start-ver=1.4 cd-journal=joma no-vol=67 cd-vols= no-issue=6 article-no= start-page=359 end-page=367 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201312 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=In Vitro Assessment of Factors Affecting the Apparent Diffusion Coefficient of Jurkat Cells Using Bio-phantoms en-subtitle= kn-subtitle= en-abstract= kn-abstract=It is well known that many tumor tissues show lower apparent diffusion coefficient (ADC) values, and that several factors are involved in the reduction of ADC values. The aim of this study was to clarify how much each factor contributes to decreases in ADC values. We investigate the roles of cell density, extracellular space, intracellular factors, apoptosis and necrosis in ADC values using bio-phantoms. The ADC values of bio-phantoms, in which Jurkat cells were encapsulated by gellan gum, were measured by a 1.5-Tesla magnetic resonance imaging device with constant diffusion time of 30sec. Heating at 42℃ was used to induce apoptosis while heating at 48℃ was used to induce necrosis. Cell death after heating was evaluated by flow cytometric analysis and electron microscopy. The ADC values of bio-phantoms including non-heated cells decreased linearly with increases in cell density, and showed a steep decline when the distance between cells became less than 3μm. The analysis of ADC values of cells after destruction of cellular structures by sonication suggested that approximately two-thirds of the ADC values of cells originate from their cellular structures. The ADC values of bio-phantoms including necrotic cells increased while those including apoptotic cells decreased. This study quantitatively clarified the role of the cellular factors and the extracellular space in determining the ADC values produced by tumor cells. The intermediate diffusion time of 30msec might be optimal to distinguish between apoptosis and necrosis. en-copyright= kn-copyright= en-aut-name=KatashimaKazunori en-aut-sei=Katashima en-aut-mei=Kazunori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KurodaMasahiro en-aut-sei=Kuroda en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AshidaMasakazu en-aut-sei=Ashida en-aut-mei=Masakazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SasakiTakanori en-aut-sei=Sasaki en-aut-mei=Takanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TaguchiTakehito en-aut-sei=Taguchi en-aut-mei=Takehito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MatsuzakiHidenobu en-aut-sei=Matsuzaki en-aut-mei=Hidenobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MurakamiJun en-aut-sei=Murakami en-aut-mei=Jun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=YanagiYoshinobu en-aut-sei=Yanagi en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=HisatomiMiki en-aut-sei=Hisatomi en-aut-mei=Miki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=HaraMarina en-aut-sei=Hara en-aut-mei=Marina kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=KatoHirokazu en-aut-sei=Kato en-aut-mei=Hirokazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=OhmuraYuichi en-aut-sei=Ohmura en-aut-mei=Yuichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=KobayashiTomoki en-aut-sei=Kobayashi en-aut-mei=Tomoki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=KanazawaSusumu en-aut-sei=Kanazawa en-aut-mei=Susumu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=HaradaSosuke en-aut-sei=Harada en-aut-mei=Sosuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=TakemotoMitsuhiro en-aut-sei=Takemoto en-aut-mei=Mitsuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=OhnoSeiichiro en-aut-sei=Ohno en-aut-mei=Seiichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=MimuraSeiichi en-aut-sei=Mimura en-aut-mei=Seiichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=AsaumiJunichi en-aut-sei=Asaumi en-aut-mei=Junichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= affil-num=1 en-affil= kn-affil=Department of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University affil-num=3 en-affil= kn-affil=Department of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University affil-num=6 en-affil= kn-affil=Department of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Department of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=11 en-affil= kn-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University affil-num=12 en-affil= kn-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University affil-num=13 en-affil= kn-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University affil-num=14 en-affil= kn-affil=Department of Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=15 en-affil= kn-affil=Department of Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=16 en-affil= kn-affil=Department of Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=17 en-affil= kn-affil=Central Division of Radiology, Okayama University Hospital affil-num=18 en-affil= kn-affil=Central Division of Radiology, Okayama University Hospital affil-num=19 en-affil= kn-affil=Department of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=ADC kn-keyword=ADC en-keyword=apoptosis kn-keyword=apoptosis en-keyword=necrosis kn-keyword=necrosis en-keyword=hyperthermia kn-keyword=hyperthermia en-keyword=cell density kn-keyword=cell density END start-ver=1.4 cd-journal=joma no-vol=66 cd-vols= no-issue=3 article-no= start-page=263 end-page=270 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201206 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=In Vitro Assessment of Factors Affecting the Apparent Diffusion Coefficient of Ramos Cells Using Bio-phantoms en-subtitle= kn-subtitle= en-abstract= kn-abstract=The roles of cell density, extracellular space, intracellular factors, and apoptosis induced by the molecularly targeted drug rituximab on the apparent diffusion coefficient (ADC) values were investigated using bio-phantoms. In these bio-phantoms, Ramos cells (a human Burkittセs lymphoma cell line) were encapsulated in gellan gum. The ADC values decreased linearly with the increase in cell density, and declined steeply when the extracellular space became less than 4 μm. The analysis of ADC values after destruction of the cellular membrane by sonication indicated that approximately 65% of the ADC values of normal cells originate from the cell structures made of membranes and that the remaining 35% originate from intracellular components. Microparticles, defined as particles smaller than the normal cells, increased in number after rituximab treatments, migrated to the extracellular space and significantly decreased the ADC values of bio-phantoms during apoptosis. An in vitro study using bio-phantoms was conducted to quantitatively clarify the roles of cellular factors and of extracellular space in determining the ADC values yielded by tumor cells and the mechanism by which apoptosis changes those values. en-copyright= kn-copyright= en-aut-name=SasakiTakanori en-aut-sei=Sasaki en-aut-mei=Takanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KurodaMasahiro en-aut-sei=Kuroda en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KatashimaKazunori en-aut-sei=Katashima en-aut-mei=Kazunori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=AshidaMasakazu en-aut-sei=Ashida en-aut-mei=Masakazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MatsuzakiHidenobu en-aut-sei=Matsuzaki en-aut-mei=Hidenobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=AsaumiJunichi en-aut-sei=Asaumi en-aut-mei=Junichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MurakamiJun en-aut-sei=Murakami en-aut-mei=Jun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=OhnoSeiichiro en-aut-sei=Ohno en-aut-mei=Seiichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KatoHirokazu en-aut-sei=Kato en-aut-mei=Hirokazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KanazawaSusumu en-aut-sei=Kanazawa en-aut-mei=Susumu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Departments of Radiology, Okayama University Graduate School of Medicine affil-num=2 en-affil= kn-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University affil-num=3 en-affil= kn-affil=Departments of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine affil-num=4 en-affil= kn-affil=Departments of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine affil-num=5 en-affil= kn-affil=Departments of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine affil-num=6 en-affil= kn-affil=Departments of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine affil-num=7 en-affil= kn-affil=Departments of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine affil-num=8 en-affil= kn-affil=Central Division of Radiology, Okayama University Hospital affil-num=9 en-affil= kn-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University affil-num=10 en-affil= kn-affil=Departments of Radiology, Okayama University Graduate School of Medicine en-keyword=apparent diffusion coefficient value kn-keyword=apparent diffusion coefficient value en-keyword=cell density kn-keyword=cell density en-keyword=extracellular space kn-keyword=extracellular space en-keyword=bio-phantom kn-keyword=bio-phantom END start-ver=1.4 cd-journal=joma no-vol=41 cd-vols= no-issue=10 article-no= start-page=984 end-page=993 dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20057 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Role of O-6-methylguanine-DNA methyltransferase and effect of O-6-benzylguanine on the anti-tumor activity of cis-diaminedichloroplatinum(II) in oral cancer cell lines en-subtitle= kn-subtitle= en-abstract= kn-abstract=

The DNA repair enzyme, O-6-methylguanine-DNA methyltransferase (MGMT) modulates the effectiveness of alkylating agents. However, the relationship between MGMT and the sensitivities to other agents has not been explored. In the present study, the association between MGMT expression and the cellular sensitivity to the platinum agent, CDDP was examined in four human oral cancer cell tines. CDDP depleted MGMT protein and mRNA levels in all four cell tines. Two cell lines with low MGMT expression were sensitive to an alkylating agent, N-methyl-N'-nitro-N-nitrosoguanidine and CDDP, whereas two other cell tines with high MGMT expression were resistant to both agents. Furthermore, the addition of the MGMT inhibitor, O-6-benzylguanine (O-6-BG), invariably enhanced CDDP sensitivity. CDDP depleted MGMT expression, and CDDP sensitivity was enhanced by O-6-BG. These results provide valuable information about the relationship between MGMT expression and CDDP sensitivity in oral cancer chemotherapy. (c) 2005 Elsevier Ltd. All rights reserved.

en-copyright= kn-copyright= en-aut-name=MakiYu en-aut-sei=Maki en-aut-mei=Yu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MurakamiJun en-aut-sei=Murakami en-aut-mei=Jun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AsaumiJun-ichi en-aut-sei=Asaumi en-aut-mei=Jun-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TsujigiwaHidetsugu en-aut-sei=Tsujigiwa en-aut-mei=Hidetsugu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NagatsukaHitoshi en-aut-sei=Nagatsuka en-aut-mei=Hitoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KokeguchiSusumu en-aut-sei=Kokeguchi en-aut-mei=Susumu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=FukuiKazuhiro en-aut-sei=Fukui en-aut-mei=Kazuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KawaiNoriko en-aut-sei=Kawai en-aut-mei=Noriko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=YanagiYoshinobu en-aut-sei=Yanagi en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KurodaMasahiro en-aut-sei=Kuroda en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=TanakaNoriaki en-aut-sei=Tanaka en-aut-mei=Noriaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=MatsubaraNagahide en-aut-sei=Matsubara en-aut-mei=Nagahide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=KishiKanji en-aut-sei=Kishi en-aut-mei=Kanji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University affil-num=8 en-affil= kn-affil=Okayama University affil-num=9 en-affil= kn-affil=Okayama University affil-num=10 en-affil= kn-affil=Okayama University affil-num=11 en-affil= kn-affil=Okayama University affil-num=12 en-affil= kn-affil=Okayama University affil-num=13 en-affil= kn-affil=Okayama University en-keyword=mgmt kn-keyword=mgmt en-keyword=cddp kn-keyword=cddp en-keyword=o-6-bg kn-keyword=o-6-bg en-keyword=oral cancer kn-keyword=oral cancer END start-ver=1.4 cd-journal=joma no-vol=56 cd-vols= no-issue=1 article-no= start-page=22 end-page=28 dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=200507 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Effects of histone deacetylase inhibitor FR901228 on expression level of telomerase reverse transcriptase in oral cancer en-subtitle= kn-subtitle= en-abstract= kn-abstract=We speculated whether or not the expression level of telomerase reverse transcriptase (hTERT) would be modulated by agents targeting epigenetics in oral cancer cell lines. Although hTERT is known to be targeted by epigenetic changes, it remains unclear how chemoagents targeting epigenetics work on hTERT transcription. In the present study, the epigenetic effects of histone deacetylase (HDAC) inhibitor FR901228 on hTERT transcription were analysed by RT-PCR in oral cancer cell lines. The mRNA expression of hTERT was upregulated after exposure to FR901228 in hTERT-negative Hep2 cells, even in the hTERT highly expressed SAS and KB cells. Moreover, co-treatment of protein synthesis inhibitor cycloheximide (CHX) resulted in the induction of hTERT transcription by FR901228. This suggests that the induction of hTERT by FR901228 requires de novo protein synthesis to some extent and is more likely a direct than an indirect effect on epigenetic changes such as histone acetylation / deacetylation. We further examined the effect of FR901228 on c-myc protein, which is one of the main hTERT transcription activators. FR901228 repressed c-myc protein only in the absence of CHX, dependent of the enhancement of de novo protein synthesis. Our results indicate that c-myc protein is repressed indirectly by FR901228 but may not contribute FR901228-induced hTERT transcription. The present study showed that the HDAC inhibitor FR901228 induced the hTERT gene by a complex mechanism that involved other transcription factors except for c-myc, in addition to the inhibition of histone deacetylation. en-copyright= kn-copyright= en-aut-name=MurakamiJun en-aut-sei=Murakami en-aut-mei=Jun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=AsaumiJun-ichi en-aut-sei=Asaumi en-aut-mei=Jun-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KawaiNoriko en-aut-sei=Kawai en-aut-mei=Noriko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TsujigiwaHidetsugu en-aut-sei=Tsujigiwa en-aut-mei=Hidetsugu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YanagiYoshinobu en-aut-sei=Yanagi en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=NagatsukaHitoshi en-aut-sei=Nagatsuka en-aut-mei=Hitoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=InoueTetsuyoshi en-aut-sei=Inoue en-aut-mei=Tetsuyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KokeguchiSusumu en-aut-sei=Kokeguchi en-aut-mei=Susumu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KawasakiShoji en-aut-sei=Kawasaki en-aut-mei=Shoji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KurodaMasahiro en-aut-sei=Kuroda en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=TanakaNoriaki en-aut-sei=Tanaka en-aut-mei=Noriaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=MatsubaraNagahide en-aut-sei=Matsubara en-aut-mei=Nagahide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=KishiKanji en-aut-sei=Kishi en-aut-mei=Kanji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= affil-num=1 en-affil= kn-affil=Department of Oral and Maxillofacial Radiology, Field of Tumor Biology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools affil-num=2 en-affil= kn-affil=Department of Oral and Maxillofacial Radiology, Field of Tumor Biology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools affil-num=3 en-affil= kn-affil=Department of Oral and Maxillofacial Radiology, Field of Tumor Biology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools affil-num=4 en-affil= kn-affil=Department of Oral Pathology, Field of Tumor Biology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools affil-num=5 en-affil= kn-affil=Department of Oral and Maxillofacial Radiology, Field of Tumor Biology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools affil-num=6 en-affil= kn-affil=Department of Oral Pathology, Field of Tumor Biology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools affil-num=7 en-affil= kn-affil=Department of Oral Microbiology, Field of Tumor Biology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools affil-num=8 en-affil= kn-affil=Department of Oral Microbiology, Field of Tumor Biology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools affil-num=9 en-affil= kn-affil=Department of Radiological Technology, Field of Tumor Biology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools affil-num=10 en-affil= kn-affil=Department of Radiology, Field of Tumor Biology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools affil-num=11 en-affil= kn-affil=Department of Surgical Oncology, Field of Tumor Biology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools affil-num=12 en-affil= kn-affil=Department of Surgical Oncology, Field of Tumor Biology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools affil-num=13 en-affil= kn-affil=Department of Oral and Maxillofacial Radiology, Field of Tumor Biology, Graduate School of Medicine and Dentistry, Okayama University Graduate Schools en-keyword=hTERT kn-keyword=hTERT en-keyword=FR901228 kn-keyword=FR901228 en-keyword=oral cancer kn-keyword=oral cancer en-keyword=HDAC inhibitor kn-keyword=HDAC inhibitor END start-ver=1.4 cd-journal=joma no-vol=40 cd-vols= no-issue=6 article-no= start-page=597 end-page=603 dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=20042 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Effects of demethylating agent 5-aza-2 '-deoxycytidine and histone deacetylase inhibitor FR901228 on maspin gene expression in oral cancer cell lines en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Maspin, which belongs to the serine protease inhibitor (serpin) superfamily, has been proposed as a potent tumor suppressor that inhibits cell motility, invasion, angiogenesis, and metastasis. In the present study, we examined the effects of 5-aza-2'-deoxycytidine (5-aza-dC), a demethylating agent, and FR901228, a histone deacetylase (HDAC) inhibitor, on maspin expression in oral cancer cell tines. The expression levels of maspin mRNA were divided into two groups, which was the maspin tow-expressed and high-expressed cell lines in the 12 oral cancer cell lines. The maspin promoter contained only a few methylated CpG sites in the maspin low-expressed cell lines. Moreover, the methylation status was not altered after 5-aza-dC treatment. However, the transcription of the maspin gene was clearly increased following 5-aza-dC treatment in a number of oral cancer cell tines. These results imply that an action of 5-aza-dC is separate from induction of promoter demethylation. Treatment with FR901228 resulted in a time-dependent stimulation of the re-expression of maspin mRNA as early as 4 h after treatment in the maspin downregulated cells. The re-expression of the maspin gene may contribute to the recuperation of biological functions linked to FR901228 such as an inhibitory effect on tumor angiogenesis and cell invasion. These results indicate that maspin and its target genes may be excellent leads for future studies on the potential benefits of FR901228, a HDAC inhibitor, in cancer therapy.

en-copyright= kn-copyright= en-aut-name=MurakamiJun en-aut-sei=Murakami en-aut-mei=Jun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=AsaumiJun-ichi en-aut-sei=Asaumi en-aut-mei=Jun-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MakiYuu en-aut-sei=Maki en-aut-mei=Yuu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TsujigiwaHidetsugu en-aut-sei=Tsujigiwa en-aut-mei=Hidetsugu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KurodaMasahiro en-aut-sei=Kuroda en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=NagaiNoriyuki en-aut-sei=Nagai en-aut-mei=Noriyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=YanagiYoshinobu en-aut-sei=Yanagi en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=InoueTetsuyoshi en-aut-sei=Inoue en-aut-mei=Tetsuyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KawasakiShoji en-aut-sei=Kawasaki en-aut-mei=Shoji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanakaNoriaki en-aut-sei=Tanaka en-aut-mei=Noriaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=MatsubaraNagahide en-aut-sei=Matsubara en-aut-mei=Nagahide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=KishiKanji en-aut-sei=Kishi en-aut-mei=Kanji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University affil-num=8 en-affil= kn-affil=Okayama University affil-num=9 en-affil= kn-affil=Okayama University affil-num=10 en-affil= kn-affil=Okayama University affil-num=11 en-affil= kn-affil=Okayama University affil-num=12 en-affil= kn-affil=Okayama University en-keyword=maspin kn-keyword=maspin en-keyword=methylation kn-keyword=methylation en-keyword=5-aza-2 '-deoxycytidine kn-keyword=5-aza-2 '-deoxycytidine en-keyword=FR901228 kn-keyword=FR901228 END start-ver=1.4 cd-journal=joma no-vol=119 cd-vols= no-issue=2 article-no= start-page=113 end-page=117 dt-received= dt-revised= dt-accepted= dt-pub-year=2007 dt-pub=20070903 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Accumulating DNA methylation in background mucosa plays a role in esophageal squamous cell carcinogenesis kn-title=食道扁平上皮癌の発癌過程におけるDNAメチル化の役割 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=IshiiTatsuhiro en-aut-sei=Ishii en-aut-mei=Tatsuhiro kn-aut-name=石井龍宏 kn-aut-sei=石井 kn-aut-mei=龍宏 aut-affil-num=1 ORCID= en-aut-name=MurakamiJun en-aut-sei=Murakami en-aut-mei=Jun kn-aut-name=村上純 kn-aut-sei=村上 kn-aut-mei=純 aut-affil-num=2 ORCID= en-aut-name=NotoharaKenji en-aut-sei=Notohara en-aut-mei=Kenji kn-aut-name=能登原憲司 kn-aut-sei=能登原 kn-aut-mei=憲司 aut-affil-num=3 ORCID= en-aut-name=SasamotoHiromi en-aut-sei=Sasamoto en-aut-mei=Hiromi kn-aut-name=笹本博美 kn-aut-sei=笹本 kn-aut-mei=博美 aut-affil-num=4 ORCID= en-aut-name=KambaraTakeshi en-aut-sei=Kambara en-aut-mei=Takeshi kn-aut-name=神原健 kn-aut-sei=神原 kn-aut-mei=健 aut-affil-num=5 ORCID= en-aut-name=ShirakawaYasuhiro en-aut-sei=Shirakawa en-aut-mei=Yasuhiro kn-aut-name=白川靖博 kn-aut-sei=白川 kn-aut-mei=靖博 aut-affil-num=6 ORCID= en-aut-name=NaomotoYoshio en-aut-sei=Naomoto en-aut-mei=Yoshio kn-aut-name=猶本良夫 kn-aut-sei=猶本 kn-aut-mei=良夫 aut-affil-num=7 ORCID= en-aut-name=OuchidaMamoru en-aut-sei=Ouchida en-aut-mei=Mamoru kn-aut-name=大内田守 kn-aut-sei=大内田 kn-aut-mei=守 aut-affil-num=8 ORCID= en-aut-name=ShimizuKenji en-aut-sei=Shimizu en-aut-mei=Kenji kn-aut-name=清水憲二 kn-aut-sei=清水 kn-aut-mei=憲二 aut-affil-num=9 ORCID= en-aut-name=JeremyR. Jass en-aut-sei=Jeremy en-aut-mei=R. Jass kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=MatsubaraNagahide en-aut-sei=Matsubara en-aut-mei=Nagahide kn-aut-name=松原長秀 kn-aut-sei=松原 kn-aut-mei=長秀 aut-affil-num=11 ORCID= en-aut-name=TanakaNoriaki en-aut-sei=Tanaka en-aut-mei=Noriaki kn-aut-name=田中紀章 kn-aut-sei=田中 kn-aut-mei=紀章 aut-affil-num=12 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 歯科口腔放射線学 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病態探究医学 affil-num=4 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 affil-num=5 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 affil-num=6 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 affil-num=7 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 affil-num=8 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 分子遺伝学 affil-num=9 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 分子遺伝学 affil-num=10 en-affil= kn-affil=Department of Pathology, McGill University affil-num=11 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 affil-num=12 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 en-keyword=食道扁平上皮癌 kn-keyword=食道扁平上皮癌 en-keyword=プロモーターメチル化 kn-keyword=プロモーターメチル化 en-keyword=p53遺伝子変異 kn-keyword=p53遺伝子変異 END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2003 dt-pub=20030325 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=口腔癌細胞におけるMGMT遺伝子のメチル化による転写抑制ならびにアルキル化剤感受性に関する研究 kn-title=Silencing of O6-methylguanine-DNA methyltransferase gene by methylation of an upstream promoter increases the sensitivity of oral cancer cells to alkylating agents used in their chemotherapy en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=MurakamiJun en-aut-sei=Murakami en-aut-mei=Jun kn-aut-name=村上純 kn-aut-sei=村上 kn-aut-mei=純 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END