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5. Heterogeneity of Phase II Enzyme Ligands on Controlling the Progression of Human Gastric Cancer Organoids as Stem Cell Therapy Model

Author

Wu, Deng-Chyang, primary, Ku, Chia-Chen, additional, Pan, Jia-Bin, additional, Wuputra, Kenly, additional, Yang, Ya-Han, additional, Liu, Chung-Jung, additional, Liu, Yi-Chang, additional, Kato, Kohsuke, additional, Saito, Shigeo, additional, Lin, Ying-Chu, additional, Chong, Inn-Wen, additional, Hsiao, Michael, additional, Hu, Huang-Ming, additional, Kuo, Chao-Hung, additional, Kuo, Kung-Kai, additional, Lin, Chang-Shen, additional, and Yokoyama, Kazunari K., additional

Published
2023
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9. Contributors

Author

Adhikari, Poulomi, primary, Bohačiaková, Dáša, additional, Bárta, Tomáš, additional, Cuda, Giovanni, additional, Dey, Chandrima, additional, Dunkenberger, Logan, additional, Farkas, Michael H., additional, Gogoi, Ranadeep, additional, Haridhasapavalan, Krishna Kumar, additional, Hochman-Mendez, Camila, additional, Husami, Nadine J., additional, Karakikes, Ioannis, additional, Kato, Kohsuke, additional, Kawabata, Kenji, additional, Lako, M., additional, Lucchino, Valeria, additional, Mesquita, Fernanda C.P., additional, Neganova, I., additional, Orozco-Fuentes, S., additional, Parichha, Arpan, additional, Parker, N.G., additional, Parrotta, Elvira Immacolata, additional, Raina, Khyati, additional, Reiner, Orly, additional, Saito, Shigeo, additional, Sapir, Tamar, additional, Scalise, Stefania, additional, Scaramuzzino, Luana, additional, Shukurov, A., additional, Sundaravadivelu, Pradeep Kumar, additional, Čajánek, Lukáš, additional, Taylor, Doris A., additional, Thool, Madhuri, additional, Thummer, Rajkumar P., additional, Wadkin, L.E., additional, Wuputra, Kenly, additional, Yamaguchi, Tomoko, additional, Yokoyama, Kazunari K., additional, and Zhang, Hongyan, additional

Published
2021
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12. Jdp2-deficient granule cell progenitors in the cerebellum are resistant to ROS-mediated apoptosis through xCT/Slc7a11 activation

Author

Ku, Chia-Chen, Wuputra, Kenly, Kato, Kohsuke, Lin, Wen-Hsin, Pan, Jia-Bin, Tsai, Shih-Chieh, Kuo, Che-Jung, Lee, Kan-Hung, Lee, Yan-Liang, Lin, Ying-Chu, Saito, Shigeo, Noguchi, Michiya, Nakamura, Yukio, Miyoshi, Hiroyuki, Eckner, Richard, Nagata, Kyosuke, Wu, Deng-Chyang, Lin, Chang-Shen, and Yokoyama, Kazunari K.

Published
2020
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13. Independent Signaling of Hepatoma Derived Growth Factor and Tumor Necrosis Factor-Alpha in Human Gastric Cancer Organoids Infected by Helicobacter pylori

Author

Wuputra, Kenly, primary, Ku, Chia-Chen, additional, Pan, Jia-Bin, additional, Liu, Chung-Jung, additional, Kato, Kohsuke, additional, Lin, Ying-Chu, additional, Liu, Yi-Chang, additional, Lin, Chang-Shen, additional, Hsiao, Michael, additional, Tai, Ming-Hong, additional, Chong, Inn-Wen, additional, Hu, Huang-Ming, additional, Kuo, Chao-Hung, additional, Wu, Deng-Chyang, additional, and Yokoyama, Kazunari K., additional

Published
2023
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15. Transcription factor TLX1 controls retinoic acid signaling to ensure spleen development

Author

Lenti, Elisa, Farinello, Diego, Yokoyama, Kazunari K., Penkov, Dmitry, Castagnaro, Laura, Lavorgna, Giovanni, Wuputra, Kenly, Sandell, Lisa L., Tjaden, Naomi E. Butler, Bernassola, Francesca, Caridi, Nicoletta, De Antoni, Anna, Wagner, Michael, Kozinc, Katja, Niederreither, Karen, Blasi, Francesco, Pasini, Diego, Majdic, Gregor, Tonon, Giovanni, Trainor, Paul A., and Brendolan, Andrea

Subjects
Tretinoin -- Genetic aspects -- Physiological aspects -- Research, Splenic diseases -- Genetic aspects -- Causes of -- Research, Transcription factors -- Analysis, Health care industry
Abstract

The molecular mechanisms that underlie spleen development and congenital asplenia, a condition linked to increased risk of overwhelming infections, remain largely unknown. The transcription factor TLX1 controls cell fate specification and organ expansion during spleen development, and Tlx1 deletion causes asplenia in mice. Deregulation of TLX1 expression has recently been proposed in the pathogenesis of congenital asplenia in patients carrying mutations of the gene-encoding transcription factor SF-1. Herein, we have shown that TLX1-dependent regulation of retinoic acid (RA) metabolism is critical for spleen organogenesis. In a murine model, loss of Tlx1 during formation of the splenic anlage increased RA signaling by regulating several genes involved in RA metabolism. Uncontrolled RA activity resulted in premature differentiation of mesenchymal cells and reduced vasculogenesis of the splenic primordium. Pharmacological inhibition of RA signaling in Tlx1- deficient animals partially rescued the spleen defect. Finally, spleen growth was impaired in mice lacking either cytochrome P450 26B1 (Cyp26b1), which results in excess RA, or retinol dehydrogenase 10 (Rdh10), which results in RA deficiency. Together, these findings establish TLX1 as a critical regulator of RA metabolism and provide mechanistic insights into the molecular determinants of human congenital asplenia., Introduction The mammalian spleen is a secondary lymphoid organ that plays a central role in host defense. As a result, asplenia or hyposplenia and postsplenectomy patients often have an increased [...]

Published
2016
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17. Stem Cell Biomarkers and Tumorigenesis in Gastric Cancer

Author

Wuputra, Kenly, primary, Ku, Chia-Chen, additional, Pan, Jia-Bin, additional, Liu, Chung-Jung, additional, Liu, Yi-Chang, additional, Saito, Shigeo, additional, Kato, Kohsuke, additional, Lin, Ying-Chu, additional, Kuo, Kung-Kai, additional, Chan, Te-Fu, additional, Chong, Inn-Wen, additional, Lin, Chang-Shen, additional, Wu, Deng-Chyang, additional, and Yokoyama, Kazunari K., additional

Published
2022
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19. Generation of Human Stomach Cancer iPSC-Derived Organoids Induced by Helicobacter pylori Infection and Their Application to Gastric Cancer Research

Author

Ku, Chia-Chen, primary, Wuputra, Kenly, additional, Pan, Jia-Bin, additional, Li, Chia-Pei, additional, Liu, Chung-Jung, additional, Liu, Yi-Chang, additional, Saito, Shigeo, additional, Chan, Te-Fu, additional, Lin, Chang-Shen, additional, Wu, Deng-Chyang, additional, and Yokoyama, Kazunari K., additional

Published
2022
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20. Therapeutic Strategies Targeting Tumor Suppressor Genes in Pancreatic Cancer

Author

Kuo, Kung-Kai, primary, Hsiao, Pi-Jung, additional, Chang, Wen-Tsan, additional, Chuang, Shih-Chang, additional, Yang, Ya-Han, additional, Wuputra, Kenly, additional, Ku, Chia-Chen, additional, Pan, Jia-Bin, additional, Li, Chia-Pei, additional, Kato, Kohsuke, additional, Liu, Chung-Jung, additional, Wu, Deng-Chyang, additional, and Yokoyama, Kazunari K., additional

Published
2021
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22. Dimethyl sulfoxide stimulates the AhR-Jdp2 axis to control ROS accumulation in mouse embryonic fibroblasts

Author

Wuputra, Kenly, primary, Tsai, Ming-Ho, additional, Kato, Kohsuke, additional, Yang, Ya-han, additional, Pan, Jia-Bin, additional, Ku, Chia-Chen, additional, Noguchi, Michiya, additional, Kishikawa, Shotaro, additional, Nakade, Koji, additional, Chen, Hua-Ling, additional, Liu, Chung-Jung, additional, Nakamura, Yukio, additional, Kuo, Kung-Kai, additional, Lin, Ying-Chu, additional, Chan, Te-Fu, additional, Wu, Deng-Chyang, additional, Hou, Ming-Feng, additional, Huang, Shau-Ku, additional, Lin, Chang-Shen, additional, and Yokoyama, Kazunari K., additional

Published
2021
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23. Reactive Oxygen Species (ROS) Homeostasis in Influenza Virus Infection

Author

Chen, Ker-Kong, Minakuchi, Moeko, Wuputra, Kenly, Ku, Chia-Chen, Pan, Jia-Bin, Kuo, Kung-Kai, Lin, Ying-Chu, Saito, Shigeo, Lin, Chang-Shen, and Yokoyama, kazunari K.

Subjects
virology
Abstract

Cellular oxidation is responsive to external and internal stimulation and is generated via signal molecules in defense mechanisms through networks of cell proliferation, differentiation, intracellular detoxification, bacterial infection, and immune reactions. Oxidative stress is not necessarily harmful per se; it depends on the balance between oxidation and antioxidation cascades, which are induced according to stimuli and can maintain oxygen homeostasis. The reactive oxygen species (ROS) that are generated during influenza virus (IV) infection have critical effects on both the virus and host cells. In this review, we outline the link between viral infection and ROS production, using IV as an example. We introduce the current state of knowledge on the molecular relationship between cellular oxidation mediated by ROS production and various effects of IV infection. We also summarize the potential anti-IV agents that act by targeting oxidative stress.

Published
2019

24. Author Correction: Jdp2-deficient granule cell progenitors in the cerebellum are resistant to ROS-mediated apoptosis through xCT/Slc7a11 activation

Author

Ku, Chia-Chen, primary, Wuputra, Kenly, additional, Kato, Kohsuke, additional, Lin, Wen-Hsin, additional, Pan, Jia-Bin, additional, Tsai, Shih-Chieh, additional, Kuo, Che-Jung, additional, Lee, Kan-Hung, additional, Lee, Yan-Liang, additional, Lin, Ying-Chu, additional, Saito, Shigeo, additional, Noguchi, Michiya, additional, Nakamura, Yukio, additional, Miyoshi, Hiroyuki, additional, Eckner, Richard, additional, Nagata, Kyosuke, additional, Wu, Deng-Chyang, additional, Lin, Chang-Shen, additional, and Yokoyama, Kazunari K., additional

Published
2020
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27. Reprogramming Antagonizes the Oncogenicity of HOXA13-Long Noncoding RNA HOTTIP Axis in Gastric Cancer Cells

Author

Wu, Deng-Chyang, primary, Wang, Sophie S.W., additional, Liu, Chung-Jung, additional, Wuputra, Kenly, additional, Kato, Kohsuke, additional, Lee, Yen-Liang, additional, Lin, Ying-Chu, additional, Tsai, Ming-Ho, additional, Ku, Chia-Chen, additional, Lin, Wen-Hsin, additional, Wang, Shin-Wei, additional, Kishikawa, Shotaro, additional, Noguchi, Michiya, additional, Wu, Chu-Chieh, additional, Chen, Yi-Ting, additional, Chai, Chee-Yin, additional, Lin, Chen-Lung Steve, additional, Kuo, Kung-Kai, additional, Yang, Ya-Han, additional, Miyoshi, Hiroyuki, additional, Nakamura, Yukio, additional, Saito, Shigeo, additional, Nagata, Kyosuke, additional, Lin, Chang-Shen, additional, and Yokoyama, Kazunari K., additional

Published
2017
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30. Positive Feedback Loop of OCT4 and c-JUN Expedites Cancer Stemness in Liver Cancer

Author

Kuo, Kung-Kai, primary, Lee, King-Teh, additional, Chen, Ker-Kong, additional, Yang, Ya-Han, additional, Lin, Ying-Chu, additional, Tsai, Ming-Ho, additional, Wuputra, Kenly, additional, Lee, Yen-Liang, additional, Ku, Chia-Chen, additional, Miyoshi, Hiroyuki, additional, Nakamura, Yukio, additional, Saito, Shigeo, additional, Wu, Chun-Chieh, additional, Chai, Chee-Yin, additional, Eckner, Richard, additional, Steve Lin, Chen-Lung, additional, Wang, Sophie S-W, additional, Wu, Deng-Chyang, additional, Lin, Chang-Shen, additional, and Yokoyama, Kazunari K., additional

Published
2016
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31. Oncogenic function of the homeobox A13-long noncoding RNA HOTTIP-insulin growth factor-binding protein 3 axis in human gastric cancer

Author

Wang, Sophie S.W., primary, Wuputra, Kenly, additional, Liu, Chung-Jung, additional, Lin, Yin-Chu, additional, Chen, Yi-Ting, additional, Chai, Chee-Yin, additional, Lin, Chen-Lung Steve, additional, Kuo, Kung-Kai, additional, Tsai, Ming-Ho, additional, Wang, Shin-Wei, additional, Chen, Ker-Kong, additional, Miyoshi, Hiroyuki, additional, Nakamura, Yukio, additional, Saito, Shigeo, additional, Hanafusa, Tadashi, additional, Wu, Deng-Chyang, additional, Lin, Chang-Shen, additional, and Yokoyama, Kazunari K., additional

Published
2016
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32. Jun dimerization protein 2 controls hypoxia-induced replicative senescence via both the p16Ink4a-pRb and Arf-p53 pathways.

Author

Nakade, Koji, Lin, Chang‐Shen, Chen, Xiao‐Yu, Tsai, Ming‐Ho, Wuputra, Kenly, Zhu, Zhi‐Wei, Pan, Jian‐Zhi, and Yokoyama, Kazunari K.

Subjects
DIMERIZATION, HYPOXEMIA, CELL cycle, OXIDATIVE stress, LYSINE
Abstract

The main regulators of replicative senescence in mice are p16Ink4a and Arf, inhibitors of cell cycle progression. Jun dimerization protein 2 (JDP2)-deficient mouse embryonic fibroblasts are resistant to replicative senescence through recruitment of the Polycomb repressive complexes 1 and 2 to the promoter of the gene that encodes p16Ink4a and inhibits the methylation of lysine 27 of the histone H3 locus. However, whether or not JDP2 is able to regulate the chromatin signaling of either p16Ink4a-pRb or Arf-p53, or both, in response to oxidative stress remains elusive. Thus, this study sought to clarify this point. We demonstrated that the introduction of JDP2 leads to upregulation of p16Ink4a and Arf and decreases cell proliferation in the presence of environmental (20% O2), but not in low (3% O2) oxygen. JDP2-mediated growth suppression was inhibited by the downregulation of both p16Ink4a and Arf. Conversely, the forced expression of p16Ink4a or Arf inhibited cell growth even in the absence of JDP2. The downregulation of both the p53 and pRb pathways, but not each individually, was sufficient to block JDP2-dependent growth inhibition. These data suggest that JDP2 induces p16Ink4a and Arf by mediating signals from oxidative stress, resulting in cell cycle arrest via both the p16Ink4a-pRb and Arf-p53 pathways. [ABSTRACT FROM AUTHOR]

Published
2017
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33. Bovine Induced Pluripotent Stem Cells Are More Resistant to Apoptosis than Testicular Cells in Response to Mono-(2-ethylhexyl) Phthalate

Author

Lin, Ying-Chu, primary, Kuo, Kung-Kai, additional, Wuputra, Kenly, additional, Lin, Shih-Han, additional, Ku, Chia-Chen, additional, Yang, Ya-Han, additional, Wang, Shin-Wei, additional, Wang, Sheng-Wen, additional, Wu, Deng-Chyang, additional, Wu, Chun-Chien, additional, Chai, Chee-Yin, additional, Lin, Cheng-Lung, additional, Lin, Chang-Shen, additional, Kajitani, Masayuki, additional, Miyoshi, Hiroyuki, additional, Nakamura, Yukio, additional, Hashimoto, Shinichi, additional, Matsushima, Kouji, additional, Jin, Chunyuan, additional, Huang, Shau-Ku, additional, Saito, Shigeo, additional, and Yokoyama, Kazunari, additional

Published
2014
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34. Control of Oxidative Stress and Generation of Induced Pluripotent Stem Cell-like Cells by Jun Dimerization Protein 2

Author

Chiou, Shyh-Shin, primary, Wang, Sophie, additional, Wu, Deng-Chyang, additional, Lin, Ying-Chu, additional, Kao, Li-Pin, additional, Kuo, Kung-Kai, additional, Wu, Chun-Chieh, additional, Chai, Chee-Yin, additional, Lin, Cheng-Lung, additional, Lee, Cheng-Yi, additional, Liao, Yu-Mei, additional, Wuputra, Kenly, additional, Yang, Ya-Han, additional, Wang, Shin-Wei, additional, Ku, Chia-Chen, additional, Nakamura, Yukio, additional, Saito, Shigeo, additional, Hasegawa, Hitomi, additional, Yamaguchi, Naoto, additional, Miyoshi, Hiroyuki, additional, Lin, Chang-Sheng, additional, Eckner, Richard, additional, and Yokoyama, Kazunari, additional

Published
2013
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35. Author Correction: Jdp2-deficient granule cell progenitors in the cerebellum are resistant to ROS-mediated apoptosis through xCT/Slc7a11 activation.

Author

Ku, Chia-Chen, Wuputra, Kenly, Kato, Kohsuke, Lin, Wen-Hsin, Pan, Jia-Bin, Tsai, Shih-Chieh, Kuo, Che-Jung, Lee, Kan-Hung, Lee, Yan-Liang, Lin, Ying-Chu, Saito, Shigeo, Noguchi, Michiya, Nakamura, Yukio, Miyoshi, Hiroyuki, Eckner, Richard, Nagata, Kyosuke, Wu, Deng-Chyang, Lin, Chang-Shen, and Yokoyama, Kazunari K.

Subjects
GRANULE cells, APOPTOSIS, CEREBELLUM
Abstract

An amendment to this paper has been published and can be accessed via a link at the top of the paper. [ABSTRACT FROM AUTHOR]

Published
2020
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36. Jun dimerization protein 2 controls hypoxia-induced replicative senescence via both the p16 Ink4a -pRb and Arf-p53 pathways.

Author

Nakade K, Lin CS, Chen XY, Tsai MH, Wuputra K, Zhu ZW, Pan JZ, and Yokoyama KK

Abstract

The main regulators of replicative senescence in mice are p16 Ink4a and Arf, inhibitors of cell cycle progression. Jun dimerization protein 2 (JDP2)-deficient mouse embryonic fibroblasts are resistant to replicative senescence through recruitment of the Polycomb repressive complexes 1 and 2 to the promoter of the gene that encodes p16 Ink4a and inhibits the methylation of lysine 27 of the histone H3 locus. However, whether or not JDP2 is able to regulate the chromatin signaling of either p16 Ink4a -pRb or Arf-p53, or both, in response to oxidative stress remains elusive. Thus, this study sought to clarify this point. We demonstrated that the introduction of JDP2 leads to upregulation of p16 Ink4a and Arf and decreases cell proliferation in the presence of environmental (20% O 2 ), but not in low (3% O 2 ) oxygen. JDP2-mediated growth suppression was inhibited by the downregulation of both p16 Ink4a and Arf. Conversely, the forced expression of p16 Ink4a or Arf inhibited cell growth even in the absence of JDP2. The downregulation of both the p53 and pRb pathways, but not each individually, was sufficient to block JDP2-dependent growth inhibition. These data suggest that JDP2 induces p16 Ink4a and Arf by mediating signals from oxidative stress, resulting in cell cycle arrest via both the p16 Ink4a -pRb and Arf-p53 pathways.

Published
2017
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37. Application of Cancer Cell Reprogramming Technology to Human Cancer Research.

Author

Pan XY, Tsai MH, Wuputra K, Ku CC, Lin WH, Lin YC, Kishikawa S, Noguchi M, Saito S, Lin CS, and Yokoyama KK

Subjects
Carcinogenesis genetics, Drug Evaluation, Preclinical methods, Humans, Induced Pluripotent Stem Cells pathology, Neoplasms genetics, Tumor Microenvironment physiology, Carcinogenesis pathology, Cellular Reprogramming physiology, Neoplasms pathology, Neoplastic Stem Cells pathology
Abstract

The cancer stem cell (CSC) hypothesis is an evolving concept of oncogenesis that has recently gained wide acceptance. By definition, CSCs exhibit continuous proliferation and self-renewal, and they have been proposed to play significant roles in oncogenesis, tumor growth, metastasis, chemoresistance, and cancer recurrence. The reprogramming of cancer cells using induced pluripotent stem cell (iPSC) technology is a potential strategy for the identification of CSC-related oncogenes and tumor-suppressor genes. This technology has some advantages for studying the interactions between CSC-related genes and the cancer microenvironment. This approach may also provide a useful platform for studying the mechanisms of CSCs underlying cancer initiation and progression. The present review summarizes the recent advances in cancer cell reprogramming using iPSC technology and discusses its potential clinical use and related drug screening., (Copyright© 2017, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

Published
2017
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