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19 results on '"Suita, Yusuke"'

2. MITF regulates IDH1 and NNT and drives a transcriptional program protecting cutaneous melanoma from reactive oxygen species

Author

Roider, Elisabeth, primary, Lakatos, Alexandra I.T., additional, McConnell, Alicia M., additional, Wang, Poguang, additional, Mueller, Alina, additional, Kawakami, Akinori, additional, Tsoi, Jennifer, additional, Szabolcs, Botond L., additional, Ascsillan, Anna A., additional, Suita, Yusuke, additional, Igras, Vivien, additional, Lo, Jennifer A., additional, Hsiao, Jennifer J., additional, Lapides, Rebecca, additional, Pal, Dorottya M.P., additional, Lengyel, Anna S., additional, Navarini, Alexander, additional, Okazaki, Arimichi, additional, Iliopoulos, Othon, additional, Nemeth, Istvan, additional, Graeber, Thomas G., additional, Zon, Leonard, additional, Giese, Roger W., additional, Kemeny, Lajos V., additional, and Fisher, David E., additional

Published
2023
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6. The germline factor DDX4 contributes to the chemoresistance of small cell lung cancer cells

Author

Noyes, Christopher, primary, Kitajima, Shunsuke, additional, Li, Fengkai, additional, Suita, Yusuke, additional, Miriyala, Saradha, additional, Isaac, Shakson, additional, Ahsan, Nagib, additional, Knelson, Erik, additional, Vajdi, Amir, additional, Tani, Tetsuo, additional, Thai, Tran C., additional, Xu, Derek, additional, Murai, Junko, additional, Tapinos, Nikos, additional, Takahashi, Chiaki, additional, Barbie, David A., additional, and Yajima, Mamiko, additional

Published
2022
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8. NNT mediates redox-dependent pigmentation via a UVB- and MITF-independent mechanism

Author

Allouche, Jennifer, primary, Rachmin, Inbal, additional, Adhikari, Kaustubh, additional, Pardo, Luba M., additional, Lee, Ju Hee, additional, McConnell, Alicia M., additional, Kato, Shinichiro, additional, Fan, Shaohua, additional, Kawakami, Akinori, additional, Suita, Yusuke, additional, Wakamatsu, Kazumasa, additional, Igras, Vivien, additional, Zhang, Jianming, additional, Navarro, Paula P., additional, Lugo, Camila Makhlouta, additional, Noonan, Haley R., additional, Christie, Kathleen A., additional, Itin, Kaspar, additional, Mujahid, Nisma, additional, Lo, Jennifer A., additional, Won, Chong Hyun, additional, Evans, Conor L., additional, Weng, Qing Yu, additional, Wang, Hequn, additional, Osseiran, Sam, additional, Lovas, Alyssa, additional, Németh, István, additional, Cozzio, Antonio, additional, Navarini, Alexander A., additional, Hsiao, Jennifer J., additional, Nguyen, Nhu, additional, Kemény, Lajos V., additional, Iliopoulos, Othon, additional, Berking, Carola, additional, Ruzicka, Thomas, additional, Gonzalez-José, Rolando, additional, Bortolini, Maria-Cátira, additional, Canizales-Quinteros, Samuel, additional, Acuna-Alonso, Victor, additional, Gallo, Carla, additional, Poletti, Giovanni, additional, Bedoya, Gabriel, additional, Rothhammer, Francisco, additional, Ito, Shosuke, additional, Schiaffino, Maria Vittoria, additional, Chao, Luke H., additional, Kleinstiver, Benjamin P., additional, Tishkoff, Sarah, additional, Zon, Leonard I., additional, Nijsten, Tamar, additional, Ruiz-Linares, Andrés, additional, Fisher, David E., additional, and Roider, Elisabeth, additional

Published
2021
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12. OCT4 impedes cell fate redirection by the melanocyte lineage master regulator MITF in mouse ESCs

Author

Sheinboim, Danna, primary, Maza, Itay, additional, Dror, Iris, additional, Parikh, Shivang, additional, Krupalnik, Vladislav, additional, Bell, Rachel E., additional, Zviran, Asaf, additional, Suita, Yusuke, additional, Hakim, Ofir, additional, Mandel-Gutfreund, Yael, additional, Khaled, Mehdi, additional, Hanna, Jacob H., additional, and Levy, Carmit, additional

Published
2017
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13. A UV-Independent Topical Small-Molecule Approach for Melanin Production in Human Skin

Author

Mujahid, Nisma, primary, Liang, Yanke, additional, Murakami, Ryo, additional, Choi, Hwan Geun, additional, Dobry, Allison S., additional, Wang, Jinhua, additional, Suita, Yusuke, additional, Weng, Qing Yu, additional, Allouche, Jennifer, additional, Kemeny, Lajos V., additional, Hermann, Andrea L., additional, Roider, Elisabeth M., additional, Gray, Nathanael S., additional, and Fisher, David E., additional

Published
2017
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14. OCT4 impedes cell fate redirection by the melanocyte lineage master regulator MITF

Author

Sheinboim, Danna, primary, Maza, Itay, additional, Dror, Iris, additional, Parikh, Shivang, additional, Krupalnik, Vladislav, additional, Bell, Rachel E, additional, Zviran, Asaf, additional, Suita, Yusuke, additional, Hakim, Ofir, additional, Gutfreund, Yael Mandel, additional, Khaled, Mehdi, additional, Hanna, Jacob H, additional, and Levy, Carmit, additional

Published
2017
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17. Towards label-free evaluation of oxidative stress in human skin exposed to sun filters (Conference Presentation)

Author

Choi, Bernard, Kollias, Nikiforos, Zeng, Haishan, Kang, Hyun Wook, Wong, Brian J. F., Ilgner, Justus F., Tearney, Guillermo J., Gregory, Kenton W., Marcu, Laura, Skala, Melissa C., Campagnola, Paul J., Mandelis, Andreas, Morris, Michael D., Osseiran, Sam, Wang, Hequn, Suita, Yusuke, Roider, Elisabeth, Fisher, David E., and Evans, Conor L.

Published
2016
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18. Machine learning on multiple epigenetic features reveals H3K27Ac as a driver of gene expression prediction across patients with glioblastoma.

Author

Suita Y, Bright H Jr, Pu Y, Toruner MD, Idehen J, Tapinos N, and Singh R

Abstract

Cancer cells show remarkable plasticity and can switch lineages in response to the tumor microenvironment. Cellular plasticity drives invasiveness and metastasis and helps cancer cells to evade therapy by developing resistance to radiation and cytotoxic chemotherapy. Increased understanding of cell fate determination through epigenetic reprogramming is critical to discover how cancer cells achieve transcriptomic and phenotypic plasticity. Glioblastoma is a perfect example of cancer evolution where cells retain an inherent level of plasticity through activation or maintenance of progenitor developmental programs. However, the principles governing epigenetic drivers of cellular plasticity in glioblastoma remain poorly understood. Here, using machine learning (ML) we employ cross-patient prediction of transcript expression using a combination of epigenetic features (ATAC-seq, CTCF ChIP-seq, RNAPII ChIP-seq, H3K27Ac ChIP-seq, and RNA-seq) of glioblastoma stem cells (GSCs). We investigate different ML and deep learning (DL) models for this task and build our final pipeline using XGBoost. The model trained on one patient generalizes to another one suggesting that the epigenetic signals governing gene transcription are consistent across patients even if GSCs can be very different. We demonstrate that H3K27Ac is the epigenetic feature providing the most significant contribution to cross-patient prediction of gene expression. In addition, using H3K27Ac signals from patients-derived GSCs, we can predict gene expression of human neural crest stem cells suggesting a shared developmental epigenetic trajectory between subpopulations of these malignant and benign stem cells. Our cross-patient ML/DL models determine weighted patterns of influence of epigenetic marks on gene expression across patients with glioblastoma and between GSCs and neural crest stem cells. We propose that broader application of this analysis could reshape our view of glioblastoma tumor evolution and inform the design of new epigenetic targeting therapies.

Published
2024
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19. MITF regulates IDH1 and NNT and drives a transcriptional program protecting cutaneous melanoma from reactive oxygen species.

Author

Roider E, Lakatos AIT, McConnell AM, Wang P, Mueller A, Kawakami A, Tsoi J, Szabolcs BL, Ascsillán AA, Suita Y, Igras V, Lo JA, Hsiao JJ, Lapides R, Pál DMP, Lengyel AS, Navarini A, Okazaki A, Iliopoulos O, Németh I, Graeber TG, Zon L, Giese RW, Kemeny LV, and Fisher DE

Abstract

Microphthalmia-associated transcription factor (MITF) plays pivotal roles in melanocyte development, function, and melanoma pathogenesis. MITF amplification occurs in melanoma and has been associated with resistance to targeted therapies. Here, we show that MITF regulates a global antioxidant program that increases survival of melanoma cell lines by protecting the cells from reactive oxygen species (ROS)-induced damage. In addition, this redox program is correlated with MITF expression in human melanoma cell lines and patient-derived melanoma samples. Using a zebrafish melanoma model, we show that MITF decreases ROS-mediated DNA damage in vivo . Some of the MITF target genes involved, such as IDH1 and NNT , are regulated through direct MITF binding to canonical enhancer box (E-BOX) sequences proximal to their promoters. Utilizing functional experiments, we demonstrate the role of MITF and its target genes in reducing cytosolic and mitochondrial ROS. Collectively, our data identify MITF as a significant driver of the cellular antioxidant state., One Sentence Summary: MITF promote melanoma survival via increasing ROS tolerance.

Published
2023
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