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257 results on '"Maruno, Takahisa"'

1. Early detection of pancreatic cancer by comprehensive serum miRNA sequencing with automated machine learning

Author

Kawai, Munenori, Fukuda, Akihisa, Otomo, Ryo, Obata, Shunsuke, Minaga, Kosuke, Asada, Masanori, Umemura, Atsushi, Uenoyama, Yoshito, Hieda, Nobuhiro, Morita, Toshihiro, Minami, Ryuki, Marui, Saiko, Yamauchi, Yuki, Nakai, Yoshitaka, Takada, Yutaka, Ikuta, Kozo, Yoshioka, Takuto, Mizukoshi, Kenta, Iwane, Kosuke, Yamakawa, Go, Namikawa, Mio, Sono, Makoto, Nagao, Munemasa, Maruno, Takahisa, Nakanishi, Yuki, Hirai, Mitsuharu, Kanda, Naoki, Shio, Seiji, Itani, Toshinao, Fujii, Shigehiko, Kimura, Toshiyuki, Matsumura, Kazuyoshi, Ohana, Masaya, Yazumi, Shujiro, Kawanami, Chiharu, Yamashita, Yukitaka, Marusawa, Hiroyuki, Watanabe, Tomohiro, Ito, Yoshito, Kudo, Masatoshi, and Seno, Hiroshi

Published
2024
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3. THBS1-producing tumor-infiltrating monocyte-like cells contribute to immunosuppression and metastasis in colorectal cancer

Author

Omatsu, Mayuki, Nakanishi, Yuki, Iwane, Kosuke, Aoyama, Naoki, Duran, Angeles, Muta, Yu, Martinez-Ordoñez, Anxo, Han, Qixiu, Agatsuma, Nobukazu, Mizukoshi, Kenta, Kawai, Munenori, Yamakawa, Go, Namikawa, Mio, Hamada, Kensuke, Fukunaga, Yuichi, Utsumi, Takahiro, Sono, Makoto, Masuda, Tomonori, Hata, Akitaka, Araki, Osamu, Nagao, Munemasa, Yoshikawa, Takaaki, Ogawa, Satoshi, Hiramatsu, Yukiko, Tsuda, Motoyuki, Maruno, Takahisa, Kogame, Toshiaki, Kasashima, Hiroaki, Kakiuchi, Nobuyuki, Nakagawa, Masahiro M., Kawada, Kenji, Yashiro, Masakazu, Maeda, Kiyoshi, Saito, Yasuyuki, Matozaki, Takashi, Fukuda, Akihisa, Kabashima, Kenji, Obama, Kazutaka, Ogawa, Seishi, Sheibani, Nader, Diaz-Meco, Maria T., Moscat, Jorge, and Seno, Hiroshi

Published
2023
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4. Brg1 controls stemness and metastasis of pancreatic cancer through regulating hypoxia pathway

Author

Araki, Osamu, Tsuda, Motoyuki, Omatsu, Mayuki, Namikawa, Mio, Sono, Makoto, Fukunaga, Yuichi, Masuda, Tomonori, Yoshikawa, Takaaki, Nagao, Munemasa, Ogawa, Satoshi, Masuo, Kenji, Goto, Norihiro, Muta, Yu, Hiramatsu, Yukiko, Maruno, Takahisa, Nakanishi, Yuki, Koyasu, Sho, Masui, Toshihiko, Hatano, Etsuro, Saur, Dieter, Fukuda, Akihisa, and Seno, Hiroshi

Published
2023
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7. Pancreatic RECK inactivation promotes cancer formation, epithelial-mesenchymal transition, and metastasis

Author

Masuda, Tomonori, Fukuda, Akihisa, Yamakawa, Go, Omatsu, Mayuki, Namikawa, Mio, Sono, Makoto, Fukunaga, Yuichi, Nagao, Munemasa, Araki, Osamu, Yoshikawa, Takaaki, Ogawa, Satoshi, Masuo, Kenji, Goto, Norihiro, Hiramatsu, Yukiko, Muta, Yu, Tsuda, Motoyuki, Maruno, Takahisa, Nakanishi, Yuki, Masui, Toshihiko, Hatano, Etsuro, Matsuzaki, Tomoko, Noda, Makoto, and Seno, Hiroshi

Subjects
Thermo Fisher Scientific Inc., Scientific equipment and supplies industry -- Health aspects -- Analysis, Metastasis -- Development and progression, Stem cells -- Analysis -- Health aspects, Liver cancer -- Development and progression, DNA binding proteins -- Health aspects -- Analysis, Health care industry
Abstract

RECK is downregulated in various human cancers; however, how RECK inactivation affects carcinogenesis remains unclear. We addressed this issue in a pancreatic ductal adenocarcinoma (PDAC) mouse model and found that pancreatic Reck deletion dramatically augmented the spontaneous development of PDAC with a mesenchymal phenotype, which was accompanied by increased liver metastases and decreased survival. Lineage tracing revealed that pancreatic Reck deletion induced epithelialmesenchymal transition (EMT) in PDAC cells, giving rise to inflammatory cancer-associated fibroblast-like cells in mice. Splenic transplantation of Reck-null PDAC cells resulted in numerous liver metastases with a mesenchymal phenotype, whereas reexpression of RECK markedly reduced metastases and changed the PDAC tumor phenotype into an epithelial one. Consistently, low RECK expression correlated with low E-cadherin expression, poor differentiation, metastasis, and poor prognosis in human PDAC. RECK reexpression in the PDAC cells was found to downregulate MMP2 and MMP3, with a concomitant increase in E-cadherin and decrease in EMT-promoting transcription factors. An MMP inhibitor recapitulated the effects of RECK on the expression of E-cadherin and EMT-promoting transcription factors and invasive activity. These results establish the authenticity of RECK as a pancreatic tumor suppressor, provide insights into its underlying mechanisms, and support the idea that RECK could be an important therapeutic effector against human PDAC., Introduction Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies. The survival rate for PDAC has remained relatively unchanged for decades, with a 5-year survival rate of approximately [...]

Published
2023
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9. TERT upregulation promotes cell proliferation via degradation of p21 and increases carcinogenic potential.

Author

Mishima, Masako, Takai, Atsushi, Takeda, Haruhiko, Iguchi, Eriko, Nakano, Shigeharu, Fujii, Yosuke, Ueno, Masayuki, Ito, Takahiko, Teramura, Mari, Eso, Yuji, Shimizu, Takahiro, Maruno, Takahisa, Hidema, Shizu, Nishimori, Katsuhiko, Marusawa, Hiroyuki, Hatano, Etsuro, and Seno, Hiroshi

Subjects
TELOMERASE reverse transcriptase, CELL cycle, LIVER cancer, HEPATOCELLULAR carcinoma, LIVER analysis
Abstract

Telomerase reverse transcriptase (TERT) gene aberration is detectable in >80% of cases with hepatocellular carcinoma (HCC). TERT reactivation is essential for cellular immortalization because it stabilizes telomere length, although the role of TERT in hepatocarcinogenesis remains unelucidated. To elucidate the significance of aberrant TERT expression in hepatocytes in inflammation‐associated hepatocarcinogenesis, we generated Alb‐Cre;TertTg mice, which overexpress TERT in the liver and examined their phenotype during chronic inflammation. Based on transcriptome data from the liver tissue of Alb‐Cre;TertTg mice, we examined the role of TERT in hepatocarcinogenesis in vitro. We also evaluated the relationship between TERT and cell‐cycle‐related molecules, including p21, in HCC samples. The liver tumor development rate was increased by TERT overexpression during chronic inflammation, especially in the absence of p53 function. Gene set enrichment analysis of liver tissues revealed that gene sets related to TNF‐NFκB signaling, cell cycle, and apoptosis were upregulated in Alb‐Cre;TertTg liver. A luciferase reporter assay and immunoprecipitation revealed that TERT interacted with NFκB p65 and enhanced NFκB promoter activity. On the other hand, TERT formed protein complexes with p21, cyclin A2, and cyclin E and promoted ubiquitin‐mediated degradation of p21, specifically in the G1 phase. In the clinical HCC samples, TERT was highly expressed but p21 was conversely downregulated, and TERT expression was associated with the upregulation of molecules related to the cell cycle. Taken together, the aberrant upregulation of TERT increased NFκB promoter activity and promoted cell cycle progression via p21 ubiquitination, leading to hepatocarcinogenesis. © 2024 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. [ABSTRACT FROM AUTHOR]

Published
2024
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10. The BRG1/SOX9 axis is critical for acinar cell–derived pancreatic tumorigenesis

Author

Tsuda, Motoyuki, Fukuda, Akihisa, Roy, Nilotpal, Hiramatsu, Yukiko, Leonhardt, Laura, Kakiuchi, Nobuyuki, Hoyer, Kaja, Ogawa, Satoshi, Goto, Norihiro, Ikuta, Kozo, Kimura, Yoshito, Matsumoto, Yoshihide, Takada, Yutaka, Yoshioka, Takuto, Maruno, Takahisa, Yamaga, Yuichi, Kim, Grace E, Akiyama, Haruhiko, Ogawa, Seishi, Wright, Christopher V, Saur, Dieter, Takaori, Kyoichi, Uemoto, Shinji, Hebrok, Matthias, Chiba, Tsutomu, and Seno, Hiroshi

Subjects
Digestive Diseases, Genetics, Rare Diseases, Cancer, Pancreatic Cancer, 2.1 Biological and endogenous factors, Aetiology, Animals, Carcinoma, Pancreatic Ductal, Cell Transformation, Neoplastic, DNA Helicases, Female, Gene Expression Regulation, Humans, Male, Mice, Mice, Transgenic, Nuclear Proteins, Pancreatic Neoplasms, Response Elements, SOX9 Transcription Factor, Signal Transduction, Transcription Factors, Tumor Suppressor Protein p53, Epigenetics, Gastroenterology, Mouse models, Oncology, Medical and Health Sciences, Immunology
Abstract

Chromatin remodeler Brahma related gene 1 (BRG1) is silenced in approximately 10% of human pancreatic ductal adenocarcinomas (PDAs). We previously showed that BRG1 inhibits the formation of intraductal pancreatic mucinous neoplasm (IPMN) and that IPMN-derived PDA originated from ductal cells. However, the role of BRG1 in pancreatic intraepithelial neoplasia-derived (PanIN-derived) PDA that originated from acinar cells remains elusive. Here, we found that exclusive elimination of Brg1 in acinar cells of Ptf1a-CreER; KrasG12D; Brg1fl/fl mice impaired the formation of acinar-to-ductal metaplasia (ADM) and PanIN independently of p53 mutation, while PDA formation was inhibited in the presence of p53 mutation. BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. SOX9 expression was downregulated in BRG1-depleted ADMs/PanINs. Notably, Sox9 overexpression canceled this PanIN-attenuated phenotype in KBC mice. Furthermore, Brg1 deletion in established PanIN by using a dual recombinase system resulted in regression of the lesions in mice. Finally, BRG1 expression correlated with SOX9 expression in human PDAs. In summary, BRG1 is critical for PanIN initiation and progression through positive regulation of SOX9. Thus, the BRG1/SOX9 axis is a potential target for PanIN-derived PDA.

Published
2018

12. Essential role of Notch/Hes1 signaling in postnatal pancreatic exocrine development

Author

Kuriyama, Katsutoshi, Kodama, Yuzo, Shiokawa, Masahiro, Nishikawa, Yoshihiro, Marui, Saiko, Kuwada, Takeshi, Sogabe, Yuko, Kakiuchi, Nobuyuki, Tomono, Teruko, Matsumori, Tomoaki, Mima, Atsushi, Morita, Toshihiro, Ueda, Tatsuki, Tsuda, Motoyuki, Yamauchi, Yuki, Sakuma, Yojiro, Ota, Yuji, Maruno, Takahisa, Uza, Norimitsu, Kageyama, Ryoichiro, Chiba, Tsutomu, and Seno, Hiroshi

Published
2021
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14. Arid1a is essential for intestinal stem cells through Sox9 regulation

Author

Hiramatsu, Yukiko, Fukuda, Akihisa, Ogawa, Satoshi, Goto, Norihiro, Ikuta, Kozo, Tsuda, Motoyuki, Matsumoto, Yoshihide, Kimura, Yoshito, Yoshioka, Takuto, Takada, Yutaka, Maruno, Takahisa, Hanyu, Yuta, Tsuruyama, Tatsuaki, Wang, Zhong, Akiyama, Haruhiko, Takaishi, Shigeo, Miyoshi, Hiroyuki, Taketo, Makoto Mark, Chiba, Tsutomu, and Seno, Hiroshi

Published
2019

16. ARID1A Maintains Differentiation of Pancreatic Ductal Cells and Inhibits Development of Pancreatic Ductal Adenocarcinoma in Mice

Author

Kimura, Yoshito, Fukuda, Akihisa, Ogawa, Satoshi, Maruno, Takahisa, Takada, Yutaka, Tsuda, Motoyuki, Hiramatsu, Yukiko, Araki, Osamu, Nagao, Munemasa, Yoshikawa, Takaaki, Ikuta, Kozo, Yoshioka, Takuto, Wang, Zong, Akiyama, Haruhiko, Wright, Christopher V., Takaori, Kyoichi, Uemoto, Shinji, Chiba, Tsutomu, and Seno, Hiroshi

Published
2018
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17. Hes1 plays an essential role in Kras-driven pancreatic tumorigenesis

Author

Nishikawa, Yoshihiro, Kodama, Yuzo, Shiokawa, Masahiro, Matsumori, Tomoaki, Marui, Saiko, Kuriyama, Katsutoshi, Kuwada, Takeshi, Sogabe, Yuko, Kakiuchi, Nobuyuki, Tomono, Teruko, Mima, Atsushi, Morita, Toshihiro, Ueda, Tatsuki, Tsuda, Motoyuki, Yamauchi, Yuki, Sakuma, Yojiro, Ota, Yuji, Maruno, Takahisa, Uza, Norimitsu, Uesugi, Motonari, Kageyama, Ryoichiro, Chiba, Tsutomu, and Seno, Hiroshi

Published
2019
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18. ELF3 suppresses gallbladder cancer development through downregulation of the EREG/EGFR/mTOR complex 1 signalling pathway

Author

Nakamura, Takeharu, primary, Nishikawa, Yoshihiro, additional, Shiokawa, Masahiro, additional, Takeda, Haruhiko, additional, Yokode, Masataka, additional, Matsumoto, Shimpei, additional, Muramoto, Yuya, additional, Ota, Sakiko, additional, Yoshida, Hiroyuki, additional, Okada, Hirokazu, additional, Kuwada, Takeshi, additional, Marui, Saiko, additional, Matsumori, Tomoaki, additional, Maruno, Takahisa, additional, Uza, Norimitsu, additional, Kodama, Yuzo, additional, Hatano, Etsuro, additional, and Seno, Hiroshi, additional

Published
2023
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19. Data from Rb and p53 Execute Distinct Roles in the Development of Pancreatic Neuroendocrine Tumors

Author

Yamauchi, Yuki, primary, Kodama, Yuzo, primary, Shiokawa, Masahiro, primary, Kakiuchi, Nobuyuki, primary, Marui, Saiko, primary, Kuwada, Takeshi, primary, Sogabe, Yuko, primary, Tomono, Teruko, primary, Mima, Atsushi, primary, Morita, Toshihiro, primary, Matsumori, Tomoaki, primary, Ueda, Tatsuki, primary, Tsuda, Motoyuki, primary, Nishikawa, Yoshihiro, primary, Kuriyama, Katsutoshi, primary, Sakuma, Yojiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Uza, Norimitsu, primary, Masuda, Atsuhiro, primary, Tatsuoka, Hisato, primary, Yabe, Daisuke, primary, Minamiguchi, Sachiko, primary, Masui, Toshihiko, primary, Inagaki, Nobuya, primary, Uemoto, Shinji, primary, Chiba, Tsutomu, primary, and Seno, Hiroshi, primary

Published
2023
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20. Data from CXCR4 in Tumor Epithelial Cells Mediates Desmoplastic Reaction in Pancreatic Ductal Adenocarcinoma

Author

Morita, Toshihiro, primary, Kodama, Yuzo, primary, Shiokawa, Masahiro, primary, Kuriyama, Katsutoshi, primary, Marui, Saiko, primary, Kuwada, Takeshi, primary, Sogabe, Yuko, primary, Matsumori, Tomoaki, primary, Kakiuchi, Nobuyuki, primary, Tomono, Teruko, primary, Mima, Atsushi, primary, Ueda, Tatsuki, primary, Tsuda, Motoyuki, primary, Yamauchi, Yuki, primary, Nishikawa, Yoshihiro, primary, Sakuma, Yojiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Uza, Norimitsu, primary, Nagasawa, Takashi, primary, Chiba, Tsutomu, primary, and Seno, Hiroshi, primary

Published
2023
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21. Supplementary Data from Hes1 Is Essential in Proliferating Ductal Cell–Mediated Development of Intrahepatic Cholangiocarcinoma

Author

Matsumori, Tomoaki, primary, Kodama, Yuzo, primary, Takai, Atsushi, primary, Shiokawa, Masahiro, primary, Nishikawa, Yoshihiro, primary, Matsumoto, Tomonori, primary, Takeda, Haruhiko, primary, Marui, Saiko, primary, Okada, Hirokazu, primary, Hirano, Tomonori, primary, Kuwada, Takeshi, primary, Sogabe, Yuko, primary, Kakiuchi, Nobuyuki, primary, Tomono, Teruko, primary, Mima, Atsushi, primary, Morita, Toshihiro, primary, Ueda, Tatsuki, primary, Tsuda, Motoyuki, primary, Yamauchi, Yuki, primary, Kuriyama, Katsutoshi, primary, Sakuma, Yojiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Uza, Norimitsu, primary, Marusawa, Hiroyuki, primary, Kageyama, Ryoichiro, primary, Chiba, Tsutomu, primary, and Seno, Hiroshi, primary

Published
2023
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22. Supplementary Table from Concurrent Activation of Kras and Canonical Wnt Signaling Induces Premalignant Lesions That Progress to Extrahepatic Biliary Cancer in Mice

Author

Nagao, Munemasa, primary, Fukuda, Akihisa, primary, Omatsu, Mayuki, primary, Namikawa, Mio, primary, Sono, Makoto, primary, Fukunaga, Yuichi, primary, Masuda, Tomonori, primary, Araki, Osamu, primary, Yoshikawa, Takaaki, primary, Ogawa, Satoshi, primary, Masuo, Kenji, primary, Goto, Norihiro, primary, Hiramatsu, Yukiko, primary, Muta, Yu, primary, Tsuda, Motoyuki, primary, Maruno, Takahisa, primary, Nakanishi, Yuki, primary, Taketo, Makoto Mark, primary, Ferrer, Jorge, primary, Tsuruyama, Tatsuaki, primary, Nakanuma, Yasuni, primary, Taura, Kojiro, primary, Uemoto, Shinji, primary, and Seno, Hiroshi, primary

Published
2023
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23. Figure S1 from CXCR4 in Tumor Epithelial Cells Mediates Desmoplastic Reaction in Pancreatic Ductal Adenocarcinoma

Author

Morita, Toshihiro, primary, Kodama, Yuzo, primary, Shiokawa, Masahiro, primary, Kuriyama, Katsutoshi, primary, Marui, Saiko, primary, Kuwada, Takeshi, primary, Sogabe, Yuko, primary, Matsumori, Tomoaki, primary, Kakiuchi, Nobuyuki, primary, Tomono, Teruko, primary, Mima, Atsushi, primary, Ueda, Tatsuki, primary, Tsuda, Motoyuki, primary, Yamauchi, Yuki, primary, Nishikawa, Yoshihiro, primary, Sakuma, Yojiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Uza, Norimitsu, primary, Nagasawa, Takashi, primary, Chiba, Tsutomu, primary, and Seno, Hiroshi, primary

Published
2023
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24. Table. S4 from Hes1 Is Essential in Proliferating Ductal Cell–Mediated Development of Intrahepatic Cholangiocarcinoma

Author

Matsumori, Tomoaki, primary, Kodama, Yuzo, primary, Takai, Atsushi, primary, Shiokawa, Masahiro, primary, Nishikawa, Yoshihiro, primary, Matsumoto, Tomonori, primary, Takeda, Haruhiko, primary, Marui, Saiko, primary, Okada, Hirokazu, primary, Hirano, Tomonori, primary, Kuwada, Takeshi, primary, Sogabe, Yuko, primary, Kakiuchi, Nobuyuki, primary, Tomono, Teruko, primary, Mima, Atsushi, primary, Morita, Toshihiro, primary, Ueda, Tatsuki, primary, Tsuda, Motoyuki, primary, Yamauchi, Yuki, primary, Kuriyama, Katsutoshi, primary, Sakuma, Yojiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Uza, Norimitsu, primary, Marusawa, Hiroyuki, primary, Kageyama, Ryoichiro, primary, Chiba, Tsutomu, primary, and Seno, Hiroshi, primary

Published
2023
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25. Supplementary Data from Concurrent Activation of Kras and Canonical Wnt Signaling Induces Premalignant Lesions That Progress to Extrahepatic Biliary Cancer in Mice

Author

Nagao, Munemasa, primary, Fukuda, Akihisa, primary, Omatsu, Mayuki, primary, Namikawa, Mio, primary, Sono, Makoto, primary, Fukunaga, Yuichi, primary, Masuda, Tomonori, primary, Araki, Osamu, primary, Yoshikawa, Takaaki, primary, Ogawa, Satoshi, primary, Masuo, Kenji, primary, Goto, Norihiro, primary, Hiramatsu, Yukiko, primary, Muta, Yu, primary, Tsuda, Motoyuki, primary, Maruno, Takahisa, primary, Nakanishi, Yuki, primary, Taketo, Makoto Mark, primary, Ferrer, Jorge, primary, Tsuruyama, Tatsuaki, primary, Nakanuma, Yasuni, primary, Taura, Kojiro, primary, Uemoto, Shinji, primary, and Seno, Hiroshi, primary

Published
2023
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26. Supplementary Figure from Concurrent Activation of Kras and Canonical Wnt Signaling Induces Premalignant Lesions That Progress to Extrahepatic Biliary Cancer in Mice

Author

Nagao, Munemasa, primary, Fukuda, Akihisa, primary, Omatsu, Mayuki, primary, Namikawa, Mio, primary, Sono, Makoto, primary, Fukunaga, Yuichi, primary, Masuda, Tomonori, primary, Araki, Osamu, primary, Yoshikawa, Takaaki, primary, Ogawa, Satoshi, primary, Masuo, Kenji, primary, Goto, Norihiro, primary, Hiramatsu, Yukiko, primary, Muta, Yu, primary, Tsuda, Motoyuki, primary, Maruno, Takahisa, primary, Nakanishi, Yuki, primary, Taketo, Makoto Mark, primary, Ferrer, Jorge, primary, Tsuruyama, Tatsuaki, primary, Nakanuma, Yasuni, primary, Taura, Kojiro, primary, Uemoto, Shinji, primary, and Seno, Hiroshi, primary

Published
2023
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27. Data from Concurrent Activation of Kras and Canonical Wnt Signaling Induces Premalignant Lesions That Progress to Extrahepatic Biliary Cancer in Mice

Author

Nagao, Munemasa, primary, Fukuda, Akihisa, primary, Omatsu, Mayuki, primary, Namikawa, Mio, primary, Sono, Makoto, primary, Fukunaga, Yuichi, primary, Masuda, Tomonori, primary, Araki, Osamu, primary, Yoshikawa, Takaaki, primary, Ogawa, Satoshi, primary, Masuo, Kenji, primary, Goto, Norihiro, primary, Hiramatsu, Yukiko, primary, Muta, Yu, primary, Tsuda, Motoyuki, primary, Maruno, Takahisa, primary, Nakanishi, Yuki, primary, Taketo, Makoto Mark, primary, Ferrer, Jorge, primary, Tsuruyama, Tatsuaki, primary, Nakanuma, Yasuni, primary, Taura, Kojiro, primary, Uemoto, Shinji, primary, and Seno, Hiroshi, primary

Published
2023
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28. Data from Hes1 Is Essential in Proliferating Ductal Cell–Mediated Development of Intrahepatic Cholangiocarcinoma

Author

Matsumori, Tomoaki, primary, Kodama, Yuzo, primary, Takai, Atsushi, primary, Shiokawa, Masahiro, primary, Nishikawa, Yoshihiro, primary, Matsumoto, Tomonori, primary, Takeda, Haruhiko, primary, Marui, Saiko, primary, Okada, Hirokazu, primary, Hirano, Tomonori, primary, Kuwada, Takeshi, primary, Sogabe, Yuko, primary, Kakiuchi, Nobuyuki, primary, Tomono, Teruko, primary, Mima, Atsushi, primary, Morita, Toshihiro, primary, Ueda, Tatsuki, primary, Tsuda, Motoyuki, primary, Yamauchi, Yuki, primary, Kuriyama, Katsutoshi, primary, Sakuma, Yojiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Uza, Norimitsu, primary, Marusawa, Hiroyuki, primary, Kageyama, Ryoichiro, primary, Chiba, Tsutomu, primary, and Seno, Hiroshi, primary

Published
2023
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29. Table S1-3 from CXCR4 in Tumor Epithelial Cells Mediates Desmoplastic Reaction in Pancreatic Ductal Adenocarcinoma

Author

Morita, Toshihiro, primary, Kodama, Yuzo, primary, Shiokawa, Masahiro, primary, Kuriyama, Katsutoshi, primary, Marui, Saiko, primary, Kuwada, Takeshi, primary, Sogabe, Yuko, primary, Matsumori, Tomoaki, primary, Kakiuchi, Nobuyuki, primary, Tomono, Teruko, primary, Mima, Atsushi, primary, Ueda, Tatsuki, primary, Tsuda, Motoyuki, primary, Yamauchi, Yuki, primary, Nishikawa, Yoshihiro, primary, Sakuma, Yojiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Uza, Norimitsu, primary, Nagasawa, Takashi, primary, Chiba, Tsutomu, primary, and Seno, Hiroshi, primary

Published
2023
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30. Fig. S4 from Hes1 Is Essential in Proliferating Ductal Cell–Mediated Development of Intrahepatic Cholangiocarcinoma

Author

Matsumori, Tomoaki, primary, Kodama, Yuzo, primary, Takai, Atsushi, primary, Shiokawa, Masahiro, primary, Nishikawa, Yoshihiro, primary, Matsumoto, Tomonori, primary, Takeda, Haruhiko, primary, Marui, Saiko, primary, Okada, Hirokazu, primary, Hirano, Tomonori, primary, Kuwada, Takeshi, primary, Sogabe, Yuko, primary, Kakiuchi, Nobuyuki, primary, Tomono, Teruko, primary, Mima, Atsushi, primary, Morita, Toshihiro, primary, Ueda, Tatsuki, primary, Tsuda, Motoyuki, primary, Yamauchi, Yuki, primary, Kuriyama, Katsutoshi, primary, Sakuma, Yojiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Uza, Norimitsu, primary, Marusawa, Hiroyuki, primary, Kageyama, Ryoichiro, primary, Chiba, Tsutomu, primary, and Seno, Hiroshi, primary

Published
2023
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31. Supplementary Data from Rb and p53 Execute Distinct Roles in the Development of Pancreatic Neuroendocrine Tumors

Author

Yamauchi, Yuki, primary, Kodama, Yuzo, primary, Shiokawa, Masahiro, primary, Kakiuchi, Nobuyuki, primary, Marui, Saiko, primary, Kuwada, Takeshi, primary, Sogabe, Yuko, primary, Tomono, Teruko, primary, Mima, Atsushi, primary, Morita, Toshihiro, primary, Matsumori, Tomoaki, primary, Ueda, Tatsuki, primary, Tsuda, Motoyuki, primary, Nishikawa, Yoshihiro, primary, Kuriyama, Katsutoshi, primary, Sakuma, Yojiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Uza, Norimitsu, primary, Masuda, Atsuhiro, primary, Tatsuoka, Hisato, primary, Yabe, Daisuke, primary, Minamiguchi, Sachiko, primary, Masui, Toshihiko, primary, Inagaki, Nobuya, primary, Uemoto, Shinji, primary, Chiba, Tsutomu, primary, and Seno, Hiroshi, primary

Published
2023
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32. Supplemental Legends from Rb and p53 Execute Distinct Roles in the Development of Pancreatic Neuroendocrine Tumors

Author

Yamauchi, Yuki, primary, Kodama, Yuzo, primary, Shiokawa, Masahiro, primary, Kakiuchi, Nobuyuki, primary, Marui, Saiko, primary, Kuwada, Takeshi, primary, Sogabe, Yuko, primary, Tomono, Teruko, primary, Mima, Atsushi, primary, Morita, Toshihiro, primary, Matsumori, Tomoaki, primary, Ueda, Tatsuki, primary, Tsuda, Motoyuki, primary, Nishikawa, Yoshihiro, primary, Kuriyama, Katsutoshi, primary, Sakuma, Yojiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Uza, Norimitsu, primary, Masuda, Atsuhiro, primary, Tatsuoka, Hisato, primary, Yabe, Daisuke, primary, Minamiguchi, Sachiko, primary, Masui, Toshihiko, primary, Inagaki, Nobuya, primary, Uemoto, Shinji, primary, Chiba, Tsutomu, primary, and Seno, Hiroshi, primary

Published
2023
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33. Supplementary Material and Methods from Activation-Induced Cytidine Deaminase Contributes to Pancreatic Tumorigenesis by Inducing Tumor-Related Gene Mutations

Author

Sawai, Yugo, primary, Kodama, Yuzo, primary, Shimizu, Takahiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Eso, Yuji, primary, Kurita, Akira, primary, Shiokawa, Masahiro, primary, Tsuji, Yoshihisa, primary, Uza, Norimitsu, primary, Matsumoto, Yuko, primary, Masui, Toshihiko, primary, Uemoto, Shinji, primary, Marusawa, Hiroyuki, primary, and Chiba, Tsutomu, primary

Published
2023
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34. Supplementary Figure S3 from Activation-Induced Cytidine Deaminase Contributes to Pancreatic Tumorigenesis by Inducing Tumor-Related Gene Mutations

Author

Sawai, Yugo, primary, Kodama, Yuzo, primary, Shimizu, Takahiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Eso, Yuji, primary, Kurita, Akira, primary, Shiokawa, Masahiro, primary, Tsuji, Yoshihisa, primary, Uza, Norimitsu, primary, Matsumoto, Yuko, primary, Masui, Toshihiko, primary, Uemoto, Shinji, primary, Marusawa, Hiroyuki, primary, and Chiba, Tsutomu, primary

Published
2023
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35. Data from Activation-Induced Cytidine Deaminase Contributes to Pancreatic Tumorigenesis by Inducing Tumor-Related Gene Mutations

Author

Sawai, Yugo, primary, Kodama, Yuzo, primary, Shimizu, Takahiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Eso, Yuji, primary, Kurita, Akira, primary, Shiokawa, Masahiro, primary, Tsuji, Yoshihisa, primary, Uza, Norimitsu, primary, Matsumoto, Yuko, primary, Masui, Toshihiko, primary, Uemoto, Shinji, primary, Marusawa, Hiroyuki, primary, and Chiba, Tsutomu, primary

Published
2023
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36. Supplementary Table S4 from Activation-Induced Cytidine Deaminase Contributes to Pancreatic Tumorigenesis by Inducing Tumor-Related Gene Mutations

Author

Sawai, Yugo, primary, Kodama, Yuzo, primary, Shimizu, Takahiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Eso, Yuji, primary, Kurita, Akira, primary, Shiokawa, Masahiro, primary, Tsuji, Yoshihisa, primary, Uza, Norimitsu, primary, Matsumoto, Yuko, primary, Masui, Toshihiko, primary, Uemoto, Shinji, primary, Marusawa, Hiroyuki, primary, and Chiba, Tsutomu, primary

Published
2023
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37. Supplemental Figure Legend from Activation-Induced Cytidine Deaminase Contributes to Pancreatic Tumorigenesis by Inducing Tumor-Related Gene Mutations

Author

Sawai, Yugo, primary, Kodama, Yuzo, primary, Shimizu, Takahiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Eso, Yuji, primary, Kurita, Akira, primary, Shiokawa, Masahiro, primary, Tsuji, Yoshihisa, primary, Uza, Norimitsu, primary, Matsumoto, Yuko, primary, Masui, Toshihiko, primary, Uemoto, Shinji, primary, Marusawa, Hiroyuki, primary, and Chiba, Tsutomu, primary

Published
2023
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38. Supplemental References from Activation-Induced Cytidine Deaminase Contributes to Pancreatic Tumorigenesis by Inducing Tumor-Related Gene Mutations

Author

Sawai, Yugo, primary, Kodama, Yuzo, primary, Shimizu, Takahiro, primary, Ota, Yuji, primary, Maruno, Takahisa, primary, Eso, Yuji, primary, Kurita, Akira, primary, Shiokawa, Masahiro, primary, Tsuji, Yoshihisa, primary, Uza, Norimitsu, primary, Matsumoto, Yuko, primary, Masui, Toshihiko, primary, Uemoto, Shinji, primary, Marusawa, Hiroyuki, primary, and Chiba, Tsutomu, primary

Published
2023
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40. THBS1-producing tumor-infiltrating monocyte-like cells contribute to immunosuppression and metastasis in colorectal cancer

Author

40838679, 10963332, 90967720, 40760567, 90839721, 90335266, Omatsu, Mayuki, Nakanishi, Yuki, Iwane, Kosuke, Aoyama, Naoki, Duran, Angeles, Muta, Yu, Martinez-Ordoñez, Anxo, Han, Qixiu, Agatsuma, Nobukazu, Mizukoshi, Kenta, Kawai, Munenori, Yamakawa, Go, Namikawa, Mio, Hamada, Kensuke, Fukunaga, Yuichi, Utsumi, Takahiro, Sono, Makoto, Masuda, Tomonori, Hata, Akitaka, Araki, Osamu, Nagao, Munemasa, Yoshikawa, Takaaki, Ogawa, Satoshi, Hiramatsu, Yukiko, Tsuda, Motoyuki, Maruno, Takahisa, Kogame, Toshiaki, Kasashima, Hiroaki, Kakiuchi, Nobuyuki, Nakagawa, Masahiro M., Kawada, Kenji, Yashiro, Masakazu, Maeda, Kiyoshi, Saito, Yasuyuki, Matozaki, Takashi, Fukuda, Akihisa, Kabashima, Kenji, Obama, Kazutaka, Ogawa, Seishi, Sheibani, Nader, Diaz-Meco, Maria T., Moscat, Jorge, Seno, Hiroshi, 40838679, 10963332, 90967720, 40760567, 90839721, 90335266, Omatsu, Mayuki, Nakanishi, Yuki, Iwane, Kosuke, Aoyama, Naoki, Duran, Angeles, Muta, Yu, Martinez-Ordoñez, Anxo, Han, Qixiu, Agatsuma, Nobukazu, Mizukoshi, Kenta, Kawai, Munenori, Yamakawa, Go, Namikawa, Mio, Hamada, Kensuke, Fukunaga, Yuichi, Utsumi, Takahiro, Sono, Makoto, Masuda, Tomonori, Hata, Akitaka, Araki, Osamu, Nagao, Munemasa, Yoshikawa, Takaaki, Ogawa, Satoshi, Hiramatsu, Yukiko, Tsuda, Motoyuki, Maruno, Takahisa, Kogame, Toshiaki, Kasashima, Hiroaki, Kakiuchi, Nobuyuki, Nakagawa, Masahiro M., Kawada, Kenji, Yashiro, Masakazu, Maeda, Kiyoshi, Saito, Yasuyuki, Matozaki, Takashi, Fukuda, Akihisa, Kabashima, Kenji, Obama, Kazutaka, Ogawa, Seishi, Sheibani, Nader, Diaz-Meco, Maria T., Moscat, Jorge, and Seno, Hiroshi

Abstract

Mesenchymal activation, characterized by dense stromal infiltration of immune and mesenchymal cells, fuels the aggressiveness of colorectal cancers (CRC), driving progression and metastasis. Targetable molecules in the tumor microenvironment (TME) need to be identified to improve the outcome in CRC patients with this aggressive phenotype. This study reports a positive link between high thrombospondin-1 (THBS1) expression and mesenchymal characteristics, immunosuppression, and unfavorable CRC prognosis. Bone marrow-derived monocyte-like cells recruited by CXCL12 are the primary source of THBS1, which contributes to the development of metastasis by inducing cytotoxic T-cell exhaustion and impairing vascularization. Furthermore, in orthotopically generated CRC models in male mice, THBS1 loss in the TME renders tumors partially sensitive to immune checkpoint inhibitors and anti-cancer drugs. Our study establishes THBS1 as a potential biomarker for identifying mesenchymal CRC and as a critical suppressor of antitumor immunity that contributes to the progression of this malignancy with a poor prognosis.

Published
2023

41. ELF3 suppresses gallbladder cancer development through downregulation of the EREG/EGFR/mTOR complex 1 signalling pathway

Author

80802785, 50737880, 40760567, 30447958, 90335266, Nakamura, Takeharu, Nishikawa, Yoshihiro, Shiokawa, Masahiro, Takeda, Haruhiko, Yokode, Masataka, Matsumoto, Shimpei, Muramoto, Yuya, Ota, Sakiko, Yoshida, Hiroyuki, Okada, Hirokazu, Kuwada, Takeshi, Marui, Saiko, Matsumori, Tomoaki, Maruno, Takahisa, Uza, Norimitsu, Kodama, Yuzo, Hatano, Etsuro, Seno, Hiroshi, 80802785, 50737880, 40760567, 30447958, 90335266, Nakamura, Takeharu, Nishikawa, Yoshihiro, Shiokawa, Masahiro, Takeda, Haruhiko, Yokode, Masataka, Matsumoto, Shimpei, Muramoto, Yuya, Ota, Sakiko, Yoshida, Hiroyuki, Okada, Hirokazu, Kuwada, Takeshi, Marui, Saiko, Matsumori, Tomoaki, Maruno, Takahisa, Uza, Norimitsu, Kodama, Yuzo, Hatano, Etsuro, and Seno, Hiroshi

Abstract

The prognosis of gallbladder cancer (GBC) remains poor, and a better understanding of GBC molecular mechanisms is important. Genome sequencing of human GBC has demonstrated that loss-of-function mutations of E74-like ETS transcription factor 3 (ELF3) are frequently observed, with ELF3 considered to be a tumour suppressor in GBC. To clarify the underlying molecular mechanisms by which ELF3 suppresses GBC development, we performed in vivo analysis using a combination of autochthonous and allograft mouse models. We first evaluated the clinical significance of ELF3 expression in human GBC tissues and found that low ELF3 expression was associated with advanced clinical stage and deep tumour invasion. For in vivo analysis, we generated Pdx1-Cre; KrasG12D; Trp53R172H; Elf3f/f (KPCE) mice and Pdx1-Cre; KrasG12D; Trp53R172H; Elf3wt/wt (KPC) mice as a control and analysed their gallbladders histologically. KPCE mice developed larger papillary lesions in the gallbladder than those developed by KPC mice. Organoids established from the gallbladders of KPCE and KPC mice were analysed in vitro. RNA sequencing showed upregulated expression of epiregulin (Ereg) in KPCE organoids, and western blotting revealed that EGFR/mechanical targets of rapamycin complex 1 (mTORC1) were upregulated in KPCE organoids. In addition, ChIP assays on Elf3-overexpressing KPCE organoids showed that ELF3 directly regulated Ereg. Ereg deletion in KPCE organoids (using CRISPR/Cas9) induced EGFR/mTORC1 downregulation, indicating that ELF3 controlled EGFR/mTORC1 activity through regulation of Ereg expression. We also generated allograft mouse models using KPCE and KPC organoids and found that KPCE organoid allograft tumours exhibited poorly differentiated structures with mTORC1 upregulation and mesenchymal phenotype, which were suppressed by Ereg deletion. Furthermore, EGFR/mTORC1 inhibition suppressed cell proliferation and epithelial–mesenchymal transition in KPCE organoids. Our results suggest that ELF3 s

Published
2023

42. Pancreatic RECK inactivation promotes cancer formation, epithelial-mesenchymal transition, and metastasis

Author

90967720, 70644897, 40760567, 40838679, 50402855, 90335266, Masuda, Tomonori, Fukuda, Akihisa, Yamakawa, Go, Omatsu, Mayuki, Namikawa, Mio, Sono, Makoto, Fukunaga, Yuichi, Nagao, Munemasa, Araki, Osamu, Yoshikawa, Takaaki, Ogawa, Satoshi, Masuo, Kenji, Goto, Norihiro, Hiramatsu, Yukiko, Muta, Yu, Tsuda, Motoyuki, Maruno, Takahisa, Nakanishi, Yuki, Masui, Toshihiko, Hatano, Etsuro, Matsuzaki, Tomoko, Noda, Makoto, Seno, Hiroshi, 90967720, 70644897, 40760567, 40838679, 50402855, 90335266, Masuda, Tomonori, Fukuda, Akihisa, Yamakawa, Go, Omatsu, Mayuki, Namikawa, Mio, Sono, Makoto, Fukunaga, Yuichi, Nagao, Munemasa, Araki, Osamu, Yoshikawa, Takaaki, Ogawa, Satoshi, Masuo, Kenji, Goto, Norihiro, Hiramatsu, Yukiko, Muta, Yu, Tsuda, Motoyuki, Maruno, Takahisa, Nakanishi, Yuki, Masui, Toshihiko, Hatano, Etsuro, Matsuzaki, Tomoko, Noda, Makoto, and Seno, Hiroshi

Abstract

RECK is downregulated in various human cancers; however, how RECK inactivation affects carcinogenesis remains unclear. We addressed this issue in a pancreatic ductal adenocarcinoma (PDAC) mouse model and found that pancreatic Reck deletion dramatically augmented the spontaneous development of PDAC with a mesenchymal phenotype, which was accompanied by increased liver metastases and decreased survival. Lineage tracing revealed that pancreatic Reck deletion induced epithelial-mesenchymal transition (EMT) in PDAC cells, giving rise to inflammatory cancer-associated fibroblast–like cells in mice. Splenic transplantation of Reck-null PDAC cells resulted in numerous liver metastases with a mesenchymal phenotype, whereas reexpression of RECK markedly reduced metastases and changed the PDAC tumor phenotype into an epithelial one. Consistently, low RECK expression correlated with low E-cadherin expression, poor differentiation, metastasis, and poor prognosis in human PDAC. RECK reexpression in the PDAC cells was found to downregulate MMP2 and MMP3, with a concomitant increase in E-cadherin and decrease in EMT-promoting transcription factors. An MMP inhibitor recapitulated the effects of RECK on the expression of E-cadherin and EMT-promoting transcription factors and invasive activity. These results establish the authenticity of RECK as a pancreatic tumor suppressor, provide insights into its underlying mechanisms, and support the idea that RECK could be an important therapeutic effector against human PDAC.

Published
2023

44. Simultaneous activation of Kras–Akt and Notch pathways induces extrahepatic biliary cancer via the mTORC1 pathway.

Author

Namikawa, Mio, Fukuda, Akihisa, Mizukoshi, Kenta, Iwane, Kosuke, Kawai, Munenori, Yamakawa, Go, Omatsu, Mayuki, Sono, Makoto, Masuda, Tomonori, Araki, Osamu, Nagao, Munemasa, Yoshikawa, Takaaki, Ogawa, Satoshi, Hiramatsu, Yukiko, Muta, Yu, Tsuda, Motoyuki, Maruno, Takahisa, Nakanishi, Yuki, Tsuruyama, Tatsuaki, and Taura, Kojiro

Subjects
BILIARY tract cancer, PRECANCEROUS conditions, RIBOSOMAL proteins, BILE ducts, CARCINOGENESIS
Abstract

Biliary tract cancer (BTC) has poor prognosis. The Notch receptor is aberrantly expressed in extrahepatic cholangiocarcinoma (eCCA). However, the role of Notch signaling in the initiation and progression of eCCA and gallbladder (GB) cancer remains unknown. Therefore, we investigated the functional role of Notch signaling during tumorigenesis of the extrahepatic bile duct (EHBD) and GB. Activation of Notch signaling and oncogenic Kras resulted in the development of biliary intraepithelial neoplasia (BilINs) in the EHBD and GB, which were premalignant lesions that progressed to adenocarcinoma in mice. The expression of genes involved in the mTORC1 pathway was increased in biliary spheroids from Hnf1b‐CreERT2; KrasLSL‐G12D; Rosa26LSL‐NotchIC mice and inhibition of the mTORC1 pathway suppressed spheroid growth. Additionally, simultaneous activation of the PI3K–AKT and Notch pathways in EHBD and GB induced biliary cancer development in mice. Consistent with this, we observed a significant correlation between activated NOTCH1 and phosphorylated Ribosomal Protein S6 (p‐S6) expression in human eCCA. Furthermore, inhibition of the mTORC1 pathway suppressed the growth of Notch‐activated human biliary cancer cells in vitro and in vivo. Mechanistically, the Kras/Notch–Myc axis activated mTORC1 through TSC2 phosphorylation in mutant biliary spheroids. These data indicate that inhibition of the mTORC1 pathway could be an effective treatment strategy for Notch‐activated human eCCA. © 2023 The Pathological Society of Great Britain and Ireland. [ABSTRACT FROM AUTHOR]

Published
2023
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45. Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice

Author

Sakuma, Yojiro, Kodama, Yuzo, Eguchi, Takaaki, Uza, Norimitsu, Tsuji, Yoshihisa, Shiokawa, Masahiro, Maruno, Takahisa, Kuriyama, Katsutoshi, Nishikawa, Yoshihiro, Yamauchi, Yuki, Tsuda, Motoyuki, Ueda, Tatsuki, Matsumori, Tomoaki, Morita, Toshihiro, Tomono, Teruko, Kakiuchi, Nobuyuki, Mima, Atsushi, Sogabe, Yuko, Marui, Saiko, Kuwada, Takeshi, Okada, Akihiko, Watanabe, Tomohiro, Nakase, Hiroshi, Chiba, Tsutomu, and Seno, Hiroshi

Published
2018
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46. JNK pathway plays a critical role for expansion of human colorectal cancer in the context of BRG1 suppression

Author

Yoshikawa, Takaaki, primary, Fukuda, Akihisa, additional, Omatsu, Mayuki, additional, Namikawa, Mio, additional, Sono, Makoto, additional, Fukunaga, Yuichi, additional, Masuda, Tomonori, additional, Araki, Osamu, additional, Nagao, Munemasa, additional, Ogawa, Satoshi, additional, Masuo, Kenji, additional, Goto, Norihiro, additional, Hiramatsu, Yukiko, additional, Muta, Yu, additional, Tsuda, Motoyuki, additional, Maruno, Takahisa, additional, Nakanishi, Yuki, additional, Kawada, Kenji, additional, Takaishi, Shigeo, additional, and Seno, Hiroshi, additional

Published
2022
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47. Loss of Arid1a and Pten in Pancreatic Ductal Cells Induces Intraductal Tubulopapillary Neoplasm via the YAP/TAZ Pathway

Author

Fukunaga, Yuichi, primary, Fukuda, Akihisa, additional, Omatsu, Mayuki, additional, Namikawa, Mio, additional, Sono, Makoto, additional, Masuda, Tomonori, additional, Araki, Osamu, additional, Nagao, Munemasa, additional, Yoshikawa, Takaaki, additional, Ogawa, Satoshi, additional, Hiramatsu, Yukiko, additional, Muta, Yu, additional, Tsuda, Motoyuki, additional, Maruno, Takahisa, additional, Nakanishi, Yuki, additional, Ferrer, Jorge, additional, Tsuruyama, Tatsuaki, additional, Masui, Toshihiko, additional, Hatano, Etsuro, additional, and Seno, Hiroshi, additional

Published
2022
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48. JNK pathway plays a critical role for expansion of human colorectal cancer in the context of BRG1 suppression

Author

70644897, 90967720, 40760567, 40838679, 90335266, Yoshikawa, Takaaki, Fukuda, Akihisa, Omatsu, Mayuki, Namikawa, Mio, Sono, Makoto, Fukunaga, Yuichi, Masuda, Tomonori, Araki, Osamu, Nagao, Munemasa, Ogawa, Satoshi, Masuo, Kenji, Goto, Norihiro, Hiramatsu, Yukiko, Muta, Yu, Tsuda, Motoyuki, Maruno, Takahisa, Nakanishi, Yuki, Kawada, Kenji, Takaishi, Shigeo, Seno, Hiroshi, 70644897, 90967720, 40760567, 40838679, 90335266, Yoshikawa, Takaaki, Fukuda, Akihisa, Omatsu, Mayuki, Namikawa, Mio, Sono, Makoto, Fukunaga, Yuichi, Masuda, Tomonori, Araki, Osamu, Nagao, Munemasa, Ogawa, Satoshi, Masuo, Kenji, Goto, Norihiro, Hiramatsu, Yukiko, Muta, Yu, Tsuda, Motoyuki, Maruno, Takahisa, Nakanishi, Yuki, Kawada, Kenji, Takaishi, Shigeo, and Seno, Hiroshi

Abstract

Tumor stem cells (TSCs), capable of self-renewal and continuous production of progeny cells, could be potential therapeutic targets. We have recently reported that chromatin remodeling regulator Brg1 is required for maintenance of murine intestinal TSCs and stemness feature of human colorectal cancer (CRC) cells by inhibiting apoptosis. However, it is still unclear how BRG1 suppression changes the underlying intracellular mechanisms of human CRC cells. We found that Brg1 suppression resulted in upregulation of the JNK signaling pathway in human CRC cells and murine intestinal TSCs. Simultaneous suppression of BRG1 and the JNK pathway, either by pharmacological inhibition or silencing of c-JUN, resulted in even stronger inhibition of the expansion of human CRC cells compared to Brg1 suppression alone. Consistently, high c-JUN expression correlated with worse prognosis for survival in human CRC patients with low BRG1 expression. Therefore, the JNK pathway plays a critical role for expansion and stemness of human CRC cells in the context of BRG1 suppression, and thus a combined blockade of BRG1 and the JNK pathway could be a novel therapeutic approach against human CRC.

Published
2022

50. Clinical impact of a novel device delivery system in the diagnosis of bile duct lesions: A single‐center experience

Author

Matsumori, Tomoaki, primary, Uza, Norimitsu, additional, Shiokawa, Masahiro, additional, Maruno, Takahisa, additional, Nishikawa, Yoshihiro, additional, Morita, Toshihiro, additional, Kuwada, Takeshi, additional, Marui, Saiko, additional, Okada, Hirokazu, additional, Taura, Kojiro, additional, Kodama, Yuzo, additional, and Seno, Hiroshi, additional

Published
2022
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