The inhibitory effects of oligonucleotides, complementary to Marek's disease virus mRNA transcribed from the BamHI-H region, on the proliferation of transformed lymphoblastoid cells, MDCC-MSB1

Kawamura, Minoru; Hayashi, Masanobu; Furuichi, Tatsuya; Nonoyama, Meihan; Isogai, Emiko; Namioka, Shigeo

doi:10.1099/0022-1317-72-5-1105

Cited by 42 publications

(34 citation statements)

References 26 publications

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“…Therefore, the inhibition of cell cycle progression by treatment with oligonucleotide A1 was reversible. This result was in good agreement with previous results of cellular growth [12]. No inhibition of progression of the cell cycle was observed by treatment with oligonucleotides other than A1 (data not shown).…”

Section: Effects Of Oligonucleotides On Cellular Dna Synthesissupporting

confidence: 83%

“…The transcripts of the BamHI-H gene family disappear, when virus loses the oncogenicity during serial in vitro passage [10,15,19]. Inhibition of the expression of the BamHI-H gene family by antisense oligonucleotides inhibits the proliferation of MDV-derived lymphoblastoid MSB1 cells [12]. Prolonged proliferation of primary CEF is observed after transfection with expression vectors of cDNA of the BamHI-H gene family [17].…”

Section: Discussionmentioning

confidence: 99%

“…These transcripts can be detected in MDV-derived chicken lymphoblastoid cell line MDCC-MSB1 (MSB1) and primary chicken embryo fibroblasts (CEF) infected with oncogenic MDV but not in primary CEF infected with attenuated MDV in which genomic DNA has undergone amplification of the 132-bp direct repeat [4,16]. Previously, we showed that an oligonucleotide complementary to the sequence of the BamHI-H gene family inhibited the proliferation of MSB1 cells [12]. Peng et al [17] also showed reduced serumdependence for growth and prolonged proliferation of CEF after in vitro transfection with expression vectors of 1.69 and 1.…”

Section: Culture Of the Cells And Cell Growth Experimentsmentioning

confidence: 99%

“…On the contrary, oligonucleotide A1, which is complementary to the BamHI-H gene family, inhibited cellular proliferation (data not shown, ref. [12]). Cellular DNA synthesis was also effectively inhibited by antisense oligonucleotide A1, but not by sense oligonucleotide (Fig.…”

Section: Effects Of Oligonucleotides On Cellular Dna Synthesismentioning

confidence: 99%

“…After incubation of the cells with antisense oligonucleotide A1 against the BamHI-H gene family (5'TTTCTCACACACATACAT3', Kawamura et al [12]) at a concentration of 5 µM for 1 hr at 37°C, the cells were diluted to a density of 5 × 10 5 /ml by addition of the medium with FCS and were again incubated in the presence of antisense oligonucleotides at 5 µM for 0-60 hr at 37°C. After staining with trypan blue, the numbers of total and viable cells were counted.…”

Section: Culture Of the Cells And Cell Growth Experimentsmentioning

confidence: 99%

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Antisence Oligonucleotide Complementary to the BamHI-H Gene Family of Marek's Disease Virus Induced Growth Arrest of MDCC-MSB1 Cells in the S-Phase.

Hayashi

Kawamura

Akaike

et al. 1999

The Journal of Veterinary Medical Science

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ABSTRACT. DNA synthesis was effectively inhibited by antisense oligonucleotide A1 complementary to the BamHI-H gene family in Marek's disease virus (MDV)-derived lymphoblastoid MDCC-MSB1 cells. When a cell cycle distribution of a total cell population was analyzed by flow cytometry, the proportion of S-phase cells increased in the cell populations by treatment with oligonucleotide A1. Approximately 60-70% of the cells appeared in the S phase for 24 and 36 hr of incubation in the presence of oligonucleotide A1 (20-30% in the untreated control cells). The inhibition of cell cycle progression by treatment with oligonucleotide A1 was reversible. When the cells were treated with 5 µM aphidicolin for 12 hr, a similar pattern of cell cycle distribution was observed to that obtained after treatment with oligonucleotide A1. Aphidicolin is an inhibitor of cellular DNA polymerase α, and it halts progression of the cell cycle at the G1/S border or early S phase. When the cells were treated with aphidicolin for 12 hr and subsequently incubated with oligonucleotide A1, no significant difference was observed in the cycle phase distribution of cells in the presence and absence of oligonucleotide A1. In contrast, when the cells were treated with oligonucleotide A1 for 12 hr and subsequently incubated with aphidicolin, the cell cycle did not progress from the G1/S border or early S phase to the next phase.-KEY WORDS: BamHI-H gene family, cell cycle arrest, DNA synthesis, Marek's disease virus, MDCC-MSB1.

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Section: Effects Of Oligonucleotides On Cellular Dna Synthesissupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Culture Of the Cells And Cell Growth Experimentsmentioning

confidence: 99%

Section: Effects Of Oligonucleotides On Cellular Dna Synthesismentioning

confidence: 99%

Section: Culture Of the Cells And Cell Growth Experimentsmentioning

confidence: 99%

See 3 more Smart Citations

Antisence Oligonucleotide Complementary to the BamHI-H Gene Family of Marek's Disease Virus Induced Growth Arrest of MDCC-MSB1 Cells in the S-Phase.

Hayashi

Kawamura

Akaike

et al. 1999

The Journal of Veterinary Medical Science

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Neoplastic Diseases

2013

Diseases of Poultry

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Latent Marek's disease virus can be activated from its chromosomally integrated state in herpesvirus-transformed lymphoma cells.

1993

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Marek's disease virus (MDV), a lymphotropic herpesvirus, induces T‐cell lymphomas in chicken, its natural host. The lymphoma cells are latently infected with MDV but the viral contribution to the transformed phenotype is not understood. To investigate the virus‐cell interaction, we focused on the status of MDV in the transformed cells. By the use of highly sensitive fluorescent in situ hybridization with metaphase chromosomes, we found (i) MDV DNA to be randomly integrated at multiple sites in the chromosomes of primary lymphoma cells from chicken tissues; (ii) extrachromosomal, circular MDV genomes were absent and linear virion DNA was usually not detectable in the latently infected lymphoma cells; (iii) the pattern of integration sites revealed the clonal origin of the tumour cells; which (iv) was retained in in vitro established cell lines derived from primary lymphomas; (v) activation of the lytic phase of MDV's life cycle occurred in vitro suggesting that MDV can escape from its integrated status by an unknown mechanism.

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The inhibitory effects of oligonucleotides, complementary to Marek's disease virus mRNA transcribed from the BamHI-H region, on the proliferation of transformed lymphoblastoid cells, MDCC-MSB1

Cited by 42 publications

References 26 publications

Antisence Oligonucleotide Complementary to the BamHI-H Gene Family of Marek's Disease Virus Induced Growth Arrest of MDCC-MSB1 Cells in the S-Phase.

Antisence Oligonucleotide Complementary to the BamHI-H Gene Family of Marek's Disease Virus Induced Growth Arrest of MDCC-MSB1 Cells in the S-Phase.

Neoplastic Diseases

Latent Marek's disease virus can be activated from its chromosomally integrated state in herpesvirus-transformed lymphoma cells.

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