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Targeting fructose metabolism by glucose transporter 5 regulation in human cholangiocarcinoma

Genes & Diseases 2022年第6期9卷 1727-1741页

作者： Nattawan Suwannakul Napat Armartmuntree Raynoo Thanan Kaoru Midorikawa Tetsuo Kon Shinji Oikawa Hatasu Kobayashi Ning Ma shosuke kawanishi Mariko Murata Department of Environmental and Molecular Medicine Mie University Graduate School of MedicineTsuMie 514-8507Japan Department of Biochemistry Faculty of MedicineKhon Kaen UniversityKhon Kaen 40002Thailand Laboratory of Functional Genomics Graduate School of BioscienceNagahama Institute of Bioscience and TechnologyNagahamaShiga 526-0829Japan Graduate School of Health Science Suzuka University of Medical ScienceSuzukaMie 513-8670Japan Faculty of Pharmaceutical Sciences Suzuka University of Medical ScienceSuzukaMie 513-8670Japan

Alterations in cellular metabolism may contribute to tumor proliferation and *** of the facilitative glucose transporter(GLUT)plays a key role in promoting ***5 mediates modulation of fructose utilization,and its overexpression has been associated with poor prognosis in several ***,its metabolic regulation remains poorly ***,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 *** exhibiting highexpression of GLUT5 showed increased rates of cell proliferation and ATP production,particularly in a fructose-supplemented *** contrast,GLUT5 silencing attenuated cell proliferation,ATP production,cell migration/invasion,and improved epithelialemesenchymal transition(EMT)***,fructose consumption increased tumor growth in a nude mouse xenograft model,and GLUT5 silencing suppressed growth,supporting the tumor-inhibitory effect of GLUT5 ***,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 *** together,these findings indicate that GLUT5 could be a potential target for CCA therapeutic approach via metabolic regulation.

关键词： Cholangiocarcinoma Fructose Glucose transporter 5 Metabolic regulation Warburg effect

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Nitrative and oxidative DNA damage in intrahepatic cholangiocarcinoma patients in relation to tumor invasion

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World Journal of Gastroenterology 2005年第30期11卷 4644-4649页

作者： Somchai Pinlaor Banchob Sripa Ning Ma Yusuke Hiraku Puangrat Yongvanit Sopit Wongkham Chawalit Pairojkul Vajarabhongsa Bhudhisawasdi Shinji Oikawa Mariko Murata Reiji Semba shosuke kawanishi Department of Parasitology Department of Pathology Department of Anatomy Department of Environmental and Molecular Medicine Department of Biochemistry Department of Surgery

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 niltric 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 = 0.042 and 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.

关键词： 8-Nitroguanine 8-Oxo-7,8-dihydro-2'-deoxyguanosine Hypoxia-inducible factor-1α Cholangiocarcinoma Tumor invasion

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