研究者詳細 - 豊國　伸哉

論文 - 豊國　伸哉

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Mechanisms of asbestos-induced carcinogenesis. 査読有り国際誌 Open Access

Toyokuni S.

Nagoya journal of medical science 71 巻 ( 1-2 ) 頁： 1 - 10 2009年2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：Nagoya journal of medical science

Respiratory exposure to asbestos fibers has been associated with diffuse malignant mesothelioma (DMM) in humans. Despite advancements in the molecular analyses of human DMM and the development of animal models, the carcinogenic mechanisms of the disease remain unclear. There are basically three hypotheses regarding the pathogenesis of asbestos-induced DMM, which may be summarized as follows: (1) the "oxidative stress theory" is based on the fact that phagocytic cells that engulf asbestos fibers produce large amounts of free radicals due to their inability to digest the fibers, and epidemiological studies indicating that iron-containing asbestos fibers appear more carcinogenic; (2) the "chromosome tangling theory" postulates that asbestos fibers damage chromosomes when cells divide; and (3) the "theory of adsorption of many specific proteins as well as carcinogenic molecules" states that asbestos fibers in vivo concentrate proteins or chemicals including the components of cigarette smoke. Elucidation of the major mechanisms underlying DMM would be helpful for the development of novel strategies to prevent DMM induction in people who have already been exposed to asbestos.

DOI： 10.18999/nagjms.71.1-2.1

Open Access

Scopus

Mechanisms of asbestos-induced carcinogenesis. Open Access

Toyokuni S

Nagoya journal of medical science 71 巻 ( 1-2 ) 頁： 1 - 10 2009年2月

Mechanisms of asbestos-induced carcinogenesis. Open Access

Toyokuni S

Nagoya J. Med. Sci. 71 巻頁： 1-10 2009年2月

Role of iron in carcinogenesis : Cancer as a ferrotoxic disease

TOYOKUNI Shinya

Cancer science 100 巻 ( 1 ) 頁： 9 - 16 2009年1月

Induction of autophagy in malignant rhabdoid tumor cells by the histone deacetylase inhibitor FK228 through AIF translocation. 査読有り国際誌 Open Access

Watanabe M, Adachi S, Matsubara H, Imai T, Yui Y, Mizushima Y, Hiraumi Y, Watanabe K, Kamitsuji Y, Toyokuni SY, Hosoi H, Sugimoto T, Toguchida J, Nakahata T

International journal of cancer 124 巻 ( 1 ) 頁： 55 - 67 2009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：International Journal of Cancer

Malignant rhabdoid tumors (MRT) exhibit a very poor prognosis because of their resistance to chemotherapeutic agents and new therapies are needed for the treatment of this cancer. Here, we show that the histone deacetylase (HDAC) inhibitor FK228 (depsipeptide) has an antitumor effect on MRT cells both in vitro and in vivo. FK228 is a unique cyclic peptide and is among the most potent inhibitors of both Class I and Class II HDACs. FK228 inhibited proliferation and induced apoptosis in all MRT cell lines tested. Preincubation with the pancaspase inhibitor zVAD-fmk did not completely rescue FK228-induced cell death, although it did inhibit apoptosis. Transmission electron microscopy (TEM) showed that FK228 could stimulate MRT cells to undergo apoptosis, necrosis or autophagy. FK228 converted unconjugated microtubule-associated protein light chain 3 (LC3-I) to conjugated light chain 3 (LC3-II) and induced localization of LC3 to autophagosomes. Apoptosis inducing factor (AIF), which plays a role in caspase-independent cell death, translocated to the nucleus in response to FK228 treatment. Moreover, small interfering RNA (siRNA) targeting of AIF prevented the morphological changes associated with autophagy and redistribution of LC3 to autophagosomes. Disrupting autophagy with chloroquine treatment enhanced FK228-induced cell death. In vivo, FK228 caused a reduction in tumor size and induced autophagy in tumor tissues. Using immunoelectron microscopy, we confirmed AIF translocation into the nucleus of FK228-induced autophagic cells in vivo. Thus, FK228 is a novel candidate for an antitumor agent for MRT cells. © 2008 Wiley-Liss, Inc.

DOI： 10.1002/ijc.23897

*Role of iron in carcinogenesis: Cancer as a ferrotoxic disease. 招待有り査読有り

Toyokuni S.

Cancer Sci. 100 巻頁： 6-16 2009年1月

Genome-wide analysis identifies a tumor suppressor role for aminoacylase 1 in iron-induced rat renal cell carcinoma. 査読有り

Zhong Y, Onuki J, Yamasaki T. Ogawa O, Akatsuka S and Toyokuni S.

Carcinogenesis 30 巻頁： 158-164 2009年1月

Biased Immunoglobulin VH Recombination and Increased Expression of Chemokine Receptor XCR1 Are Distinct Features of Bone Marrow-Derived Diffuse Large B-Cell Lymphoma 国際誌

Yamashita, Y; Kajiura, D; Nakamura, S; Toyokuni, S; Mori, N

LABORATORY INVESTIGATION 89 巻頁： 292A - 292A 2009年1月

Biased Immunoglobulin VH Recombination and Increased Expression of Chemokine Receptor XCR1 Are Distinct Features of Bone Marrow-Derived Diffuse Large B-Cell Lymphoma 国際誌

Yamashita, Y; Kajiura, D; Nakamura, S; Toyokuni, S; Mori, N

MODERN PATHOLOGY 22 巻頁： 292A - 292A 2009年1月

Genome-wide analysis identifies a tumor suppressor role for aminoacylase 1 in iron-induced rat renal cell carcinoma. 査読有り国際誌

Zhong Y, Onuki J, Yamasaki T, Ogawa O, Akatsuka S, Toyokuni S

Carcinogenesis 30 巻 ( 1 ) 頁： 158 - 64 2009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

A growing number of studies indicate a link between oxidative stress and cancer. We previously developed a rat model of renal cell carcinoma (RCC) induced by ferric nitrilotriacetate (Fe-NTA). Here, we performed a genome-wide analysis to study characteristics of genomic alteration and identify putative genes involved in the development of Fe-NTA-induced RCCs. Array-based comparative genomic hybridization analyses revealed a chromosomal loss spanning chromosome 8 in most of the RCCs studied, with a common deletion at 8q31-32, which was confirmed by loss of heterozygosity (LOH) analysis. Studies of gene expression in RCCs or following Fe-NTA treatment revealed globally decreased transcription levels of 34 genes derived from chromosome 8 that are expressed in the kidney. Among them, the aminoacylase 1 (Acy1) gene, which maps to 8q32 and is highly expressed in the kidney, displayed a significantly decreased level of expression in RCCs. Significant amounts of the Acy1 protein were detected in the cytoplasm as well as in the nuclei of renal proximal tubular cells of untreated rats. Transfection of Acy1 into RCC cell lines inhibited proliferation and colony formation on soft agar. An increased number of apoptotic cells were observed following Acy1 transfection. The rat 8q31-32 chromosomal region corresponds to human 3p21.31-24.1, a hot spot where LOH is frequently found in various human cancers. Thus, Fe-NTA-induced renal tumor model is ideal for studying the link between deletions within this region and tumor formation. Our data demonstrate that Acy1 functions as a tumor suppressor in this rat RCC model. © The Author 2008. Published by Oxford University Press. All rights reserved.

DOI： 10.1093/carcin/bgn255

Role of iron in carcinogenesis: cancer as a ferrotoxic disease. 査読有り国際誌 Open Access

Toyokuni S

Cancer science 100 巻 ( 1 ) 頁： 9 - 16 2009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：Cancer Science

Iron is abundant universally. During the evolutionary processes, humans have selected iron as a carrier of oxygen inside the body. However, iron works as a double-edged sword, and its excess is a risk for cancer, presumably via generation of reactive oxygen species. Thus far, pathological conditions such as hemochromatosis, chronic viral hepatitis B and C, exposure to asbestos fibers, as well as endometriosis have been recognized as iron overload-associated risks for human cancer. Indeed, iron is carcinogenic in animal experiments. These reports unexpectedly revealed that there are target genes in iron-induced carcinogenesis and that iron-catalyzed oxidative DNA damage is not random in.vivo. Several iron transporters and hepcidin, a peptide hormone regulating iron metabolism, were discovered in the past decade. Furthermore, a recent epidemiological study reported that iron reduction by phlebotomy decreased cancer risk in the apparently normal population. These results warrant reconsideration of the role of iron in carcinogenesis and suggest that fine control of body iron stores would be a wise strategy for cancer prevention. © 2009 Japanese Cancer Association.

DOI： 10.1111/j.1349-7006.2008.01001.x

*Role of iron in carcinogenesis: Cancer as a ferrotoxic disease. 招待有り査読有り

Toyokuni S

Cancer Sci. 100 巻頁： 6-16 2009年1月

Intermittent microwave irradiation facilitates antigen-antibody reaction in Western blot analysis. 招待有り

Liu YT, Toyokuni S.

Methods Mol. Biol. 536 巻頁： 307-312 2009年

Lipid Peroxidation Generates a Body Odor Component Trans-2-Nonenal Covalently Bound to Protein in vivo 国際誌

Ishino Kousuke, Wakita Chika, Shibata Takahiro, Toyokuni Shinya, Machida Sachiko, Matsuda Shun, Matsuda Tomonari, Uchida Koji

FREE RADICAL BIOLOGY AND MEDICINE 47 巻頁： S76 - S76 2009年

Intermittent microwave irradiation facilitates antigen-antibody reaction in Western blot analysis. 招待有り

Liu YT, Toyokuni S

Methods Mol. Biol. 536 巻頁： 307-312 2009年

Lipid Peroxidation Generates a Body Odor Component Trans-2-Nonenal Covalently Bound to Protein in vivo 査読有り

Kousuke Ishino, Chika Wakita, Takahiro Shibata, Shinya Toyokuni, Sachiko Machida, Shun Matsuda, Tomonari Matsuda, Koji Uchida

FREE RADICAL BIOLOGY AND MEDICINE 47 巻頁： S76 - S76 2009年

Intermittent microwave irradiation facilitates antigen-antibody reaction in Western blot analysis. 査読有り国際誌

Liu YT, Toyokuni S

Methods in molecular biology (Clifton, N.J.) 536 巻頁： 307 - 12 2009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：Methods in molecular biology (Clifton, N.J.)

We established a shortened protocol for western blot analysis using intermittent microwave irradiation. With this method, the procedure is completed within 1 h after applying the primary antibody, and thus greatly saves time. This procedure appears to be applicable to any antibody based on our experience of several years.

DOI： 10.1007/978-1-59745-542-8_33

S1-3 アスベスト誘発中皮腫の発がん機構の解明とその予防への応用(シンポジウム1:「生活習慣・環境因子とバイオマーカー」) Open Access

豊國伸哉

日本環境変異原学会大会プログラム・要旨集 ( 38 ) 2009年

Characteristics and modifying factors of asbestos-induced oxidative DNA damage

JIANG Li, NAGAI Hirotaka, OHARA Hiroki, HARA Shigeo, TACHIBANA Mitsuhiro, HIRANO Seishiro, SHINOHARA Yasushi, KOHYAMA Norihiko, AKATSUKA Shinya, TOYOKUNI Shinya

Cancer science 99 巻 ( 11 ) 頁： 2142 - 2151 2008年11月

*Characteristics and modifying factors of asbestos-induced oxidative DNA damage. 査読有り

Jiang L, Nagai H; Ohara H, Hara S, Tachibana M, Hirano S, Shinohara Y, Kohyama N, Akatsuka S and Toyokuni S.

Cancer Sci. 99 巻 ( 11 ) 頁： 2142-2151 2008年11月

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