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1. Editorial: Acute leukemias: molecular characterization, leukemia-initiating cells, and influence of the microenvironment, volume II.

Author

Varisli, Lokman, Dancik, Garrett M., Copland, John A., and Vlahopoulos, Spiros A.

Subjects
GENE expression, ACUTE leukemia, HEMATOPOIETIC stem cells, PROGNOSIS, REFERENCE values
Abstract

The editorial in Frontiers in Oncology discusses the molecular characterization of acute leukemias, focusing on leukemia-initiating cells and the influence of the tissue microenvironment. Various studies highlighted in the editorial explore different aspects of acute leukemias, such as identifying biomarkers, treatment approaches, and prognostic factors. The research aims to enhance the understanding of the molecular mechanisms underlying acute leukemias to develop more effective treatment strategies and improve patient outcomes. The authors express gratitude to all contributors and emphasize the importance of continued research in this field. [Extracted from the article]

Published
2025
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7. European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

Author

Egea, Javier, Fabregat, Isabel, Frapart, Yves M., Ghezzi, Pietro, Görlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G., Lopez, Manuela G., Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vina, Jose, Winyard, Paul, Abbas, Kahina, Ademowo, Opeyemi S., Afonso, Catarina B., Andreadou, Ioanna, Antelmann, Haike, Antunes, Fernando, Aslan, Mutay, Bachschmid, Markus M., Barbosa, Rui M., Belousov, Vsevolod, Berndt, Carsten, Bernlohr, David, Bertrán, Esther, Bindoli, Alberto, Bottari, Serge P., Brito, Paula M., Carrara, Guia, Casas, Ana I., Chatzi, Afroditi, Chondrogianni, Niki, Conrad, Marcus, Cooke, Marcus S., Costa, João G., Cuadrado, Antonio, My-Chan Dang, Pham, De Smet, Barbara, Debelec–Butuner, Bilge, Dias, Irundika H.K., Dunn, Joe Dan, Edson, Amanda J., El Assar, Mariam, El-Benna, Jamel, Ferdinandy, Péter, Fernandes, Ana S., Fladmark, Kari E., Förstermann, Ulrich, Giniatullin, Rashid, Giricz, Zoltán, Görbe, Anikó, Griffiths, Helen, Hampl, Vaclav, Hanf, Alina, Herget, Jan, Hernansanz-Agustín, Pablo, Hillion, Melanie, Huang, Jingjing, Ilikay, Serap, Jansen-Dürr, Pidder, Jaquet, Vincent, Joles, Jaap A., Kalyanaraman, Balaraman, Kaminskyy, Danylo, Karbaschi, Mahsa, Kleanthous, Marina, Klotz, Lars-Oliver, Korac, Bato, Korkmaz, Kemal Sami, Koziel, Rafal, Kračun, Damir, Krause, Karl-Heinz, Křen, Vladimír, Krieg, Thomas, Laranjinha, João, Lazou, Antigone, Li, Huige, Martínez-Ruiz, Antonio, Matsui, Reiko, McBean, Gethin J., Meredith, Stuart P., Messens, Joris, Miguel, Verónica, Mikhed, Yuliya, Milisav, Irina, Milković, Lidija, Miranda-Vizuete, Antonio, Mojović, Miloš, Monsalve, María, Mouthuy, Pierre-Alexis, Mulvey, John, Münzel, Thomas, Muzykantov, Vladimir, Nguyen, Isabel T.N., Oelze, Matthias, Oliveira, Nuno G., Palmeira, Carlos M., Papaevgeniou, Nikoletta, Pavićević, Aleksandra, Pedre, Brandán, Peyrot, Fabienne, Phylactides, Marios, Pircalabioru, Gratiela G., Pitt, Andrew R., Poulsen, Henrik E., Prieto, Ignacio, Rigobello, Maria Pia, Robledinos-Antón, Natalia, Rodríguez-Mañas, Leocadio, Rolo, Anabela P., Rousset, Francis, Ruskovska, Tatjana, Saraiva, Nuno, Sasson, Shlomo, Schröder, Katrin, Semen, Khrystyna, Seredenina, Tamara, Shakirzyanova, Anastasia, Smith, Geoffrey L., Soldati, Thierry, Sousa, Bebiana C., Spickett, Corinne M., Stancic, Ana, Stasia, Marie José, Steinbrenner, Holger, Stepanić, Višnja, Steven, Sebastian, Tokatlidis, Kostas, Tuncay, Erkan, Turan, Belma, Ursini, Fulvio, Vacek, Jan, Vajnerova, Olga, Valentová, Kateřina, Van Breusegem, Frank, Varisli, Lokman, Veal, Elizabeth A., Yalçın, A. Suha, Yelisyeyeva, Olha, Žarković, Neven, Zatloukalová, Martina, Zielonka, Jacek, Touyz, Rhian M., Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H.H.W., Di Lisa, Fabio, and Daiber, Andreas

Published
2017
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8. Epithelial–Mesenchymal Transition in Acute Leukemias.

Author

Varisli, Lokman and Vlahopoulos, Spiros

Subjects
*ACUTE leukemia, *EPITHELIAL-mesenchymal transition, *PHENOTYPIC plasticity, *HEMATOLOGIC malignancies, *TISSUE differentiation
Abstract

Epithelial–mesenchymal transition (EMT) is a metabolic process that confers phenotypic flexibility to cells and the ability to adapt to new functions. This transition is critical during embryogenesis and is required for the differentiation of many tissues and organs. EMT can also be induced in advanced-stage cancers, leading to further malignant behavior and chemotherapy resistance, resulting in an unfavorable prognosis for patients. Although EMT was long considered and studied only in solid tumors, it has been shown to be involved in the pathogenesis of hematological malignancies, including acute leukemias. Indeed, there is increasing evidence that EMT promotes the progression of acute leukemias, leading to the emergence of a more aggressive phenotype of the disease, and also causes chemotherapy resistance. The current literature suggests that the levels and activities of EMT inducers and markers can be used to predict prognosis, and that targeting EMT in addition to conventional therapies may increase treatment success in acute leukemias. [ABSTRACT FROM AUTHOR]

Published
2024
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9. OGG1 as an Epigenetic Reader Affects NFκB: What This Means for Cancer.

Author

Vlahopoulos, Spiros, Pan, Lang, Varisli, Lokman, Dancik, Garrett M., Karantanos, Theodoros, and Boldogh, Istvan

Subjects
CYTOKINES, DNA, GENETIC mutation, NEOVASCULARIZATION, NF-kappa B, GENETIC polymorphisms, CELL survival, OXIDATIVE stress, CELLULAR signal transduction, EPITHELIAL-mesenchymal transition, GENE expression, GLYCOSIDASES, ENZYMES, CELL proliferation, TUMORS
Abstract

Simple Summary: OGG1-enabled NFκB activity can promote cancer progression via a number of key mechanisms that include phenotypic transitions of cancer and stromal cells, expression and secretion of molecules that modulate innate immunity, and alteration of the vascular network. Under oxidative stress, the supraphysiological levels of nongenotoxic 8-oxoGua, along with redox inactivation of OGG1 via cysteine oxidation and potential dimerization, provide multiple interfaces with redox-activated/modulated NFκB and other transacting factors, including Myc. This promotes not only cell proliferation, the expression of innate immune genes, and angiogenesis but also the metastatic capability of cells involving the expression of epithelial–mesenchymal transition genes. Mounting evidence supports the idea that increased levels of oxidative stress play a crucial role in the onset and progression of solid and lymphoid malignancies. This is achieved by gaining mutations and by activating signaling pathways that promote cell survival, cell proliferation, and resistance to treatment modalities. 8-oxoguanine glycosylase 1 (OGG1), which was initially identified as the enzyme that catalyzes the first step in the DNA base excision repair pathway, is now also recognized as a modulator of gene expression. What is important for cancer is that OGG1 acts as a modulator of NFκB-driven gene expression. Specifically, oxidant stress in the cell transiently halts enzymatic activity of substrate-bound OGG1. The stalled OGG1 facilitates DNA binding of transactivators, such as NFκB to their cognate sites, enabling the expression of cytokines and chemokines, with ensuing recruitment of inflammatory cells. Recently, we highlighted chief aspects of OGG1 involvement in regulation of gene expression, which hold significance in lung cancer development. However, OGG1 has also been implicated in the molecular underpinning of acute myeloid leukemia. This review analyzes and discusses how these cells adapt through redox-modulated intricate connections, via interaction of OGG1 with NFκB, which provides malignant cells with alternative molecular pathways to transform their microenvironment, enabling adjustment, promoting cell proliferation, metastasis, and evading killing by therapeutic agents. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Silencing of HN1L suppresses the proliferation and migration of cancer cells

Author

Varisli, Lokman, Tolan, Veysel, Varisli, Lokman, and Tolan, Veysel

Abstract

Background and purpose: HN1L is a member of the HN1 gene family and shares about 30% similarity with HN1 which is another member of the family on the primary protein sequence. Since HN1 is an important gene that is involved in various cellular mechanisms and also differentially expressed in carcinogenesis, we investigated the effect of HN1L on some malignant behaviors of various cancer cells.Material and methods: Co-expression analysis, Gene Ontology enrichment, and database searches were performed to predict the cellular roles of HN1, and to investigate its expression in cancers and their corresponding normal tissues. Western blotting and Real-Time PCR were used to compare the expression of HN1L in the normal prostate cells and prostate cancer cells. Cell proliferation and migration assays were used to investigate the effects of HN1L depletion on cell proliferation and migration.Results: The results of co-expression and Gene Ontology enrichment analyses showed that HN1L is co-expressed with DNA replication and DNA damage response/repair associated genes. The database search results revealed that HN1L expression increases in at least 10 diverse cancer types compared to their normal corresponding tissues. This result was confirmed in the prostate cancer cell model, experimentally. Silencing of HN1L inhibited proliferative and migrative behaviors of prostate, breast, colon, and cervix cancer cells.Conclusions: HN1L probably is a novel proto-oncogene that is involved in the DNA metabolism-related mechanisms, and high HN1L level promotes further proliferation and migration in the cancer cells.

Published
2022

24. Dissecting pharmacological effects of chloroquine in cancer treatment: interference with inflammatory signaling pathways.

Author

Varisli, Lokman, Cen, Osman, and Vlahopoulos, Spiros

Subjects
*CANCER treatment, *OCCUPATIONAL roles, *CANCER invasiveness, *DRUG abuse, *IMMUNE system
Abstract

Summary: Chloroquines are 4‐aminoquinoline‐based drugs mainly used to treat malaria. At pharmacological concentrations, they have significant effects on tissue homeostasis, targeting diverse signaling pathways in mammalian cells. A key target pathway is autophagy, which regulates macromolecule turnover in the cell. In addition to affecting cellular metabolism and bioenergetic flow equilibrium, autophagy plays a pivotal role at the interface between inflammation and cancer progression. Chloroquines consequently have critical effects in tissue metabolic activity and importantly, in key functions of the immune system. In this article, we will review the work addressing the role of chloroquines in the homeostasis of mammalian tissue, and the potential strengths and weaknesses concerning their use in cancer therapy. [ABSTRACT FROM AUTHOR]

Published
2020
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25. European contribution to the study of ROS:a summary of the findings and prospects for the future from the COST Action BM1203 (EU-ROS)

Author

Egea, Javier, Fabregat, Isabel, Frapart, Yves M., Ghezzi, Pietro, Görlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G., Lopez, Manuela G., Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vina, Jose, Winyard, Paul, Abbas, Kahina, Ademowo, Stella, Afonso, Catarina B., Andreadou, Ioanna, Antelmann, Haike, Antunes, Fernando, Aslan, Mutay, Bachschmid, Markus M., Barbosa, Rui M., Belousov, Vsevolod, Berndt, Carsten, Bernlohr, David, Bertrán, Esther, Bindoli, Alberto, Bottari, Serge P., Brito, Paula M., Carrara, Guia, Casas, Ana I., Chatzi, Afroditi, Chondrogianni, Niki, Conrad, Marcus, Cooke, Marcus S., Costa, João G., Cuadrado, Antonio, My-Chan Dang, Pham, De Smet, Barbara, Debelec–butuner, Bilge, Dias, Irundika, Dunn, Joe Dan, Edson, Amanda J., El Assar, Mariam, El-Benna, Jamel, Ferdinandy, Péter, Fernandes, Ana S., Fladmark, Kari E., Förstermann, Ulrich, Giniatullin, Rashid, Giricz, Zoltán, Görbe, Anikó, Griffiths, Helen, Hampl, Vaclav, Hanf, Alina, Herget, Jan, Hernansanz-Agustín, Pablo, Hillion, Melanie, Huang, Jinjing, Ilikay, Serap, Jansen-Dürr, Pidder, Jaquet, Vincent, Joles, Jaap A., Kalyanaraman, Balaraman, Kaminskyy, Danylo, Karbaschi, Mahsa, Kleanthous, Marina, Klotz, Lars-Oliver, Korac, Bato, Korkmaz, Kemal Sami, Koziel, Rafal, Kračun, Damir, Krause, Karl-Heinz, Křen, Vladimír, Krieg, Thomas, Laranjinha, João, Lazou, Antigone, Li, Huige, Martínez-Ruiz, Antonio, Matsui, Reiko, Mcbean, Gethin J., Meredith, Stuart P., Messens, Joris, Miguel, Verónica, Mikhed, Yuliya, Milisav, Irina, Milković, Lidija, Miranda-Vizuete, Antonio, Mojović, Milos, Monsalve, María, Mouthuy, Pierre-Alexis, Mulvey, John, Münzel, Thomas, Muzykantov, Vladimir, Nguyen, Isabel T.N., Oelze, Matthias, Oliveira, Nuno G., Palmeira, Carlos M., Papaevgeniou, Nikoletta, Pavićević, Aleksandra, Pedre, Brandán, Peyrot, Fabienne, Phylactides, Marios, Pircalabioru, Gratiela G., Pitt, Andrew R., Poulsen, Henrik E., Prieto, Ignacio, Rigobello, Maria Pia, Robledinos-Antón, Natalia, Rodríguez-mañas, Leocadio, Rolo, Anabela P., Rousset, Francis, Ruskovska, Tatjana, Saraiva, Nuno, Sasson, Shlomo, Schröder, Katrin, Semen, Khrystyna, Seredenina, Tamara, Shakirzyanova, Anastasia, Smith, Geoffrey L., Soldati, Thierry, Sousa, Bebiana C., Spickett, Corinne M., Stancic, Ana, Stasia, Marie José, Steinbrenner, Holger, Stepanić, Višnja, Steven, Sebastian, Tokatlidis, Kostas, Tuncay, Erkan, Turan, Belma, Ursini, Fulvio, Vacek, Jan, Vajnerova, Olga, Valentová, Kateřina, van Breusegem, Frank, Varisli, Lokman, Veal, Elizabeth A., Yalçın, A. Suha, Yelisyeyeva, Olha, Žarković, Neven, Zatloukalová, Martina, Zielonka, Jacek, Touyz, Rhian M., Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H.H.W., di Lisa, Fabio, Daiber, Andreas, Egea, Javier, Fabregat, Isabel, Frapart, Yves M., Ghezzi, Pietro, Görlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G., Lopez, Manuela G., Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vina, Jose, Winyard, Paul, Abbas, Kahina, Ademowo, Stella, Afonso, Catarina B., Andreadou, Ioanna, Antelmann, Haike, Antunes, Fernando, Aslan, Mutay, Bachschmid, Markus M., Barbosa, Rui M., Belousov, Vsevolod, Berndt, Carsten, Bernlohr, David, Bertrán, Esther, Bindoli, Alberto, Bottari, Serge P., Brito, Paula M., Carrara, Guia, Casas, Ana I., Chatzi, Afroditi, Chondrogianni, Niki, Conrad, Marcus, Cooke, Marcus S., Costa, João G., Cuadrado, Antonio, My-Chan Dang, Pham, De Smet, Barbara, Debelec–butuner, Bilge, Dias, Irundika, Dunn, Joe Dan, Edson, Amanda J., El Assar, Mariam, El-Benna, Jamel, Ferdinandy, Péter, Fernandes, Ana S., Fladmark, Kari E., Förstermann, Ulrich, Giniatullin, Rashid, Giricz, Zoltán, Görbe, Anikó, Griffiths, Helen, Hampl, Vaclav, Hanf, Alina, Herget, Jan, Hernansanz-Agustín, Pablo, Hillion, Melanie, Huang, Jinjing, Ilikay, Serap, Jansen-Dürr, Pidder, Jaquet, Vincent, Joles, Jaap A., Kalyanaraman, Balaraman, Kaminskyy, Danylo, Karbaschi, Mahsa, Kleanthous, Marina, Klotz, Lars-Oliver, Korac, Bato, Korkmaz, Kemal Sami, Koziel, Rafal, Kračun, Damir, Krause, Karl-Heinz, Křen, Vladimír, Krieg, Thomas, Laranjinha, João, Lazou, Antigone, Li, Huige, Martínez-Ruiz, Antonio, Matsui, Reiko, Mcbean, Gethin J., Meredith, Stuart P., Messens, Joris, Miguel, Verónica, Mikhed, Yuliya, Milisav, Irina, Milković, Lidija, Miranda-Vizuete, Antonio, Mojović, Milos, Monsalve, María, Mouthuy, Pierre-Alexis, Mulvey, John, Münzel, Thomas, Muzykantov, Vladimir, Nguyen, Isabel T.N., Oelze, Matthias, Oliveira, Nuno G., Palmeira, Carlos M., Papaevgeniou, Nikoletta, Pavićević, Aleksandra, Pedre, Brandán, Peyrot, Fabienne, Phylactides, Marios, Pircalabioru, Gratiela G., Pitt, Andrew R., Poulsen, Henrik E., Prieto, Ignacio, Rigobello, Maria Pia, Robledinos-Antón, Natalia, Rodríguez-mañas, Leocadio, Rolo, Anabela P., Rousset, Francis, Ruskovska, Tatjana, Saraiva, Nuno, Sasson, Shlomo, Schröder, Katrin, Semen, Khrystyna, Seredenina, Tamara, Shakirzyanova, Anastasia, Smith, Geoffrey L., Soldati, Thierry, Sousa, Bebiana C., Spickett, Corinne M., Stancic, Ana, Stasia, Marie José, Steinbrenner, Holger, Stepanić, Višnja, Steven, Sebastian, Tokatlidis, Kostas, Tuncay, Erkan, Turan, Belma, Ursini, Fulvio, Vacek, Jan, Vajnerova, Olga, Valentová, Kateřina, van Breusegem, Frank, Varisli, Lokman, Veal, Elizabeth A., Yalçın, A. Suha, Yelisyeyeva, Olha, Žarković, Neven, Zatloukalová, Martina, Zielonka, Jacek, Touyz, Rhian M., Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H.H.W., di Lisa, Fabio, and Daiber, Andreas

Abstract

The European Cooperation in Science and Technology (COST) provides an ideal framework to establish multi-disciplinary research networks. COST Action BM1203 (EU-ROS) represents a consortium of researchers from different disciplines who are dedicated to providing new insights and tools for better understanding redox biology and medicine and, in the long run, to finding new therapeutic strategies to target dysregulated redox processes in various diseases. This report highlights the major achievements of EU-ROS as well as research updates and new perspectives arising from its members. The EU-ROS consortium comprised more than 140 active members who worked together for four years on the topics briefly described below. The formation of reactive oxygen and nitrogen species (RONS) is an established hallmark of our aerobic environment and metabolism but RONS also act as messengers via redox regulation of essential cellular processes. The fact that many diseases have been found to be associated with oxidative stress established the theory of oxidative stress as a trigger of diseases that can be corrected by antioxidant therapy. However, while experimental studies support this thesis, clinical studies still generate controversial results, due to complex pathophysiology of oxidative stress in humans. For future improvement of antioxidant therapy and better understanding of redox-associated disease progression detailed knowledge on the sources and targets of RONS formation and discrimination of their detrimental or beneficial roles is required. In order to advance this important area of biology and medicine, highly synergistic approaches combining a variety of diverse and contrasting disciplines are needed.

Published
2017

26. European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

Author

MS Nefrologie, Regenerative Medicine and Stem Cells, Circulatory Health, Nefro Vasculaire Geneeskunde, Other research (not in main researchprogram), Egea, Javier, Fabregat, Isabel, Frapart, Yves M, Ghezzi, Pietro, Görlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G, Lopez, Manuela G, Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vina, Jose, Winyard, Paul J, Abbas, Kahina, Ademowo, Opeyemi S, Afonso, Catarina B, Andreadou, Ioanna, Antelmann, Haike, Antunes, Fernando, Aslan, Mutay, Bachschmid, Markus M, Barbosa, Rui M, Belousov, Vsevolod, Berndt, Carsten, Bernlohr, David, Bertrán, Esther, Bindoli, Alberto, Bottari, Serge P, Brito, Paula M, Carrara, Guia, Casas, Ana I, Chatzi, Afroditi, Chondrogianni, Niki, Conrad, Marcus, Cooke, Marcus S, Costa, João G, Cuadrado, Antonio, My-Chan Dang, Pham, De Smet, Barbara, Debelec-Butuner, Bilge, Dias, Irundika H K, Dunn, Joe Dan, Edson, Amanda J, El Assar, Mariam, El-Benna, Jamel, Ferdinandy, Péter, Fernandes, Ana S, Fladmark, Kari E, Förstermann, Ulrich, Giniatullin, Rashid, Giricz, Zoltán, Görbe, Anikó, Griffiths, Helen L, Hampl, Vaclav, Hanf, Alina, Herget, Jan, Hernansanz-Agustín, Pablo, Hillion, Melanie, Huang, Jingjing, Ilikay, Serap, Jansen-Dürr, Pidder, Jaquet, Vincent, Joles, Jaap A, Kalyanaraman, Balaraman, Kaminskyy, Danylo, Karbaschi, Mahsa, Kleanthous, Marina, Klotz, Lars-Oliver, Korac, Bato, Korkmaz, Kemal Sami, Koziel, Rafal, Kračun, Damir, Krause, Karl-Heinz, Křen, Vladimír, Krieg, Thomas, Laranjinha, João, Lazou, Antigone, Li, Huige, Martínez-Ruiz, Antonio, Matsui, Reiko, McBean, Gethin J, Meredith, Stuart P, Messens, Joris, Miguel, Verónica, Mikhed, Yuliya, Milisav, Irina, Milković, Lidija, Miranda-Vizuete, Antonio, Mojović, Miloš, Monsalve, María, Mouthuy, Pierre-Alexis, Mulvey, John, Münzel, Thomas, Muzykantov, Vladimir, Nguyen, Isabel T N, Oelze, Matthias, Oliveira, Nuno G, Palmeira, Carlos M, Papaevgeniou, Nikoletta, Pavićević, Aleksandra, Pedre, Brandán, Peyrot, Fabienne, Phylactides, Marios, Pircalabioru, Gratiela G, Pitt, Andrew R, Poulsen, Henrik E, Prieto, Ignacio, Rigobello, Maria Pia, Robledinos-Antón, Natalia, Rodríguez-Mañas, Leocadio, Rolo, Anabela P, Rousset, Francis, Ruskovska, Tatjana, Saraiva, Nuno, Sasson, Shlomo, Schröder, Katrin, Semen, Khrystyna, Seredenina, Tamara, Shakirzyanova, Anastasia, Smith, Geoffrey L, Soldati, Thierry, Sousa, Bebiana C, Spickett, Corinne M, Stancic, Ana, Stasia, Marie José, Steinbrenner, Holger, Stepanić, Višnja, Steven, Sebastian, Tokatlidis, Kostas, Tuncay, Erkan, Turan, Belma, Ursini, Fulvio, Vacek, Jan, Vajnerova, Olga, Valentová, Kateřina, Van Breusegem, Frank, Varisli, Lokman, Veal, Elizabeth A, Yalçın, A Suha, Yelisyeyeva, Olha, Žarković, Neven, Zatloukalová, Martina, Zielonka, Jacek, Touyz, Rhian M, Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H H W, Di Lisa, Fabio, Daiber, Andreas, MS Nefrologie, Regenerative Medicine and Stem Cells, Circulatory Health, Nefro Vasculaire Geneeskunde, Other research (not in main researchprogram), Egea, Javier, Fabregat, Isabel, Frapart, Yves M, Ghezzi, Pietro, Görlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G, Lopez, Manuela G, Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vina, Jose, Winyard, Paul J, Abbas, Kahina, Ademowo, Opeyemi S, Afonso, Catarina B, Andreadou, Ioanna, Antelmann, Haike, Antunes, Fernando, Aslan, Mutay, Bachschmid, Markus M, Barbosa, Rui M, Belousov, Vsevolod, Berndt, Carsten, Bernlohr, David, Bertrán, Esther, Bindoli, Alberto, Bottari, Serge P, Brito, Paula M, Carrara, Guia, Casas, Ana I, Chatzi, Afroditi, Chondrogianni, Niki, Conrad, Marcus, Cooke, Marcus S, Costa, João G, Cuadrado, Antonio, My-Chan Dang, Pham, De Smet, Barbara, Debelec-Butuner, Bilge, Dias, Irundika H K, Dunn, Joe Dan, Edson, Amanda J, El Assar, Mariam, El-Benna, Jamel, Ferdinandy, Péter, Fernandes, Ana S, Fladmark, Kari E, Förstermann, Ulrich, Giniatullin, Rashid, Giricz, Zoltán, Görbe, Anikó, Griffiths, Helen L, Hampl, Vaclav, Hanf, Alina, Herget, Jan, Hernansanz-Agustín, Pablo, Hillion, Melanie, Huang, Jingjing, Ilikay, Serap, Jansen-Dürr, Pidder, Jaquet, Vincent, Joles, Jaap A, Kalyanaraman, Balaraman, Kaminskyy, Danylo, Karbaschi, Mahsa, Kleanthous, Marina, Klotz, Lars-Oliver, Korac, Bato, Korkmaz, Kemal Sami, Koziel, Rafal, Kračun, Damir, Krause, Karl-Heinz, Křen, Vladimír, Krieg, Thomas, Laranjinha, João, Lazou, Antigone, Li, Huige, Martínez-Ruiz, Antonio, Matsui, Reiko, McBean, Gethin J, Meredith, Stuart P, Messens, Joris, Miguel, Verónica, Mikhed, Yuliya, Milisav, Irina, Milković, Lidija, Miranda-Vizuete, Antonio, Mojović, Miloš, Monsalve, María, Mouthuy, Pierre-Alexis, Mulvey, John, Münzel, Thomas, Muzykantov, Vladimir, Nguyen, Isabel T N, Oelze, Matthias, Oliveira, Nuno G, Palmeira, Carlos M, Papaevgeniou, Nikoletta, Pavićević, Aleksandra, Pedre, Brandán, Peyrot, Fabienne, Phylactides, Marios, Pircalabioru, Gratiela G, Pitt, Andrew R, Poulsen, Henrik E, Prieto, Ignacio, Rigobello, Maria Pia, Robledinos-Antón, Natalia, Rodríguez-Mañas, Leocadio, Rolo, Anabela P, Rousset, Francis, Ruskovska, Tatjana, Saraiva, Nuno, Sasson, Shlomo, Schröder, Katrin, Semen, Khrystyna, Seredenina, Tamara, Shakirzyanova, Anastasia, Smith, Geoffrey L, Soldati, Thierry, Sousa, Bebiana C, Spickett, Corinne M, Stancic, Ana, Stasia, Marie José, Steinbrenner, Holger, Stepanić, Višnja, Steven, Sebastian, Tokatlidis, Kostas, Tuncay, Erkan, Turan, Belma, Ursini, Fulvio, Vacek, Jan, Vajnerova, Olga, Valentová, Kateřina, Van Breusegem, Frank, Varisli, Lokman, Veal, Elizabeth A, Yalçın, A Suha, Yelisyeyeva, Olha, Žarković, Neven, Zatloukalová, Martina, Zielonka, Jacek, Touyz, Rhian M, Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H H W, Di Lisa, Fabio, and Daiber, Andreas

Published
2017

27. Hn1 Negatively Influences The Beta-Catenin/E-Cadherin Interaction, And Contributes To Migration In Prostate Cells

Author

Varisli, Lokman, Ozturk, Bilge E., Akyuz, Gencer K., and Korkmaz, Kemal S.

Abstract

Previously, it has been reported that HN1 is involved in cytoplasmic retention and degradation of androgen receptor in an AKT dependent manner. As HN1 is a hormone inducible gene, and has been shown that it is upregulated in various cancers, we studied the importance of HN1 function in -catenin signaling in prostate cancer cell line, PC-3 and mammary cancer cell line MDA-MB231. Here, we demonstrated that HN1 physically associates with GSK3/-catenin destruction complex and abundantly localizes to cytoplasm, especially when the GSK3 is phosphorylated on S9 residue. Further, ectopic HN1 expression results an increase in the -catenin degradation leading to loss of E-cadherin interaction, concurrently contributing to actin re-organization, colony formation and migration in cancer cell lines. Thus, we report that HN1 is an essential factor for -catenin turnover and signaling, augments cell growth and migration in prostate cancer cells. J. Cell. Biochem. 116: 170-178, 2015. (c) 2014 Wiley Periodicals, Inc.

Published
2015

29. Ubiquitously Expressed Hematological And Neurological Expressed 1 Downregulates Akt-Mediated Gsk3 Beta Signaling, And Its Knockdown Results In Deregulated G2/M Transition In Prostate Cells

Author

Varisli, Lokman, Gonen-Korkmaz, Ceren, Debelec-Butuner, Bilge, Erbaykent-Tepedelen, Burcu, Muhammed, Hamid Syed, Bogurcu, Nuray, Saatcioglu, Fahri, and Korkmaz, Kemal Sami

Abstract

As the molecular mechanism of beta-catenin deregulation is not well understood, and stabilized beta-catenin is known to translocate into the nucleus and activate genes for proliferation, a novel regulatory factor, hematological and neurological expressed 1 (HN1), for Akt-GSK3 beta-beta-catenin axis is reported here. In our studies, HN1 gene structure was characterized. HN1 expression was found to be epidermal growth factor-responsive in PC-3 cells, and protein expression was also upregulated in PC-3 and LNCaP but not in DU145 cells. Additionally, HN1 was found to be downregulated by the specific AKT inhibitor wortmannin but not with PI3K or MAPK inhibitors, LY294002 and PD98059, respectively, in PC-3 and MCF-7 cells. Further, siRNA-mediated knockdown of HN1 resulted in considerable increase in Akt((S473)) and GSK3 beta((S9),(Y216)) phosphorylations; moreover, subsequent accumulation of beta-catenin, increase in c-myc expression, and nuclear accumulation of cyclin D1 were observed in PC-3 cells. Knockdown of HN1 also resulted in prolongation of G(1) phase in cell cycle, increasing tetraploidy, presumably because of cells escaping from abnormal mitosis in PC-3 cells. Consistently, overexpression of HN1 reversed the cell-cycle-specific observations, resulted in accumulation of cells in G(2)/M, and reduced the proliferation rate, which were investigated using flow cytometry and methylthiazol tetrazolium assays. As activating mutations of beta-catenin have been demonstrated in late-stage tumors, and beta-catenin stabilization was correlated with poor prognosis in previous reports, epidermal growth factor-upregulated HN1 expression might have a role in deregulating the AKT-GSK3 beta((S9))-mediated signaling as a novel compensating mechanism.

Published
2011

31. Identification and Characterization of Rat ETV6 Gene by Using Bioinformatics Tools

Author

VARISLI, Lokman and CEN, Osman

Subjects
Bioinformatics,comparative genomics,ETV6,rat genome
Abstract

The products of ETS (erythroblast transformation specific domain) family genes are essential for a variety of developmental processes. This group of genes is frequently involved in leukemia and sarcoma as the result of specific chromosomal translocations. The ETV6 (ETS variant gene 6) gene, also called Tel or Tel1, is a member of the ETS family transcriptional regulators. Using in silico bioinformatic tools, we identified and characterized the rat ETV6 gene in this study. It has 8 exons and is located on the rat genomic contig NW_047696 of the rat chromosome 4. Its protein product has a predicted nuclear localization signal, one SAM_PNT (SAM-Pointed domain), and one ETS conserved domain. It has high homology to those of other vertebrate species. This is the first report on identification and characterization of the rat ETV6 gene

Published
2007

38. Ubiquitously Expressed Hematological and Neurological Expressed 1 Downregulates Akt-Mediated GSK3β Signaling, and Its Knockdown Results in Deregulated G2/M Transition in Prostate Cells

Author

Varisli, Lokman, primary, Gonen-Korkmaz, Ceren, additional, Debelec-Butuner, Bilge, additional, Erbaykent-Tepedelen, Burcu, additional, Muhammed, Hamid Syed, additional, Bogurcu, Nuray, additional, Saatcioglu, Fahri, additional, and Korkmaz, Kemal Sami, additional

Published
2011
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40. Biyoinformatik araçlarla VDR geni ve ürününün karşılaştırmalı analizi

Author

VARISLI, Lokman, OZGONUL, Abdullah, and CEN, Osman

Subjects
VDR,Biyoinformatik,Karşılaştırmalı genomik,in silico Biyoloji, VDR,Bioinformatics,Comparative genomics,in silico Biology
Abstract

Amaç: Bu çalışma, insan VDR molekülüne homolog protein dizileri, promotor dizileri üzerinde genel transkripsiyon faktör bağlanma yerleri, korunan bölgelerin filogenetik ilişkileri ve araştırılan ESTdb’lerin varlığında EST verilerine bağlı ekspresyon profilleri gibi genin ve onun ürünlerinin özelliklerini araştırmak amacı ile planlandı. Gereç-Yöntem: Biz, farklı anlı türlerinde biyoinformatik araçları kullanarak ESTdb’den EST verilerine dayanarak VDR genin homolojisini, korunan bölgelerini, promotor ve ekspresyon profillerini inceledik. Sonuçlar: Bu çalışmanın sonuçları, VDR molekülünün çalışılan tüm organizmalar arasında, örneğin Macaca mulatta 98% , Saguinus oedipus 98% ve Petromyzon marinus 59% ’un insana benzediğini ve orta derecede korunduğunu gösterdi. ZnF_C4 nükleer hormon reseptöründe C4 çinko ucu ve HOLI hormonların ligand bağlama alanı alanlarına göre bir kaç benzer motif belirlendi. Ayrıca insanın normal ve kanserli dokuları arasında gen ekspresyonu bakımından anlamlı fark olduğu gösterildi. Yorum: Bu çalışma, farklı canlı türlerinde VDR gen promotoru üzerinde herhangi bir genel transkripsiyon bağlama yerinin olmadığını kanıtladı. Yakınlık metodu NJ ’na dayanarak oluşturulan filogenetik ağaçlar, ZnF_C4 ve HOLI dizilerinin yakın evrimsel ilişkisini gösterdi, Background: The aims of this study was to analyze some properties of this gene and its products; such as the homologous protein sequences to human VDR molecule, the common transcription factor binding sites on promoter sequences, phylogenetic relationships of the conserved domains, and in silico expression profiles based on EST data that presence in ESTdb in all investigated. Methods: We investigated the homology, conserved domain, promoter and expression profiles of the VDR gene based on EST data from the ESTdb by using bioinformatics tools in different species. Results: The results of this study indicated that VDR molecule is middling conserved among all studied organisms; for example, human similar to Macaca mulatta 98% and Saguinus oedipus 98% , to Petromyzon marinus 59% . From the point of view of ZnF_C4 C4 zinc finger in nuclear hormone receptors and HOLI Ligand binding domain of hormones domains, it was obtained several similar motifs. Separately, it was seen that there was significantly difference gene expression in normal and cancer tissues of brain in human. Conclusion: This study demonstrated that there was no common transcription factor binding sites in promoter VDR gene in different species. Phylogenetic trees constructed using the neighbor-joining method NJ revealed a close evolutionary relationship of ZnF_C4 and HOLI in various species

41. European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

Author

YALÇIN, AHMET SUHA, Egea, Javier, Fabregat, Isabel, Frapart, Yves M., Ghezzi, Pietro, Gorlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G., Lopez, Manuela G., Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vinal, Jose, Winyard, Paul, Abbas, Kahina, Ademowo, Opeyemi S., Afonso, Catarina B., Andreadou, Ioanna, Antelmann, Haike, Antunes, Fernando, Aslan, Mutay, Bachschmid, Markus M., Barbosa, Rui M., Belousov, Vsevolod, Berndt, Carsten, Bernlohr, David, Bertran, Esther, Bindoli, Alberto, Bottari, Serge P., Brito, Paula M., Carrara, Guia, Casas, Ana I., Chatzi, Afroditi, Chondrogianni, Niki, Conrad, Marcus, Cooke, Marcus S., Costa, Joao G., Cuadrado, Antonio, Dang, Pham My-Chan, De Smet, Barbara, Butuner, Bilge Debelec, Dias, Irundika H. K., Dunn, Joe Dan, Edson, Amanda J., El Assar, Mariam, El-Benna, Jamel, Ferdinandy, Peter, Fernandes, Ana S., Fladmark, Kari E., Forstermann, Ulrich, Giniatullin, Rashid, Giricz, Zoltan, Gorbe, Aniko, Griffiths, Helen, Hampl, Vaclav, Hanf, Alina, Herget, Jan, Hernansanz-Agustin, Pablo, Hillion, Melanie, Huang, Jingjing, Ilikay, Serap, Jansen-Durr, Pidder, Jaquet, Vincent, Joles, Jaap A., Kalyanaraman, Balaraman, Kaminskyy, Danylo, Karbaschi, Mahsa, Kleanthous, Marina, Klotz, Lars-Oliver, Korac, Bato, Sami Korkmaz, Kemal, Koziel, Rafal, Kracun, Damir, Krause, Karl-Heinz, Kren, Vladimir, Krieg, Thomas, Laranjinha, Joao, Lazou, Antigone, Li, Huige, Martinez-Ruiz, Antonio, Matsui, Reiko, McBean, Gethin J., Meredith, Stuart P., Messens, Joris, Miguel, Veronica, Mikhed, Yuliya, Milisav, Irina, Milkovic, Lidija, Miranda-Vizuete, Antonio, Mojovic, Milos, Monsalve, Maria, Mouthuy, Pierre-Alexis, Mulvey, John, Munzel, Thomas, Muzykantov, Vladimir, Nguyen, Isabel T. N., Oelze, Matthias, Oliveira, Nuno G., Palmeira, Carlos M., Papaevgeniou, Nikoletta, Pavicevic, Aleksandra, Pedre, Brandan, Peyrot, Fabienne, Phylactides, Marios, Pircalabioru, Gratiela G., Pitt, Andrew R., Poulsen, Henrik E., Prieto, Ignacio, Pia Rigobello, Maria, Robledinos-Anton, Natalia, Rodriguez-Manas, Leocadio, Rolo, Anabela P., Rousset, Francis, Ruskovska, Tatjana, Saraiva, Nuno, Sasson, Shlomo, Schroeder, Katrin, Semen, Khrystyna, Seredenina, Tamara, Shakirzyanova, Anastasia, Smith, Geoffrey L., Soldati, Thierry, Sousa, Bebiana C., Spickett, Corinne M., Stancic, Ana, Stasia, Marie Jose, Steinbrenner, Holger, Stepanic, Visnja, Steven, Sebastian, Tokatlidis, Kostas, Tuncay, Erkan, Turan, Belma, Ursini, Fulvio, Vacek, Jan, Vajnerova, Olga, Valentova, Katerina, Van Breusegem, Frank, Varisli, Lokman, Veal, Elizabeth A., Yalcin, A. Suha, Yelisyeyeva, Olha, Zarkovic, Neven, Zatloukalova, Martina, Zielonka, Jacek, Touyz, Rhian M., Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H. H. W., Di Lisa, Fabio, and Daiber, Andreas

Subjects
Redox therapeutics, PULMONARY ARTERIAL-HYPERTENSION, Redox signaling, GROWTH-FACTOR-BETA, Reactive nitrogen species, MICROCYSTIN-INDUCED APOPTOSIS, Antioxidants, MANGANESE SUPEROXIDE-DISMUTASE, CHRONIC GRANULOMATOUS-DISEASE, ENDOPLASMIC-RETICULUM STRESS, Oxidative stress, ENDOTHELIAL-CELL MIGRATION, ADENINE-DINUCLEOTIDE PHOSPHATE, NITRIC-OXIDE SYNTHASE, Reactive oxygen species, MITOCHONDRIAL OXIDATIVE STRESS
Abstract

The European Cooperation in Science and Technology (COST) provides an ideal framework to establish multi-disciplinary research networks. COST Action BM1203 (EU-ROS) represents a consortium of researchers from different disciplines who are dedicated to providing new insights and tools for better understanding redox biology and medicine and, in the long run, to finding new therapeutic strategies to target dysregulated redox processes in various diseases. This report highlights the major achievements of EU-ROS as well as research updates and new perspectives arising from its members. The EU-ROS consortium comprised more than 140 active members who worked together for four years on the topics briefly described below. The formation of reactive oxygen and nitrogen species (RONS) is an established hallmark of our aerobic environment and metabolism but RONS also act as messengers via redox regulation of essential cellular processes. The fact that many diseases have been found to be associated with oxidative stress established the theory of oxidative stress as a trigger of diseases that can be corrected by antioxidant therapy. However, while experimental studies support this thesis, clinical studies still generate controversial results, due to complex pathophysiology of oxidative stress in humans. For future improvement of antioxidant therapy and better understanding of redox-associated disease progression detailed knowledge on the sources and targets of RONS formation and discrimination of their detrimental or beneficial roles is required. In order to advance this important area of biology and medicine, highly synergistic approaches combining a variety of diverse and contrasting disciplines are needed.

Published
2017

42. Dissecting the effects of androgen deprivation therapy on cadherin switching in advanced prostate cancer: A molecular perspective.

Author

Varisli L, Tolan V, Cen JH, Vlahopoulos S, and Cen O

Subjects
Male, Humans, Androgen Antagonists adverse effects, Androgens, Cadherins, Epithelial-Mesenchymal Transition, Prostatic Neoplasms drug therapy, Prostatic Neoplasms genetics
Abstract

Prostate cancer is one of the most often diagnosed malignancies in males and its prevalence is rising in both developed and developing countries. Androgen deprivation therapy has been used as a standard treatment approach for advanced prostate cancer for more than 80 years. The primary aim of androgen deprivation therapy is to decrease circulatory androgen and block androgen signaling. Although a partly remediation is accomplished at the beginning of treatment, some cell populations become refractory to androgen deprivation therapy and continue to metastasize. Recent evidences suggest that androgen deprivation therapy may cause cadherin switching, from E-cadherin to N-cadherin, which is the hallmark of epithelial-mesenchymal transition. Diverse direct and indirect mechanisms are involved in this switching and consequently, the cadherin pool changes from E-cadherin to N-cadherin in the epithelial cells. Since E-cadherin represses invasive and migrative behaviors of the tumor cells, the loss of E-cadherin disrupts epithelial tissue structure leading to the release of tumor cells into surrounding tissues and circulation. In this study, we review the androgen deprivation therapy-dependent cadherin switching in advanced prostate cancer with emphasis on its molecular basis especially the transcriptional factors regulated through TFG-β pathway., Competing Interests: The authors declare that they have no conflicts of interest to report regarding the present study., (© 2022 Varisli et al.)

Published
2023
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