demonstrate that miR-34a directly targets the messenger ribonucleic acid (mRNA) encoding E2F3 and significantly reduces the levels of E2F3 protein, a potent transcriptional inducer of cell-cycle progression. Furthermore, miR-34a expression increases during retinoic acid-induced differentiation of the SK-N-BE cell line, whereas E2F3 protein levels decrease. Thus, adding to the increasing role of miRNAs in cancer, miR-34a may act as a suppressor of NB tumorgenesis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>17297439</pmid><doi>10.1038/sj.onc.1210293</doi><tpages>6</tpages></addata></record>
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subjects Ageing, cell death
Apoptosis
Biological and medical sciences
Cancer
Caspase
Cell Biology
Cell differentiation
Cell Line, Tumor
Cell physiology
Cell proliferation
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Child
Chromosome 1
Chromosome Deletion
Chromosomes, Human, Pair 1
E2F3 protein
E2F3 Transcription Factor - genetics
Fundamental and applied biological sciences. Psychology
Gene deletion
Gene Expression Regulation, Neoplastic
Genes, Tumor Suppressor
Genetic aspects
Genetics
Health aspects
Human Genetics
Humans
Internal Medicine
Medical sciences
Medicine
Medicine & Public Health
MicroRNAs
MicroRNAs - genetics
MicroRNAs - metabolism
MicroRNAs - physiology
miRNA
Molecular and cellular biology
Neuroblastoma
Neuroblastoma - genetics
Neuroblastoma - metabolism
Neuroblastoma - pathology
Neuroblastoma cells
Neurology
Oncology
Pediatrics
Physiological aspects
Ploidy
Proteins
Retinoic acid
Ribonucleic acid
Risk factors
RNA
short-communication
Transcription
Tumor suppressor genes
Tumors
Tumors of the nervous system. Phacomatoses
title MicroRNA-34a functions as a potential tumor suppressor by inducing apoptosis in neuroblastoma cells
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