Transcriptional control of the endogenous MYC protooncogene by antisense RNA.

Yokoyama, Kazushige; Imamoto, Fumio

doi:10.1073/pnas.84.21.7363

Cited by 129 publications

(60 citation statements)

References 23 publications

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“…The data suggest that HOXB4 is directly involved in 1,25-(OH) 2 D 3 down-regulation of c-myc and the antisense effect observed on cell differentiation may be a result of reduced c-myc concentrations. This is consistent with studies demonstrating that a c-myc antisense construct partially promoted HL-60 cell differentiation (Yokoyama & Imamoto 1987, Holt et al 1988.…”

Section: Discussionsupporting

confidence: 81%

Antisense knockout of HOXB4 blocks 1,25-dihydroxyvitamin D3 inhibition of c-myc expression

Pan

Simpson²

2001

Journal of Endocrinology

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The expression of c-myc is decreased by 1,25-(OH) 2 D 3 during HL-60 cell differentiation. Concomitantly, 1,25-(OH) 2 D 3 increases the expression and DNA binding activity of HOXB4, a homeobox gene. HOXB4 binds to the c-myc gene at sites involved in blocking c-myc transcription elongation. In this study, a phosphorothioate antisense oligonucleotide targeted against HOXB4 was examined for its effect on 1,25-(OH) 2 D 3 inhibition of c-myc expression. Alone, 1,25-(OH) 2 D 3 (20 nM) increased HOXB4 levels by 103 7% (mean .., n=3) and decreased c-myc levels by 89 5% (mean ..., n=3) at 48 h of treatment. HOXB4 antisense treatment completely blocked the induction of HOXB4 by 1,25-(OH) 2 D 3 . In addition, HOXB4 antisense partially blocked 1,25-(OH) 2 D 3 -mediated decrease in c-myc levels (46 6% inhibition) and promotion of HL-60 cell differentiation (20 2% and 25 3% inhibition as assessed by nitroblue tetrazolium and non-specific esterase assays respectively). The data further establish that HOXB4 levels are regulated by 1,25-(OH) 2 D 3 and reveal that HOXB4 participates in the down-regulation of c-myc expression.

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Section: Discussionsupporting

confidence: 81%

Antisense knockout of HOXB4 blocks 1,25-dihydroxyvitamin D3 inhibition of c-myc expression

Pan

Simpson²

2001

Journal of Endocrinology

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“…Antisense knockdown has been widely applied in both in vitro and in vivo studies to block the translation of endogenous mRNA. 11,12 After gene transfer, a germline-transmitted zebrafish carrying a heart-specific Tet-On system was generated to conditionally produce the antisense RNA of the cTnC gene. Under the impediment of translation of the endogenous cTnC gene, cardiac functional assays were carried out in this transgenic zebrafish after induction.…”

Section: Editorial P 1595mentioning

confidence: 99%

Conditional Antisense-Knockdown of Zebrafish Cardiac Troponin C as a New Animal Model for Dilated Cardiomyopathy

Lin

Tsai

et al. 2009

Circ J

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“…Antisense RNA can bind in a highly specific manner to complementary sequences, blocking the ability of the bound RNA to be processed or translated or, possibly, even to interact with sequence-specific binding proteins (17)(18)(19)(20). To test the efficacy of antisense RNA complementary to the sequences of a murine retrovirus in blocking retroviral replication, transgenic mice expressing RNA sequences complementary to the q, sequences of Moloney murine leukemia virus (M-MuLV) were produced and then challenged with this virus.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Moloney murine leukemia virus-induced leukemia in transgenic mice expressing antisense RNA complementary to the retroviral packaging sequences.

Han

Yun

Wagner

1991

Proc. Natl. Acad. Sci. U.S.A.

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Recombinant plasmids pLP/as and pCP*as were constructed by positioning the Moloney murine leukemia virus (M-MuLV) proviral packaging (at) sequences in reverse orientation under the transcriptional regulation of lymphotropic promoter/regulatory elements from the M-MuLV long terminal repeat or the cytomegalovirus immediate-early region. Linear fragments containing the antisense 'I' and the appropriate transcriptional regulatory sequences from these plasmids were introduced into the mouse germ line by zygote microinjection. The chromosomal integration, germ-line transmission, and lymphocyte-directed expression of the antisense ## RNA were confirmed. Control (nontransgenic) and transgenic mice containing either the pLPqas or the pCPaas sequences were infected with M-MuLV on the day of birth and assayed for signs ofleukemia between 12 and 14 weeks of age with standard assay procedures. While 31% (11 of 36) of the control, nontransgenic, mice developed leukemia, none of the antisense 4i transgenic mice developed any symptoms of leukemia. The pCPabas sequences were also introduced into mouse NIH 3T3 cells and stably transformed cell lines were isolated. When infected with M-MuLV these cells were shown to produce virus devoid of packaged viral RNA.Retroviruses require only a very limited number of genes and genetic regulatory sequences to complete their cycle of infection in host cells or organisms (1-4). This remarkable molecular efficiency partially explains why retroviruses such as human immunodeficiency virus (HIV) act so effectively as pathogens, but may also suggest targets for molecular attenuation of retroviral replication in host organisms. Among the most stringent requirements for retroviral replication are cis-acting viral genomic sequences necessary for the specific encapsidation of genomic viral RNA molecules into virus particles (4-10). These packaging (4i) sequences have been identified and used extensively as the basis of retroviral vectors designed for gene transfer (10-13). Results from these combined studies suggest that interference with the specific interactions between these 4i sequences and virion capsid proteins will block the retroviral replication cycle.The use of antisense RNA to inhibit RNA function within cells and whole organism has provided a valuable molecular method (14-16). Antisense RNA can bind in a highly specific manner to complementary sequences, blocking the ability of the bound RNA to be processed or translated or, possibly, even to interact with sequence-specific binding proteins (17)(18)(19)(20). To test the efficacy of antisense RNA complementary to the sequences of a murine retrovirus in blocking retroviral replication, transgenic mice expressing RNA sequences complementary to the q, sequences of Moloney murine leukemia virus (M-MuLV) were produced and then challenged with this virus. MATERIALS AND METHODSPlasmids. Recombinant plasmids pLPqias and pCP/as were constructed as shown in Fig. 1. Plasmid pLJ (21) was cleaved with Sma I and the 540-bp Sma I fragment containi...

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Transcriptional control of the endogenous MYC protooncogene by antisense RNA.

Cited by 129 publications

References 23 publications

Antisense knockout of HOXB4 blocks 1,25-dihydroxyvitamin D3 inhibition of c-myc expression

Antisense knockout of HOXB4 blocks 1,25-dihydroxyvitamin D3 inhibition of c-myc expression

Conditional Antisense-Knockdown of Zebrafish Cardiac Troponin C as a New Animal Model for Dilated Cardiomyopathy

Inhibition of Moloney murine leukemia virus-induced leukemia in transgenic mice expressing antisense RNA complementary to the retroviral packaging sequences.

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