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| 1 | Nitrative and oxidative DNA damage in intrahepatic cholangiocarcinoma patients in relation to tumor invasion显示文摘AIM: Nitrative and oxidative DNA damage such as 8-nitroguanine and 8-oxo-7,8-dihydro-2'-deoxyguanosine(8-oxodG) formation has been implicated in initiation and/or promotion of inflammation-mediated carcinogenesis.The aim of this study is to clarify whether these DNA lesions participate in the progression of intrahepatic cholangiocarcinoma.METHODS: We investigated the relation of the formation of 8-nitroguanine and 8-oxodG and the expression of hypoxia-inducible factor-1α (HIF-1α) with tumor invasion in 37 patients with intra-hepatic cholangiocarcinoma.RESULTS: Immunohistochemical analyses revealed that 8-nitroguanine and 8-oxodG formation occurred to a much greater extent in cancerous tissues than in non-cancerous tissues. HIF-1α could be detected in cancerous tissues in all patients, suggesting low oxygen tension in the tumors.HIF-1α expression was correlated with inducible nitric oxide synthase (iNOS) expression (r= 0.369 and P = 0.025)and 8-oxodG formation (r = 0.398 and P = 0.015).Double immunofluorescence study revealed that iNOS and HIF-1α co-localized in cancerous tissues. Notably, the formation of 8-oxodG was correlated significantly with lymphatic invasion (r = 0.386 and P= 0.018). Moreover, 8-nitroguanine and 8-oxodG in non-cancerous tissues were associated significantly with neural invasion (P = 0.042and P = 0.026, respectively). These results suggest that reciprocal activation between HIF-1α and iNOS mediates persistent DNA damage, which induces tumor invasiveness via mutations, resulting in poor prognosis.CONCLUSION: The formation of 8-nitroguanine and 8-oxodG plays an important role in multiple steps of genetic changes leading to tumor progression, including invasiveness. | Somchai Pinlaor Banchob Sripa Ning Ma Yusuke Hiraku Puangrat Yongvanit Sopit Wongkham Chawalit Pairojkul Vajarabhongsa Bhudhisawasdi Shinji Oikawa Mariko Murata Reiji Semba Shosuke Kawanishi | 2005 | World Journal of Gastroenterology2005，11，30： | 9 |
| 2 | A nationwide survey of outdoor radon concentra-tion in Japan显示文摘 | Shinji Oikawa | | 0，，02： | 1 |
| 3 | Wind tunnel experiments on how thermal stratification affects flow in and above urban street canyons显示文摘 | Kiyoshi Uehara Shuzo Murakami Susumu Oikawa Shinji Wakamatsu | 2000 | Atmospheric Environment2000，，10： | 1 |
| 4 | metabolism of carcinogenic urethane to nitric oxide is involved in oxidative dna damage显示文摘 | katsuhisa sakano shinji oikawa yusuke hiraku | 2002 | Free Radical Biology& Medicine2002，33，5： | 1 |
| 5 | Pro- teomic analysis of aging brain in SAMPI0 mouse: a model of age- related cerebral degeneration 显示文摘 | Ayako Furukawa Shinji Oikawa Sanae Hasegawa-Ishii | 2010 | Mech Ageing Dev2010，131，6： | 1 |
| 6 | Carcinogenic semicarbazide induces sequence-specific DNA damage through the generation of reactive oxygen species and the derived organic radicals显示文摘 | Kazutaka Hirakawa Kaoru Midorikawa Shinji Oikawa Shosuke Kawanishi | 2003 | -Genetic Toxicology and Environmental Mutagenesis2003，，1： | 1 |
| 7 | (?)-Epigallocatechin gallate causes oxidative damage to isolated and cellular DNA显示文摘 | Ayako Furukawa Shinji Oikawa Mariko Murata Yusuke Hiraku Shosuke Kawanishi | 2003 | Biochemical Pharmacology2003，，9： | 1 |
| 8 | A survey of indoor workplace radon concentration in Japan 显示文摘 | Shinji Oikawa Nobuyuki Kanno Tetsuya Sanada | 2006 | Journal of Environmental Radioactivity2006，87，： | 1 |
| 9 | A nationwide survey of outdoor radon concentration in Japan 显示文摘 | Shinji Oikawa Nobuyuki Kanno Tetsuya Sanada | 2003 | Journal of EnvironmentalRadioactivity2003，65，： | 1 |
| 10 | Targeting fructose metabolism by glucose transporter 5 regulation in human cholangiocarcinoma显示文摘Alterations in cellular metabolism may contribute to tumor proliferation and survival.Upregulation of the facilitative glucose transporter(GLUT)plays a key role in promoting cancer.GLUT5 mediates modulation of fructose utilization,and its overexpression has been associated with poor prognosis in several cancers.However,its metabolic regulation remains poorly understood.Here,we demonstrated elevated GLUT5 expression in human cholangiocarcinoma(CCA),using RNA sequencing data from samples of human tissues and cell lines,as compared to normal liver tissues or a cholangiocyte cell line.Cells exhibiting highexpression of GLUT5 showed increased rates of cell proliferation and ATP production,particularly in a fructose-supplemented medium.In contrast,GLUT5 silencing attenuated cell proliferation,ATP production,cell migration/invasion,and improved epithelialemesenchymal transition(EMT)balance.Correspondingly,fructose consumption increased tumor growth in a nude mouse xenograft model,and GLUT5 silencing suppressed growth,supporting the tumor-inhibitory effect of GLUT5 downregulation.Furthermore,in the metabolic pathways of fructolysis-Warburg effect,the expression levels of relative downstream genes,including ketohexokinase(KHK),aldolase B(ALDOB),lactate dehydrogenase A(LDHA),and monocarboxylate transporter 4(MCT4),as well as hypoxia-inducible factor 1 alpha(HIF1A),were altered in a GLUT5 expression-dependent manner.Taken together,these findings indicate that GLUT5 could be a potential target for CCA therapeutic approach via metabolic regulation. | Nattawan Suwannakul Napat Armartmuntree Raynoo Thanan Kaoru Midorikawa Tetsuo Kon Shinji Oikawa Hatasu Kobayashi Ning Ma Shosuke Kawanishi Mariko Murata | 2022 | Genes & Diseases2022，9，6： | 0 |
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