研究者詳細 - 豊國　伸哉

論文 - 豊國　伸哉

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Cancer-promoting role of adipocytes in asbestos-induced mesothelial carcinogenesis through dysregulated adipocytokine production. 査読有り国際誌

Chew SH, Okazaki Y, Nagai H, Misawa N, Akatsuka S, Yamashita K, Jiang L, Yamashita Y, Noguchi M, Hosoda K, Sekido Y, Takahashi T, Toyokuni S

Carcinogenesis 35 巻 ( 1 ) 頁： 164 - 72 2014年1月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Carcinogenesis

Like many other human cancers, the development of malignant mesothelioma is closely associated with a chronic inflammatory condition. Both macrophages and mesothelial cells play crucial roles in the inflammatory response caused by asbestos exposure. Here, we show that adipocytes can also contribute to asbestos-induced inflammation through dysregulated adipocytokine production. 3T3-L1 preadipocytes were differentiated into mature adipocytes prior to use. These cells took up asbestos fibers (chrysotile, crocidolite and amosite) but were more resistant to asbestos-induced injury than macrophages and mesothelial cells. Expression microarray analysis followed by reverse transcription-PCR revealed that adipocytes respond directly to asbestos exposure with an increased production of proinflammatory adipocytokines [e.g. monocyte chemoattractant protein-1 (MCP-1)], whereas the production of anti-inflammatory adipocytokines (e.g. adiponectin) is suppressed. This was confirmed in epididymal fat pad of mice after intraperitoneal injection of asbestos fibers. Such dysregulated adipocytokine production favors the establishment of a proinflammatory environment. Furthermore, MCP-1 marginally promoted the growth of MeT-5A mesothelial cells and significantly enhanced the wound healing of Y-MESO-8A and Y-MESO-8D human mesothelioma cells. Our results suggest that increased levels of adipocytokines, such as MCP-1, can potentially contribute to the promotion of mesothelial carcinogenesis through the enhanced recruitment of inflammatory cells as well as a direct growth and migration stimulatory effect on mesothelial and mesothelioma cells. Taken together, our findings support a potential cancer-promoting role of adipocytes in asbestos-induced mesothelial carcinogenesis. © The Author 2013. Published by Oxford University Press. All rights reserved.

DOI： 10.1093/carcin/bgt267

Iron overload as a major targetable pathogenesis of asbestos-induced mesothelial carcinogenesis 査読有り国際誌 Open Access

Toyokuni, S

REDOX REPORT 19 巻 ( 1 ) 頁： 1 - 7 2014年1月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Redox Report

Few people expected that asbestos, a fibrous mineral, would be carcinogenic to humans. In fact, asbestos is a definite carcinogen in humans, causing a rare but aggressive cancer called malignant mesothelioma (MM). Mesothelial cells line the three somatic cavities and thus do not face the outer surface, but reduce the friction among numerous moving organs. MM has several characteristics: extremely long incubation period of 30-40 years after asbestos exposure, difficulty in clinical diagnosis at an early stage, and poor prognosis even under the current multimodal therapies. In Japan, 'Kubota shock' attracted considerable social attention in 2005 for asbestos-induced mesothelioma and, thereafter, the government enacted a law to provide the people suffering from MM a financial allowance. Several lines of recent evidence suggest that the major pathology associated with asbestos-induced MM is local iron overload, associated with asbestos exposure. Preclinical studies to prevent MM after asbestos exposure with iron reduction are in progress. In addition, novel target genes in mesothelial carcinogenesis have been discovered with recently recognized mesothelioma-prone families. Development of an effective preventive strategy is eagerly anticipated because of the long incubation period for MM. © W. S. Maney & Son Ltd 2014.

DOI： 10.1179/1351000213Y.0000000075

As a host society to SFRRI 2014 in Kyoto. Open Access

Handa O, Naito Y, Toyokuni S

Journal of clinical biochemistry and nutrition 54 巻 ( 1 ) 頁： 1 - 1 2014年1月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Journal of Clinical Biochemistry and Nutrition

It is our great honor to host the 17th Biennial Meeting of Society for Free Radical Research International (SFRRI 2014) that is being held at the Kyoto International Conference Center, in Kyoto, Japan on March 23rd–26th, 2014. Previously we had this biennial meeting twice in Kyoto, in the year 1988 and 2000. This meeting has a great meaning not only for every member in SFRRI but also for those in SFRR Japan, since the SFRRI 1998 meeting was a key event behind the establishment of SFRR Japan. Since 1998, SFRR Japan has expanded the number of the members and has developed a variety of original research activities. The International Scientific Program Committee (ISPC) representing each region of SFRR has worked hard all together to develop what we believe will be an exciting and informative meeting to both young and senior participants. As a result, the congress will include award lectures and symposia on novel aspects of free radical research, which was democratically selected after the application during December 2012 and January 2013 by the voting of ISPC. Concurrent symposia will address in-depth and cutting-edge scientific topics in free radical chemistry, biology and medicine. In addition, the meeting will have four plenary lectures presented by Prof. Rafael Radi (Uruguay), Prof. Harold. M Swartz (USA), Prof. Arturo Zychlinsky (Germany) and Prof. Hideyuki Saya (Japan). Each lecture would reveal novel aspects of free radical research. It has been our sincere wish to make the meeting affordable and attractive especially to young scientists. There will be several awards from each region of SFRR as well as from this meeting. Sunrise lecture for the beginner of free radical research will be presented. Several satellite meetings are now planned in order to allow participants with special interests to meet. The congress venue, Kyoto city, is a UNESCO World Heritage site with a long and rich history going back over 1,200 years and was the original imperial capital of Japan. With more than 3,000 temples and shrines, full of traditional Japanese culture, with cherry blossoms presumably in full bloom, Kyoto city will deeply inspire your sixth sense. Besides traditional atmosphere, Kyoto city is thriving and exciting modern city with excellent facilities and easy links to the rest of the world. We believe that SFRRI 2014 meeting will be rich in science, and a great opportunity to hear cutting edge advances in the free radical research, as well as an opportunity to renew old friendships and establish new collaborations and associations. We look forward to meeting all of you in Kyoto in March 2014.

DOI： 10.3164/jcbn.54-1E1

Cancer-promoting role of adipocytes in asbestos-induced mesothelial carcinogenesis through dysregulated adipocytokine production. 査読有り

Chew SH, Okazaki Y, Nagai H, Misawa N, Akatsuka S, Yamashita K, Jiang L, Noguchi M, Hosoda K, Sekido Y, Takahashi T and Toyokuni S.

Carcinogenesis 35 巻頁： 164-172 2014年

Preclinical evaluation of an O(6)-methylguanine-DNA methyltransferase-siRNA/liposome complex administered by convection-enhanced delivery to rat and porcine brains. 査読有り

Tsujiuchi T, Natsume A, Motomura K, Kondo G, Ranjit M, Hachisu R, Sugimura I, Tomita S, Takehara I, Woolley M, Barua NU, Gill SS, Bienemann AS, Yamashita Y, Toyokuni S, Wakabayashi T.

Am J Transl Res 15 巻頁： 169-178 2014年

Dexamethasone palmitate ameliorates macrophages-1 rich graft-versus-host disease by inhibiting macrophage functions. 査読有り Open Access

Nishiwaki S, Nakayama T, Murata M, Nishida T, Terakura S, Saito S, Kato T. Mizuno H, Imahashi N, Seto S, Ozawa Y, Miyamura K, Ito M, Takeshita K, Kato H, Toyokuni S, Nagao K, Ueda R and Naoe T.

PLoS ONE 9 巻頁： e96252 2014年

Histological detection of catalytic ferrous iron with the selective turn-on fluorescent probe RhoNox-1 in a Fenton reaction-based rat renal carcinogenesis model. 査読有り

Mukaide T, Hatori Y, Misawa N, Funahashi S, Jiang L, Hirayama T, Nagasawa H and Toyokuni S.

Free Radic Res 48 巻頁： 990-995 2014年

Rat model demonstrates a high risk of tremolite but a low risk of anthophyllite for mesothelial carcinogenesis. 査読有り Open Access

Aierken D, Okazaki Y, Chew SH, Sakai A, Wang Y, Nagai H, Misawa N, Kohyama N and Toyokuni S.

Nagoya J Med Sci 76 巻頁： 149-160 2014年

Maternal molecular hydrogen administration ameliorates rat fetal hippocampal damage by in ut ero ischemia-reperfusion. 査読有り

Mano Y, Kotani T, Ito M, Nagai T, Ichinohashi Y, Yamada K, Ohno K, Kikkawa F and Toyokuni S.

Free Radic Biol Med 69 巻頁： 324-330 2014年

Lack of presence of the human cytomegalovirus in human glioblastoma. Modern Pathol 27: 922-929, 2014. 査読有り

Yamashita Y, Ito Y, Isomura H, Takemura N, Okamoto A, Motomura K, Tsujiuchi T, Natsume A, Wakabayashi T, Toyokuni S and Tsurumi T.

Modern Pathology 27 巻頁： 922-929 2014年

Ovarian mucinous tumors arising from mature cystic teratomas-a molecular genetic approach for understanding the cellular origin. 査読有り

Fujii K, Yamashita Y, Yamamoto T, Takahashi K, Hashimoto K, Miyata T, Kawai K, Kikkawa F, Toyokuni S, Nagasaka T.

Human Pathol 45 巻頁： 717-724 2014年

Iron as a major targetable pathogenesis of asbestos-induced mesothelial carcinogenesis. 査読有り

Toyokuni, S.

Redox Rep. 19 巻頁： 1-7 2014年

Iron and thiols as two major players in carcinogenesis: friends or foes? 招待有り査読有り

Toyokuni S.

Front Pharmacol 5 巻頁： 200 2014年

Genome-wide profiling of 8-oxoguanine reveals its association with spatial positioning in nucleus. 査読有り

Yoshihara M, Jiang L, Akatsuka S, Suyama M and Toyokuni S.

DNA Res 21 巻頁： 603-612 2014年

Direct exposure of non-equilibrium atmospheric pressure plasma confers simultaneous oxidative and ultraviolet modifications in biomolecules. 査読有り

Okazaki Y, Wang Y, Tanaka H, Mizuno M, Nakamura K, Kajiyama H, Kano H, Uchida K, Kikkawa F, Hori M and Toyokuni S.

J Clin Biochem Nutr 55 巻頁： 207-215 2014年

Plasma medical science for cancer therapy using non-thermal atomospheric pressure plasma. 査読有り

Tanaka H, Mizuno M, Ishikawa K, Takeda K, Nakamura K, Utsumi F, Kajiyama H, Nano H, Okazaki Y, Toyokuni S, Maruyama S, Kikkawa F and Hori M.

IEEE Trans Plasma Sci 42 巻頁： 3760-3764 2014年

Iron and thiols as two major players in carcinogenesis: friends or foes? 査読有り国際誌 Open Access

Toyokuni S

Frontiers in pharmacology 5 巻頁： 200 - 200 2014年

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Frontiers in Pharmacology

Iron is the most abundant metal in the human body and mainly works as a cofactor for proteins such as hemoglobin and various enzymes. No independent life forms on earth can survive without iron. However, excess iron is intimately associated with carcinogenesis by increasing oxidative stress via its catalytic activity to generate hydroxyl radicals. Biomolecules with redox-active sulfhydryl function(s) (thiol compounds) are necessary for the maintenance of mildly reductive cellular environments to counteract oxidative stress, and for the execution of redox reactions for metabolism and detoxification. Involvement of glutathione S-transferase and thioredoxin has long attracted the attention of cancer researchers. Here, I update recent findings on the involvement of iron and thiol compounds during carcinogenesis and in cancer cells. It is now recognized that the cystine/glutamate transporter (antiporter) is intimately associated with ferroptosis, an iron-dependent, non-apoptotic form of cell death, observed in cancer cells, and also with cancer stem cells; the former with transporter blockage but the latter with its stabilization. Excess iron in the presence of oxygen appears the most common known mutagen. Ironically, the persistent activation of antioxidant systems via genetic alterations in Nrf2 and Keap1 also contributes to carcinogenesis. Therefore, it is difficult to conclude the role of iron and thiol compounds as friends or foes, which depends on the quantity/distribution and induction/flexibility, respectively. Avoiding further mutation would be the most helpful strategy for cancer prevention, and myriad of efforts are being made to sort out the weaknesses of cancer cells. © 2014 Toyokuni.

DOI： 10.3389/fphar.2014.00200

Iron and thiols as two major players in carcinogenesis: friends or foes? 招待有り査読有り Open Access

Toyokuni S

Front Pharmacol 5 巻頁： 200 2014年

Preclinical evaluation of an O(6)-methylguanine-DNA methyltransferase-siRNA/liposome complex administered by convection-enhanced delivery to rat and porcine brains.

Tsujiuchi T, Natsume A, Motomura K, Kondo G, Ranjit M, Hachisu R, Sugimura I, Tomita S, Takehara I, Woolley M, Barua NU, Gill SS, Bienemann AS, Yamashita Y, Toyokuni S, Wakabayashi T

American journal of translational research 6 巻 ( 2 ) 頁： 169 - 78 2014年

Preclinical evaluation of an O<sup>6</sup>-methylguanine-DNA methyltransferase-siRNA/liposome complex administered by convection-enhanced delivery to rat and porcine brains 査読有り国際誌

Tsujiuchi T., Natsume A., Motomura K., Kondo G., Ranjit M., Hachisu R., Sugimura I., Tomita S., Takehara I., Woolley M., Barua N.U., Gill S.S., Bienemann A.S., Yamashita Y., Toyokuni S., Wakabayashi T.

American Journal of Translational Research 6 巻 ( 2 ) 頁： 169 - 178 2014年

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：American Journal of Translational Research

The main determinant of glioblastoma (GBM) resistance to temozolomide (TMZ) is thought to be O6-methylguanine-DNA methyltransferase (MGMT), which is a DNA-repair enzyme that removes alkyl groups from the O6-position of guanine. Previously, we reported that a MGMT-siRNA/cationic liposome complex exerted a clear synergistic antitumor effect in combination with TMZ. Translation to a clinical setting might be desirable for reinforcing the efficacy of TMZ therapy for GBM. In this study, we aim to evaluate the safety of MGMT-siRNA/cationic liposome complexes and determine whether the convection-enhanced delivery of these complexes is suitable for clinical use by undertaking preclinical testing in laboratory animals. No significant adverse events were observed in rats receiving infusions of MGMT-siRNA/cationic liposome complex directly into the brain with or without TMZ administration. A pig which received the complex administered by CED also showed no evidence of neurological dysfunction or histological abnormalities. However, the complex did not appear to achieve effective distribution by CED in either the rat or the porcine brain tissue. Considering these results together, we concluded that insufficient distribution of cationic liposomes was achieved for tumor treatment by CED.

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