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Your search keyword '"Aoki, Takeshi"' showing total 6 results
Start Over Author "Aoki, Takeshi" Journal plos one
6 results on '"Aoki, Takeshi"'

1. Stromal expression of hemopexin is associated with lymph-node metastasis in pancreatic ductal adenocarcinoma

Author

Suzuki, Yukie, primary, Takadate, Tatsuyuki, additional, Mizuma, Masamichi, additional, Shima, Hiroki, additional, Suzuki, Takashi, additional, Tachibana, Tomoyoshi, additional, Shimura, Mitsuhiro, additional, Hata, Tatsuo, additional, Iseki, Masahiro, additional, Kawaguchi, Kei, additional, Aoki, Takeshi, additional, Hayashi, Hiroki, additional, Morikawa, Takanori, additional, Nakagawa, Kei, additional, Motoi, Fuyuhiko, additional, Naitoh, Takeshi, additional, Igarashi, Kazuhiko, additional, and Unno, Michiaki, additional

Published
2020
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2. High expression of olfactomedin-4 is correlated with chemoresistance and poor prognosis in pancreatic cancer

Author

Ohkuma, Ryotaro, primary, Yada, Erica, additional, Ishikawa, Shumpei, additional, Komura, Daisuke, additional, Ishizaki, Hidenobu, additional, Tamada, Koji, additional, Kubota, Yutaro, additional, Hamada, Kazuyuki, additional, Ishida, Hiroo, additional, Hirasawa, Yuya, additional, Ariizumi, Hirotsugu, additional, Satoh, Etsuko, additional, Shida, Midori, additional, Watanabe, Makoto, additional, Onoue, Rie, additional, Ando, Kiyohiro, additional, Tsurutani, Junji, additional, Yoshimura, Kiyoshi, additional, Yokobori, Takehiko, additional, Sasada, Tetsuro, additional, Aoki, Takeshi, additional, Murakami, Masahiko, additional, Norose, Tomoko, additional, Ohike, Nobuyuki, additional, Takimoto, Masafumi, additional, Izumizaki, Masahiko, additional, Kobayashi, Shinichi, additional, Tsunoda, Takuya, additional, and Wada, Satoshi, additional

Published
2020
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4. The Co-Transplantation of Bone Marrow Derived Mesenchymal Stem Cells Reduced Inflammation in Intramuscular Islet Transplantation

Author

Yoshimatsu, Gumpei, primary, Sakata, Naoaki, additional, Tsuchiya, Haruyuki, additional, Minowa, Takashi, additional, Takemura, Taro, additional, Morita, Hiromi, additional, Hata, Tatsuo, additional, Fukase, Masahiko, additional, Aoki, Takeshi, additional, Ishida, Masaharu, additional, Motoi, Fuyuhiko, additional, Naitoh, Takeshi, additional, Katayose, Yu, additional, Egawa, Shinichi, additional, and Unno, Michiaki, additional

Published
2015
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5. A GNAS Mutation Found in Pancreatic Intraductal Papillary Mucinous Neoplasms Induces Drastic Alterations of Gene Expression Profiles with Upregulation of Mucin Genes

Author

Komatsu, Hirotake, primary, Tanji, Etsuko, additional, Sakata, Naoaki, additional, Aoki, Takeshi, additional, Motoi, Fuyuhiko, additional, Naitoh, Takeshi, additional, Katayose, Yu, additional, Egawa, Shinichi, additional, Unno, Michiaki, additional, and Furukawa, Toru, additional

Published
2014
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6. A GNAS Mutation Found in Pancreatic Intraductal Papillary Mucinous Neoplasms Induces Drastic Alterations of Gene Expression Profiles with Upregulation of Mucin Genes.

Author

Komatsu, Hirotake, Tanji, Etsuko, Sakata, Naoaki, Aoki, Takeshi, Motoi, Fuyuhiko, Naitoh, Takeshi, Katayose, Yu, Egawa, Shinichi, Unno, Michiaki, and Furukawa, Toru

Subjects
PANCREATIC cancer, GENETIC mutation, PAPILLARY carcinoma, GENE expression, MUCIN genetics, PROTEIN genetics, GASTROINTESTINAL tumors
Abstract

GNAS, a gene encoding G protein stimulating α subunit, is frequently mutated in intraductal papillary mucinous neoplasms (IPMNs), which are indolent and slow-growing pancreatic tumors that secrete abundant mucin. The GNAS mutation is not observed in conventional ductal adenocarcinomas of the pancreas. To determine the functional significance of the GNAS mutation in pancreatic ductal lineage cells, we examined in vitro phenotypes of cells of pancreatic ductal lineage, HPDE, PK-8, PCI-35, and MIA PaCa-2, with exogenous expression of either wild-type or mutated (R201H) GNAS. We found that exogenous GNAS upregulated intracellular cyclic adenine monophosphate (cAMP), particularly in mutated GNAS transfectants, and upregulated expression of MUC2 and MUC5AC in HPDE and PK-8 cells. By contrast, exogenous GNAS inhibited expression of mucin genes in PCI-35 and MIA PaCa-2 cells, despite upregulation of cAMP. We examined global gene expression profiles of some of the cells transfected with exogenous mutated GNAS (PK-8, PCI-35, and MIA PaCa-2), and found that PK-8 cells exhibited drastic alterations of the gene expression profile, which contrasted with modest alterations in PCI-35 and MIA PaCa-2 cells. To identify a cause of these different effects of exogenous mutated GNAS on phenotypes of the cells, we examined effects of interactions of the signaling pathways of G protein-coupled receptor (GPCR), mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3-kinase (PI3K) on expression of mucin genes. The MAPK and PI3K pathways significantly influenced the expression of mucin genes. Exogenous GNAS did not promote cell growth but suppressed it in some of the cells. In conclusion, mutated GNAS found in IPMNs may extensively alter gene expression profiles, including expression of mucin genes, through the interaction with MAPK and PI3K pathways in pancreatic ductal cells; these changes may determine the characteristic phenotype of IPMN. PK-8 cells expressing exogenous mutated GNAS may be an ideal in vitro model of IPMN. [ABSTRACT FROM AUTHOR]

Published
2014
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