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2. Enhancer infestation drives tumorigenic activation of inactive B compartment in Epstein-Barr virus-positive nasopharyngeal carcinoma

Author

Mizokami, Harue, Okabe, Atsushi, Choudhary, Ruchi, Mima, Masato, Saeda, Kenta, Fukuyo, Masaki, Rahmutulla, Bahityar, Seki, Motoaki, Goh, Boon-Cher, Kondo, Satoru, Dochi, Hirotomo, Moriyama-Kita, Makiko, Misawa, Kiyoshi, Hanazawa, Toyoyuki, Tan, Patrick, Yoshizaki, Tomokazu, Fullwood, Melissa Jane, and Kaneda, Atsushi

Published
2024
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3. An integrative transcriptional logic model of hepatic insulin resistance

Author

Kitamoto, Takumi, Kuo, Taiyi, Okabe, Atsushi, Kaneda, Atsushi, and Accili, Domenico

Subjects
Biochemistry and Cell Biology, Biological Sciences, Liver Disease, Nutrition, Digestive Diseases, Genetics, Diabetes, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Metabolic and endocrine, Animals, Fasting, Forkhead Box Protein O1, Gene Expression Regulation, Insulin Resistance, Liver, Male, Mice, Mice, Inbred C57BL, Models, Biological, Transcription, Genetic, diabetes, insulin sensitizers, drug failures, chromatin structure, animal models of human disease
Abstract

Abnormalities of lipid/lipoprotein and glucose metabolism are hallmarks of hepatic insulin resistance in type 2 diabetes. The former antedate the latter, but the latter become progressively refractory to treatment and contribute to therapeutic failures. It's unclear whether the two processes share a common pathogenesis and what underlies their progressive nature. In this study, we investigated the hypothesis that genes in the lipid/lipoprotein pathway and those in the glucose metabolic pathway are governed by different transcriptional regulatory logics that affect their response to physiologic (fasting/refeeding) as well as pathophysiologic cues (insulin resistance and hyperglycemia). To this end, we obtained genomic and transcriptomic maps of the key insulin-regulated transcription factor, FoxO1, and integrated them with those of CREB, PPAR-α, and glucocorticoid receptor. We found that glucose metabolic genes are primarily regulated by promoter and intergenic enhancers in a fasting-dependent manner, while lipid genes are regulated through fasting-dependent intron enhancers and fasting-independent enhancerless introns. Glucose genes also showed a remarkable transcriptional resiliency (i.e., the ability to compensate following constitutive FoxO1 ablation through an enrichment of active marks at shared PPAR-α/FoxO1 regulatory elements). Unexpectedly, insulin resistance and hyperglycemia were associated with a "spreading" of FoxO1 binding to enhancers and the emergence of unique target sites. We surmise that this unusual pattern correlates with the progressively intractable nature of hepatic insulin resistance. This transcriptional logic provides an integrated model to interpret the combined lipid and glucose abnormalities of type 2 diabetes.

Published
2021

9. Chemical catalyst manipulating cancer epigenome and transcription.

Author

Yamanashi, Yuki, Takamaru, Shinpei, Okabe, Atsushi, Kaito, Satoshi, Azumaya, Yuto, Kamimura, Yugo R., Yamatsugu, Kenzo, Kujirai, Tomoya, Kurumizaka, Hitoshi, Iwama, Atsushi, Kaneda, Atsushi, Kawashima, Shigehiro A., and Kanai, Motomu

Subjects
ELONGATION factors (Biochemistry), GENETIC engineering, HISTONE acetylation, GENETIC transcription, CANCER chemotherapy
Abstract

The number and variety of identified histone post-translational modifications (PTMs) are continually increasing. However, the specific consequences of each histone PTM remain largely unclear, primarily due to the lack of methods for selectively and rapidly introducing a desired histone PTM in living cells without genetic engineering. Here, we report the development of a cell-permeable histone acetylation catalyst, BAHA-LANA-PEG-CPP44, which selectively enters leukemia cells, binds to chromatin, and acetylates H2BK120 of endogenous histones in a short reaction time. Time-course analyses of this in-cell catalytic reaction revealed that H2BK120 acetylation attenuates the chromatin binding of negative elongation factor E (NELFE), an onco-transcription factor. This H2BK120 acetylation-mediated removal of NELFE from chromatin reshapes transcription, slows leukemia cell viability, and reduces their tumorigenic potential in mice. Therefore, this histone acetylation catalyst provides a unique tool for elucidating the time-resolved consequences of histone PTMs and may offer a modality for cancer chemotherapy. Here, the authors develop a cell-permeable chemical catalyst that acetylates histone H2BK120 in leukemia cells, attenuates NELFE chromatin binding, reprograms transcription, and reduces the tumorigenic potential of leukemia cells in mice. [ABSTRACT FROM AUTHOR]

Published
2025
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11. Identification of AR-V7 downstream genes commonly targeted by AR/AR-V7 and specifically targeted by AR-V7 in castration resistant prostate cancer

Author

Sugiura, Masahiro, Sato, Hiroaki, Okabe, Atsushi, Fukuyo, Masaki, Mano, Yasunobu, Shinohara, Ken-ichi, Rahmutulla, Bahityar, Higuchi, Kosuke, Maimaiti, Maihulan, Kanesaka, Manato, Imamura, Yusuke, Furihata, Tomomi, Sakamoto, Shinichi, Komiya, Akira, Anzai, Naohiko, Kanai, Yoshikatsu, Luo, Jun, Ichikawa, Tomohiko, and Kaneda, Atsushi

Published
2021
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12. Dose‐dependent effects of histone methyltransferase NSD2 on site‐specific double‐strand break repair.

Author

Iwasaki, Koh, Tojo, Akari, Kobayashi, Haruka, Shimizu, Kai, Kamimura, Yoshitaka, Horikoshi, Yasunori, Fukuto, Atsuhiko, Sun, Jiying, Yasui, Manabu, Honma, Masamitsu, Okabe, Atsushi, Fujiki, Ryoji, Nakajima, Nakako Izumi, Kaneda, Atsushi, Tashiro, Satoshi, Sassa, Akira, and Ura, Kiyoe

Subjects
HOMOLOGOUS recombination, HISTONE methylation, GENETIC transcription, METHYLTRANSFERASES, THYMIDINE, DNA repair, DOUBLE-strand DNA breaks
Abstract

Histone modifications are catalyzed and recognized by specific proteins to regulate dynamic DNA metabolism processes. NSD2 is a histone H3 lysine 36 (H3K36)‐specific methyltransferase that is associated with both various transcription regulators and DNA repair factors. Specifically, it has been implicated in the repair of DNA double‐strand breaks (DSBs); however, the role of NSD2 during DSB repair remains enigmatic. Here, we show that NSD2 does not accumulate at DSB sites and that it is not further mobilized by DSB formation. Using three different DSB repair reporter systems, which contained the endonuclease site in the active thymidine kinase gene (TK) locus, we demonstrated separate dose‐dependent effects of NSD2 on homologous recombination (HR), canonical‐non‐homologous end joining (c‐NHEJ), and non‐canonical‐NHEJ (non‐c‐NHEJ). Endogenous NSD2 has a role in repressing non‐c‐NHEJ, without affecting DSB repair efficiency by HR or total NHEJ. Furthermore, overexpression of NSD2 promotes c‐NHEJ repair and suppresses HR repair. Therefore, we propose that NSD2 has functions in chromatin integrity at the active regions during DSB repair. [ABSTRACT FROM AUTHOR]

Published
2024
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14. Chemical catalyst manipulating cancer epigenome and transcription

Author

Yamanashi, Yuki, primary, Takamaru, Shinpei, additional, Okabe, Atsushi, additional, Kaito, Satoshi, additional, Azumaya, Yuto, additional, Kamimura, Yugo, additional, Yamatsugu, Kenzo, additional, Kujirai, Tomoya, additional, Kurumizaka, Hitoshi, additional, Iwama, Atsushi, additional, Kaneda, Atsushi, additional, Kawashima, Shigehiro, additional, and Kanai, Motomu, additional

Published
2024
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15. Integrated enhancer regulatory network by enhancer–promoter looping in gastric cancer

Author

Zhu, Tianhui, primary, Okabe, Atsushi, additional, Usui, Genki, additional, Fujiki, Ryoji, additional, Komiyama, Daichi, additional, Huang, Kie Kyon, additional, Seki, Motoaki, additional, Fukuyo, Masaki, additional, Abe, Hiroyuki, additional, Ning, Meng, additional, Okada, Tomoka, additional, Minami, Mizuki, additional, Matsumoto, Makoto, additional, Fan, Qin, additional, Rahmutulla, Bahityar, additional, Hoshii, Takayuki, additional, Tan, Patrick, additional, Morikawa, Teppei, additional, Ushiku, Tetsuo, additional, and Kaneda, Atsushi, additional

Published
2024
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17. FIGURE 5 from Aberrant Upregulation of RUNX3 Activates Developmental Genes to Drive Metastasis in Gastric Cancer

Author

Suda, Kazuto, primary, Okabe, Atsushi, primary, Matsuo, Junichi, primary, Chuang, Linda Shyue Huey, primary, Li, Ying, primary, Jangphattananont, Nawaphat, primary, Mon, Naing Naing, primary, Myint, Khine Nyein, primary, Yamamura, Akihiro, primary, So, Jimmy Bok-Yan, primary, Voon, Dominic Chih-Cheng, primary, Yang, Henry, primary, Yeoh, Khay Guan, primary, Kaneda, Atsushi, primary, and Ito, Yoshiaki, primary

Published
2024
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18. Supplementary Figure S4 from Aberrant Upregulation of RUNX3 Activates Developmental Genes to Drive Metastasis in Gastric Cancer

Author

Suda, Kazuto, primary, Okabe, Atsushi, primary, Matsuo, Junichi, primary, Chuang, Linda Shyue Huey, primary, Li, Ying, primary, Jangphattananont, Nawaphat, primary, Mon, Naing Naing, primary, Myint, Khine Nyein, primary, Yamamura, Akihiro, primary, So, Jimmy Bok-Yan, primary, Voon, Dominic Chih-Cheng, primary, Yang, Henry, primary, Yeoh, Khay Guan, primary, Kaneda, Atsushi, primary, and Ito, Yoshiaki, primary

Published
2024
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19. FIGURE 1 from Aberrant Upregulation of RUNX3 Activates Developmental Genes to Drive Metastasis in Gastric Cancer

Author

Suda, Kazuto, primary, Okabe, Atsushi, primary, Matsuo, Junichi, primary, Chuang, Linda Shyue Huey, primary, Li, Ying, primary, Jangphattananont, Nawaphat, primary, Mon, Naing Naing, primary, Myint, Khine Nyein, primary, Yamamura, Akihiro, primary, So, Jimmy Bok-Yan, primary, Voon, Dominic Chih-Cheng, primary, Yang, Henry, primary, Yeoh, Khay Guan, primary, Kaneda, Atsushi, primary, and Ito, Yoshiaki, primary

Published
2024
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20. FIGURE 3 from Aberrant Upregulation of RUNX3 Activates Developmental Genes to Drive Metastasis in Gastric Cancer

Author

Suda, Kazuto, primary, Okabe, Atsushi, primary, Matsuo, Junichi, primary, Chuang, Linda Shyue Huey, primary, Li, Ying, primary, Jangphattananont, Nawaphat, primary, Mon, Naing Naing, primary, Myint, Khine Nyein, primary, Yamamura, Akihiro, primary, So, Jimmy Bok-Yan, primary, Voon, Dominic Chih-Cheng, primary, Yang, Henry, primary, Yeoh, Khay Guan, primary, Kaneda, Atsushi, primary, and Ito, Yoshiaki, primary

Published
2024
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21. FIGURE 6 from Aberrant Upregulation of RUNX3 Activates Developmental Genes to Drive Metastasis in Gastric Cancer

Author

Suda, Kazuto, primary, Okabe, Atsushi, primary, Matsuo, Junichi, primary, Chuang, Linda Shyue Huey, primary, Li, Ying, primary, Jangphattananont, Nawaphat, primary, Mon, Naing Naing, primary, Myint, Khine Nyein, primary, Yamamura, Akihiro, primary, So, Jimmy Bok-Yan, primary, Voon, Dominic Chih-Cheng, primary, Yang, Henry, primary, Yeoh, Khay Guan, primary, Kaneda, Atsushi, primary, and Ito, Yoshiaki, primary

Published
2024
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22. FIGURE 4 from Aberrant Upregulation of RUNX3 Activates Developmental Genes to Drive Metastasis in Gastric Cancer

Author

Suda, Kazuto, primary, Okabe, Atsushi, primary, Matsuo, Junichi, primary, Chuang, Linda Shyue Huey, primary, Li, Ying, primary, Jangphattananont, Nawaphat, primary, Mon, Naing Naing, primary, Myint, Khine Nyein, primary, Yamamura, Akihiro, primary, So, Jimmy Bok-Yan, primary, Voon, Dominic Chih-Cheng, primary, Yang, Henry, primary, Yeoh, Khay Guan, primary, Kaneda, Atsushi, primary, and Ito, Yoshiaki, primary

Published
2024
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23. Supplementary Data S1 from Aberrant Upregulation of RUNX3 Activates Developmental Genes to Drive Metastasis in Gastric Cancer

Author

Suda, Kazuto, primary, Okabe, Atsushi, primary, Matsuo, Junichi, primary, Chuang, Linda Shyue Huey, primary, Li, Ying, primary, Jangphattananont, Nawaphat, primary, Mon, Naing Naing, primary, Myint, Khine Nyein, primary, Yamamura, Akihiro, primary, So, Jimmy Bok-Yan, primary, Voon, Dominic Chih-Cheng, primary, Yang, Henry, primary, Yeoh, Khay Guan, primary, Kaneda, Atsushi, primary, and Ito, Yoshiaki, primary

Published
2024
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24. FIGURE 2 from Aberrant Upregulation of RUNX3 Activates Developmental Genes to Drive Metastasis in Gastric Cancer

Author

Suda, Kazuto, primary, Okabe, Atsushi, primary, Matsuo, Junichi, primary, Chuang, Linda Shyue Huey, primary, Li, Ying, primary, Jangphattananont, Nawaphat, primary, Mon, Naing Naing, primary, Myint, Khine Nyein, primary, Yamamura, Akihiro, primary, So, Jimmy Bok-Yan, primary, Voon, Dominic Chih-Cheng, primary, Yang, Henry, primary, Yeoh, Khay Guan, primary, Kaneda, Atsushi, primary, and Ito, Yoshiaki, primary

Published
2024
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25. Data from Aberrant Upregulation of RUNX3 Activates Developmental Genes to Drive Metastasis in Gastric Cancer

Author

Suda, Kazuto, primary, Okabe, Atsushi, primary, Matsuo, Junichi, primary, Chuang, Linda Shyue Huey, primary, Li, Ying, primary, Jangphattananont, Nawaphat, primary, Mon, Naing Naing, primary, Myint, Khine Nyein, primary, Yamamura, Akihiro, primary, So, Jimmy Bok-Yan, primary, Voon, Dominic Chih-Cheng, primary, Yang, Henry, primary, Yeoh, Khay Guan, primary, Kaneda, Atsushi, primary, and Ito, Yoshiaki, primary

Published
2024
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26. Aberrant Upregulation of RUNX3 Activates Developmental Genes to Drive Metastasis in Gastric Cancer

Author

Suda, Kazuto, primary, Okabe, Atsushi, additional, Matsuo, Junichi, additional, Chuang, Linda Shyue Huey, additional, Li, Ying, additional, Jangphattananont, Nawaphat, additional, Mon, Naing Naing, additional, Myint, Khine Nyein, additional, Yamamura, Akihiro, additional, So, Jimmy Bok-Yan, additional, Voon, Dominic Chih-Cheng, additional, Yang, Henry, additional, Yeoh, Khay Guan, additional, Kaneda, Atsushi, additional, and Ito, Yoshiaki, additional

Published
2024
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27. Contributors

Author

Balasubramanian, Adithya, primary, Bijlsma, Maarten F., additional, Bougen-Zhukov, Nicola, additional, Boussioutas, Alex, additional, Busuttil, Rita A., additional, Carneiro, Fátima, additional, Chuang, Linda Shyue Huey, additional, Davis, Jeremy L., additional, Dawson, Ruby, additional, Dings, Mark P.G., additional, Douchi, Daisuke, additional, Echizen, Kanae, additional, Ferrero, Richard L., additional, Frentzas, Sophia, additional, Guilford, Parry, additional, Gullo, Irene, additional, Han, Tae-Su, additional, Hatakeyama, Masanori, additional, Ito, Yoshiaki, additional, Jenkins, Brendan J., additional, John, Alexius, additional, Jones, David W., additional, Ju, Xiaoli, additional, Kaneda, Atsushi, additional, Koulis, Athanasios, additional, Li, Wenzhe, additional, Lum, Caroline, additional, Matsuo, Junichi, additional, Noto, Jennifer M., additional, Okabe, Atsushi, additional, Oliveira, Carla, additional, Oshima, Hiroko, additional, Oshima, Masanobu, additional, Segelov, Eva, additional, van der Post, Rachel S., additional, van Dieren, Jolanda M., additional, Vermeulen, Louis, additional, and Zavros, Yana, additional

Published
2021
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29. The Link of mRNA and rRNA Transcription by PUF60/FIR through TFIIH/P62 as a Novel Therapeutic Target for Cancer

Author

Kitamura, Kouichi, primary, Hoshino, Tyuji, additional, Okabe, Atsushi, additional, Fukuyo, Masaki, additional, Rahmutulla, Bahityar, additional, Tanaka, Nobuko, additional, Kobayashi, Sohei, additional, Tanaka, Tomoaki, additional, Shida, Takashi, additional, Ueda, Mashiro, additional, Minamoto, Toshinari, additional, Matsubara, Hisahiro, additional, Kaneda, Atsushi, additional, Ishii, Hideshi, additional, and Matsushita, Kazuyuki, additional

Published
2023
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31. Supplementary Methods, Figures 1-8, Tables 1-4 from Tumor Suppressor miR-22 Determines p53-Dependent Cellular Fate through Post-transcriptional Regulation of p21

Author

Tsuchiya, Naoto, primary, Izumiya, Masashi, primary, Ogata-Kawata, Hiroko, primary, Okamoto, Koji, primary, Fujiwara, Yuko, primary, Nakai, Makiko, primary, Okabe, Atsushi, primary, Schetter, Aaron J., primary, Bowman, Elise D., primary, Midorikawa, Yutaka, primary, Sugiyama, Yasuyuki, primary, Aburatani, Hiroyuki, primary, Harris, Curtis C., primary, and Nakagama, Hitoshi, primary

Published
2023
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32. Data from Tumor Suppressor miR-22 Determines p53-Dependent Cellular Fate through Post-transcriptional Regulation of p21

Author

Tsuchiya, Naoto, primary, Izumiya, Masashi, primary, Ogata-Kawata, Hiroko, primary, Okamoto, Koji, primary, Fujiwara, Yuko, primary, Nakai, Makiko, primary, Okabe, Atsushi, primary, Schetter, Aaron J., primary, Bowman, Elise D., primary, Midorikawa, Yutaka, primary, Sugiyama, Yasuyuki, primary, Aburatani, Hiroyuki, primary, Harris, Curtis C., primary, and Nakagama, Hitoshi, primary

Published
2023
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33. Comprehensive molecular phenotyping ofARID1A-deficient gastric cancer reveals pervasive epigenomic reprogramming and therapeutic opportunities

Author

Xu, Chang, primary, Huang, Kie Kyon, additional, Law, Jia Hao, additional, Chua, Joy Shijia, additional, Sheng, Taotao, additional, Flores, Natasha M, additional, Pizzi, Melissa Pool, additional, Okabe, Atsushi, additional, Tan, Angie Lay Keng, additional, Zhu, Feng, additional, Kumar, Vikrant, additional, Lu, Xiaoyin, additional, Benitez, Ana Morales, additional, Lian, Benedict Shi Xiang, additional, Ma, Haoran, additional, Ho, Shamaine Wei Ting, additional, Ramnarayanan, Kalpana, additional, Anene-Nzelu, Chukwuemeka George, additional, Razavi-Mohseni, Milad, additional, Abdul Ghani, Siti Aishah Binte, additional, Tay, Su Ting, additional, Ong, Xuewen, additional, Lee, Ming Hui, additional, Guo, Yu Amanda, additional, Ashktorab, Hassan, additional, Smoot, Duane, additional, Li, Shang, additional, Skanderup, Anders Jacobsen, additional, Beer, Michael A, additional, Foo, Roger Sik Yin, additional, Wong, Joel Shi Hao, additional, Sanghvi, Kaushal, additional, Yong, Wei Peng, additional, Sundar, Raghav, additional, Kaneda, Atsushi, additional, Prabhakar, Shyam, additional, Mazur, Pawel Karol, additional, Ajani, Jaffer A, additional, Yeoh, Khay Guan, additional, So, Jimmy Bok-Yan, additional, and Tan, Patrick, additional

Published
2023
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34. Correction: Chromatin Rewiring by Mismatch Repair Protein MSH2 Alters Cell Adhesion Pathways and Sensitivity to BET Inhibition in Gastric Cancer

Author

Nargund, Amrita M., primary, Xu, Chang, additional, Mandoli, Amit, additional, Okabe, Atsushi, additional, Chen, Gao Bin, additional, Huang, Kie Kyon, additional, Sheng, Taotao, additional, Yao, Xiaosai, additional, Teo, Jia Ming Nickolas, additional, Sundar, Raghav, additional, Kok, Yee Jiun, additional, See, Yi Xiang, additional, Xing, Manjie, additional, Li, Zhimei, additional, Yong, Chern Han, additional, Anand, Aparna, additional, Bin Adam Isa, Zul Fazreen, additional, Poon, Lai Fong, additional, Ng, Michelle Shu Wen, additional, Koh, Javier Yu Peng, additional, Ooi, Wen Fong, additional, Tay, Su Ting, additional, Ong, Xuewen, additional, Tan, Angie Lay Keng, additional, Smoot, Duane T., additional, Ashktorab, Hassan, additional, Grabsch, Heike I., additional, Fullwood, Melissa J., additional, Teh, Bin Tean, additional, Bi, Xuezhi, additional, Kaneda, Atsushi, additional, Li, Shang, additional, and Tan, Patrick, additional

Published
2023
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36. [Chiba Medical Society Young Investigator Award Minireview] Epigenetic contribution to tumorigenesis of host cells by Epstein-Barr virus infection

Author

FUJII, Takahiro, OKABE, Atsushi, and KANEDA, Atsushi

Subjects
hemic and lymphatic diseases
Abstract

[ABSTRACT] Epstein-Barr virus (EBV) is known as an oncogenic virus and causes tumors in a variety of tissues, including lymphocytes and epithelial cells. EBV infects host cells latently as an episome and affects the host genome and epigenome while switching between three types of latent stages and a lytic stage. In recent years, the development of analytic methods using next generation sequencing and chromosome conformation capture technologies has enabled us to identify abnormalities at the molecular level in cancer cells. In EBV-positive tumors, pigenetic alterations such as DNA methylation, viral miRNA-mediated expression changes, and aberrations in histone modification and 3D chromatin structure, together with the involvement of EBV, have been revealed by analysis of tumor cells and in vitro EBV infection experiments. Further understanding of host-EBV interactions and their roles in the cancer pathogenesis is expected to lead to the development of revolutionary therapies targeting the epigenome. Here we review epigenetic contribution to tumorigenesis by EBV infection in host cells.

Published
2022

37. Tumorigenic activation around HPV integrated sites in head and neck squamous cell carcinoma

Author

Mima, Masato, primary, Okabe, Atsushi, additional, Hoshii, Takayuki, additional, Nakagawa, Takuya, additional, Kurokawa, Tomoya, additional, Kondo, Satoru, additional, Mizokami, Harue, additional, Fukuyo, Masaki, additional, Fujiki, Ryoji, additional, Rahmutulla, Bahityar, additional, Yoshizaki, Tomokazu, additional, Hanazawa, Toyoyuki, additional, Misawa, Kiyoshi, additional, and Kaneda, Atsushi, additional

Published
2023
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39. A novel target for cancer therapy on the RNA stimulation by FUBP1- interacting repressor (FIR) via TFIIH/P62

Author

Kitamura, Kouichi, primary, Hoshino, Tyuji, additional, Okabe, Atsushi, additional, Fukuyo, Masaki, additional, Rahmutulla, Bahityar, additional, Tanaka, Nobuko, additional, Kobayashi, Sohei, additional, Tanaka, Tomoaki, additional, Shida, Takashi, additional, Ueda, Mashiro, additional, Minamoto, Toshinari, additional, Matsubara, Hisahiro, additional, Kaneda, Atsushi, additional, and Matsushita, Kazuyuki, additional

Published
2022
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40. Chromatin Rewiring by Mismatch Repair Protein MSH2 Alters Cell Adhesion Pathways and Sensitivity to BET Inhibition in Gastric Cancer

Author

Nargund, Amrita M., primary, Xu, Chang, additional, Mandoli, Amit, additional, Okabe, Atsushi, additional, Chen, Gao Bin, additional, Huang, Kie Kyon, additional, Sheng, Taotao, additional, Yao, Xiaosai, additional, Teo, Jia Ming Nickolas, additional, Sundar, Raghav, additional, Kok, Yee Jiun, additional, See, Yi Xiang, additional, Xing, Manjie, additional, Li, Zhimei, additional, Yong, Chern Han, additional, Anand, Aparna, additional, Bin Adam Isa, Zul Fazreen, additional, Poon, Lai Fong, additional, Ng, Michelle Shu Wen, additional, Koh, Javier Yu Peng, additional, Ooi, Wen Fong, additional, Tay, Su Ting, additional, Ong, Xuewen, additional, Tan, Angie Lay Keng, additional, Smoot, Duane T., additional, Ashktorab, Hassan, additional, Grabsch, Heike I., additional, Fullwood, Melissa J., additional, Teh, Bin Tean, additional, Bi, Xuezhi, additional, Kaneda, Atsushi, additional, Li, Shang, additional, and Tan, Patrick, additional

Published
2022
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42. Activation of EHF via STAT3 phosphorylation by LMP2A in Epstein‐Barr virus–positive gastric cancer

Author

Li, Wenzhe, primary, Okabe, Atsushi, additional, Usui, Genki, additional, Fukuyo, Masaki, additional, Matsusaka, Keisuke, additional, Rahmutulla, Bahityar, additional, Mano, Yasunobu, additional, Hoshii, Takayuki, additional, Funata, Sayaka, additional, Hiura, Nobuhiro, additional, Fukayama, Masashi, additional, Tan, Patrick, additional, Ushiku, Tetsuo, additional, and Kaneda, Atsushi, additional

Published
2021
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43. TET1 upregulation drives cancer cell growth through aberrant enhancer hydroxymethylation of HMGA2 in hepatocellular carcinoma

Author

Shirai, Kiyokazu, primary, Nagae, Genta, additional, Seki, Motoaki, additional, Kudo, Yotaro, additional, Kamio, Asuka, additional, Hayashi, Akimasa, additional, Okabe, Atsushi, additional, Ota, Satoshi, additional, Tsutsumi, Shuichi, additional, Fujita, Takanori, additional, Yamamoto, Shogo, additional, Nakaki, Ryo, additional, Kanki, Yasuharu, additional, Osawa, Tsuyoshi, additional, Midorikawa, Yutaka, additional, Tateishi, Keisuke, additional, Ichinose, Masao, additional, and Aburatani, Hiroyuki, additional

Published
2021
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46. Comprehensive molecular phenotyping of ARID1A-deficient gastric cancer reveals pervasive epigenomic reprogramming and therapeutic opportunities

Author

Xu, Chang, Huang, Kie Kyon, Law, Jia Hao, Chua, Joy Shijia, Sheng, Taotao, Flores, Natasha M, Pizzi, Melissa Pool, Okabe, Atsushi, Tan, Angie Lay Keng, Zhu, Feng, Kumar, Vikrant, Lu, Xiaoyin, Benitez, Ana Morales, Lian, Benedict Shi Xiang, Ma, Haoran, Ho, Shamaine Wei Ting, Ramnarayanan, Kalpana, Anene-Nzelu, Chukwuemeka George, Razavi-Mohseni, Milad, Abdul Ghani, Siti Aishah Binte, Tay, Su Ting, Ong, Xuewen, Lee, Ming Hui, Guo, Yu Amanda, Ashktorab, Hassan, Smoot, Duane, Li, Shang, Skanderup, Anders Jacobsen, Beer, Michael A, Foo, Roger Sik Yin, Wong, Joel Shi Hao, Sanghvi, Kaushal, Yong, Wei Peng, Sundar, Raghav, Kaneda, Atsushi, Prabhakar, Shyam, Mazur, Pawel Karol, Ajani, Jaffer A, Yeoh, Khay Guan, So, Jimmy Bok-Yan, and Tan, Patrick

Abstract

ObjectiveGastric cancer (GC) is a leading cause of cancer mortality, with ARID1Abeing the second most frequently mutated driver gene in GC. We sought to decipher ARID1A-specific GC regulatory networks and examine therapeutic vulnerabilities arising from ARID1Aloss.DesignGenomic profiling of GC patients including a Singapore cohort (>200 patients) was performed to derive mutational signatures of ARID1Ainactivation across molecular subtypes. Single-cell transcriptomic profiles of ARID1A-mutated GCs were analysed to examine tumour microenvironmental changes arising from ARID1Aloss. Genome-wide ARID1A binding and chromatin profiles (H3K27ac, H3K4me3, H3K4me1, ATAC-seq) were generated to identify gastric-specific epigenetic landscapes regulated by ARID1A. Distinct cancer hallmarks of ARID1A-mutated GCs were converged at the genomic, single-cell and epigenomic level, and targeted by pharmacological inhibition.ResultsWe observed prevalent ARID1Ainactivation across GC molecular subtypes, with distinct mutational signatures and linked to a NFKB-driven proinflammatory tumour microenvironment. ARID1A-depletion caused loss of H3K27ac activation signals at ARID1A-occupied distal enhancers, but unexpectedly gain of H3K27ac at ARID1A-occupied promoters in genes such as NFKB1and NFKB2. Promoter activation in ARID1A-mutated GCs was associated with enhanced gene expression, increased BRD4 binding, and reduced HDAC1 and CTCF occupancy. Combined targeting of promoter activation and tumour inflammation via bromodomain and NFKB inhibitors confirmed therapeutic synergy specific to ARID1A-genomic status.ConclusionOur results suggest a therapeutic strategy for ARID1A-mutated GCs targeting both tumour-intrinsic (BRD4-assocatiated promoter activation) and extrinsic (NFKB immunomodulation) cancer phenotypes.

Published
2023
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48. Epstein‐Barr virus‐positive gastric cancer involves enhancer activation through activating transcription factor 3

Author

Asakawa, Yuta, primary, Okabe, Atsushi, additional, Fukuyo, Masaki, additional, Li, Wenzhe, additional, Ikeda, Eriko, additional, Mano, Yasunobu, additional, Funata, Sayaka, additional, Namba, Hiroe, additional, Fujii, Takahiro, additional, Kita, Kazuko, additional, Matsusaka, Keisuke, additional, and Kaneda, Atsushi, additional

Published
2020
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50. Ethyl β-d-glucoside: a novel chemoattractant of Ralstonia solanacearum isolated from tomato root exudates by a bioassay-guided fractionation

Author

Hasegawa, Takuya, Okabe, Atsushi, Kato, Yusuke, Ooshiro, Atsushi, Kawaide, Hiroshi, and Natsume, Masahiro

Subjects
fungi, food and beverages, biochemical phenomena, metabolism, and nutrition, equipment and supplies
Abstract

A chemoattractant of Ralstonia solanacearum isolated from the activated charcoal-adsorbed fraction of tomato root exudates was identified as ethyl β-d-glucopyranoside by instrumental analyses and comparison with synthetic preparations. Ethyl β-D-glucopyranoside showed unambiguous activity at above 1 µmol/disc. Its stereoisomers and D-glucose were inactive. Structure of chemoattractant for Ralstonia solanacearum isolated from tomato root exudates with the guidance of bioassay was identified as ethyl β-D-glucopyranoside.

Published
2018
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