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2. Membrane to cortex attachment determines different mechanical phenotypes in LGR5+ and LGR5- colorectal cancer cells

Author

Conti, Sefora, Venturini, Valeria, Cañellas-Socias, Adrià, Cortina, Carme, Abenza, Juan F., Stephan-Otto Attolini, Camille, Middendorp Guerra, Emily, Xu, Catherine K., Li, Jia Hui, Rossetti, Leone, Stassi, Giorgio, Roca-Cusachs, Pere, Diz-Muñoz, Alba, Ruprecht, Verena, Guck, Jochen, Batlle, Eduard, Labernadie, Anna, and Trepat, Xavier

Published
2024
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4. The efficacy of chemotherapy is limited by intratumoral senescent cells expressing PD-L2

Author

Chaib, Selim, López-Domínguez, José Alberto, Lalinde-Gutiérrez, Marta, Prats, Neus, Marin, Ines, Boix, Olga, García-Garijo, Andrea, Meyer, Kathleen, Muñoz, María Isabel, Aguilera, Mònica, Mateo, Lidia, Stephan-Otto Attolini, Camille, Llanos, Susana, Pérez-Ramos, Sandra, Escorihuela, Marta, Al-Shahrour, Fatima, Cash, Timothy P., Tchkonia, Tamara, Kirkland, James L., Abad, María, Gros, Alena, Arribas, Joaquín, and Serrano, Manuel

Published
2024
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6. Iron accumulation drives fibrosis, senescence and the senescence-associated secretory phenotype

Author

Maus, Mate, López-Polo, Vanessa, Mateo, Lidia, Lafarga, Miguel, Aguilera, Mònica, De Lama, Eugenia, Meyer, Kathleen, Sola, Anna, Lopez-Martinez, Cecilia, López-Alonso, Ines, Guasch-Piqueras, Marc, Hernandez-Gonzalez, Fernanda, Chaib, Selim, Rovira, Miguel, Sanchez, Mayka, Faner, Rosa, Agusti, Alvar, Diéguez-Hurtado, Rodrigo, Ortega, Sagrario, Manonelles, Anna, Engelhardt, Stefan, Monteiro, Freddy, Stephan-Otto Attolini, Camille, Prats, Neus, Albaiceta, Guillermo, Cruzado, Josep M., and Serrano, Manuel

Published
2023
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9. Mex3a marks drug-tolerant persister colorectal cancer cells that mediate relapse after chemotherapy

Author

Álvarez-Varela, Adrián, Novellasdemunt, Laura, Barriga, Francisco M., Hernando-Momblona, Xavier, Cañellas-Socias, Adrià, Cano-Crespo, Sara, Sevillano, Marta, Cortina, Carme, Stork, Diana, Morral, Clara, Turon, Gemma, Slebe, Felipe, Jiménez-Gracia, Laura, Caratù, Ginevra, Jung, Peter, Stassi, Giorgio, Heyn, Holger, Tauriello, Daniele V. F., Mateo, Lidia, Tejpar, Sabine, Sancho, Elena, Stephan-Otto Attolini, Camille, and Batlle, Eduard

Published
2022
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10. Functional patient-derived organoid screenings identify MCLA-158 as a therapeutic EGFR × LGR5 bispecific antibody with efficacy in epithelial tumors

Author

Herpers, Bram, Eppink, Berina, James, Mark I., Cortina, Carme, Cañellas-Socias, Adrià, Boj, Sylvia F., Hernando-Momblona, Xavier, Glodzik, Dominik, Roovers, Rob C., van de Wetering, Marc, Bartelink-Clements, Carina, Zondag-van der Zande, Vanessa, Mateos, Jara García, Yan, Kuan, Salinaro, Lucia, Basmeleh, Abdul, Fatrai, Szabolcs, Maussang, David, Lammerts van Bueren, Jeroen J., Chicote, Irene, Serna, Garazi, Cabellos, Laia, Ramírez, Lorena, Nuciforo, Paolo, Salazar, Ramon, Santos, Cristina, Villanueva, Alberto, Stephan-Otto Attolini, Camille, Sancho, Elena, Palmer, Hector G., Tabernero, Josep, Stratton, Michael R., de Kruif, John, Logtenberg, Ton, Clevers, Hans, Price, Leo S., Vries, Robert G. J., Batlle, Eduard, and Throsby, Mark

Published
2022
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11. pTINCR microprotein promotes epithelial differentiation and suppresses tumor growth through CDC42 SUMOylation and activation

Author

Boix, Olga, Martinez, Marion, Vidal, Santiago, Giménez-Alejandre, Marta, Palenzuela, Lluís, Lorenzo-Sanz, Laura, Quevedo, Laura, Moscoso, Olivier, Ruiz-Orera, Jorge, Ximénez-Embún, Pilar, Ciriaco, Nikaoly, Nuciforo, Paolo, Stephan-Otto Attolini, Camille, Albà, M. Mar, Muñoz, Javier, Tian, Tian V., Varela, Ignacio, Vivancos, Ana, Ramón y Cajal, Santiago, Muñoz, Purificación, Rivas, Carmen, and Abad, María

Published
2022
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12. Global hyperactivation of enhancers stabilizes human and mouse naive pluripotency through inhibition of CDK8/19 Mediator kinases

Author

Lynch, Cian J., Bernad, Raquel, Martínez-Val, Ana, Shahbazi, Marta N., Nóbrega-Pereira, Sandrina, Calvo, Isabel, Blanco-Aparicio, Carmen, Tarantino, Carolina, Garreta, Elena, Richart-Ginés, Laia, Alcazar, Noelia, Graña-Castro, Osvaldo, Gómez-Lopez, Gonzalo, Aksoy, Irene, Muñoz-Martín, Maribel, Martinez, Sonia, Ortega, Sagrario, Prieto, Susana, Simboeck, Elisabeth, Camasses, Alain, Stephan-Otto Attolini, Camille, Fernandez, Agustin F., Sierra, Marta I., Fraga, Mario F., Pastor, Joaquin, Fisher, Daniel, Montserrat, Nuria, Savatier, Pierre, Muñoz, Javier, Zernicka-Goetz, Magdalena, and Serrano, Manuel

Published
2020
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16. MSK1 regulates luminal cell differentiation and metastatic dormancy in ER+ breast cancer

Author

Gawrzak, Sylwia, Rinaldi, Lorenzo, Gregorio, Sara, Arenas, Enrique J., Salvador, Fernando, Urosevic, Jelena, Figueras-Puig, Cristina, Rojo, Federico, del Barco Barrantes, Ivan, Cejalvo, Juan Miguel, Palafox, Marta, Guiu, Marc, Berenguer-Llergo, Antonio, Symeonidi, Aikaterini, Bellmunt, Anna, Kalafatovic, Daniela, Arnal-Estapé, Anna, Fernández, Esther, Müllauer, Barbara, Groeneveld, Rianne, Slobodnyuk, Konstantin, Stephan-Otto Attolini, Camille, Saura, Cristina, Arribas, Joaquín, Cortes, Javier, Rovira, Ana, Muñoz, Montse, Lluch, Ana, Serra, Violeta, Albanell, Joan, Prat, Aleix, Nebreda, Angel R., Benitah, Salvador Aznar, and Gomis, Roger R.

Published
2018
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18. Induction of senescence renders cancer cells highly immunogenic

Author

Marín, Inés, primary, Boix, Olga, additional, García, Andrea, additional, Sirois, Isabelle, additional, Caballe, Adrià, additional, Zarzuela, Eduardo, additional, Ruano, Irene, additional, Stephan-Otto Attolini, Camille, additional, Prats, Neus, additional, López-Domínguez, José Alberto, additional, Kovatcheva, Marta, additional, Garralda, Elena, additional, Muñoz, Javier, additional, Caron, Etienne, additional, Abad, María, additional, Gros, Alena, additional, Pietrocola, Federico, additional, and Serrano, Manuel, additional

Published
2022
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19. pTINCR microprotein promotes epithelial differentiation and suppresses tumor growth through CDC42 SUMOylation and activation

Author

Fundación Fero, Fundación la Caixa, Asociación Española Contra el Cáncer, Fundación Mutua Madrileña, Ministerio de Economía y Competitividad (España), Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Generalitat de Catalunya, Boix, Olga, Martínez, Marion, Vidal, Santiago, Giménez-Alejandre, Marta, Palenzuela, Lluís, Lorenzo-Sanz, Laura, Quevedo, Laura, Moscoso, Olivier, Ruiz-Orera, Jorge, Ximénez-Embún, Pilar, Ciriaco, Nikaoly, Nuciforo, Paolo, Stephan-Otto Attolini, Camille, Albà, M. Mar, Muñoz, Javier, Tian, Tian V., Varela, Ignacio, Vivancos, Ana, Ramón y Cajal, S., Muñoz, Purificación, Rivas, Carmen, Abad, M., Fundación Fero, Fundación la Caixa, Asociación Española Contra el Cáncer, Fundación Mutua Madrileña, Ministerio de Economía y Competitividad (España), Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Generalitat de Catalunya, Boix, Olga, Martínez, Marion, Vidal, Santiago, Giménez-Alejandre, Marta, Palenzuela, Lluís, Lorenzo-Sanz, Laura, Quevedo, Laura, Moscoso, Olivier, Ruiz-Orera, Jorge, Ximénez-Embún, Pilar, Ciriaco, Nikaoly, Nuciforo, Paolo, Stephan-Otto Attolini, Camille, Albà, M. Mar, Muñoz, Javier, Tian, Tian V., Varela, Ignacio, Vivancos, Ana, Ramón y Cajal, S., Muñoz, Purificación, Rivas, Carmen, and Abad, M.

Abstract

The human transcriptome contains thousands of small open reading frames (sORFs) that encode microproteins whose functions remain largely unexplored. Here, we show that TINCR lncRNA encodes pTINCR, an evolutionary conserved ubiquitin-like protein (UBL) expressed in many epithelia and upregulated upon differentiation and under cellular stress. By gain- and loss-of-function studies, we demonstrate that pTINCR is a key inducer of epithelial differentiation in vitro and in vivo. Interestingly, low expression of TINCR associates with worse prognosis in several epithelial cancers, and pTINCR overexpression reduces malignancy in patient-derived xenografts. At the molecular level, pTINCR binds to SUMO through its SUMO interacting motif (SIM) and to CDC42, a Rho-GTPase critical for actin cytoskeleton remodeling and epithelial differentiation. Moreover, pTINCR increases CDC42 SUMOylation and promotes its activation, triggering a pro-differentiation cascade. Our findings suggest that the microproteome is a source of new regulators of cell identity relevant for cancer.

Published
2022

20. Multi-omic rejuvenation of naturally aged tissues by a single cycle of transient reprogramming

Author

Fundación la Caixa, Fundación Científica Asociación Española Contra el Cáncer, Principado de Asturias, European Commission, Instituto de Salud Carlos III, Agence Nationale de la Recherche (France), Ligue Nationale contre le Cancer (France), Association de la Recherche Contre le Cancer (France), Cancéropôle Île-de-France, Chancellerie des Universités de Paris, Fondation pour la Recherche Médicale, European Research Area Network on Cardiovascular Diseases, Institut National du Cancer (France), Fondation Leducq, Université de Paris, Biotechnology and Biological Sciences Research Council (UK), European Research Council, Ministerio de Economía y Competitividad (España), Generalitat de Catalunya, Chondronasiou, Dafni, Gill, Diljeet, Mosteiro, Lluc, Urdinguio, Rocío G., Berenguer-Llergo, Antonio, Aguilera,Mònica, Durand, Sylvère, Aprahamian, Fanny, Nirmalathasan, Nitharsshini, Abad, Maria, Martin-Herranz, Daniel E., Stephan-Otto Attolini, Camille, Prats, Neus, Kroemer, Guido, Fraga, Mario F., Reik, Wolf, Serrano, Manuel, Fundación la Caixa, Fundación Científica Asociación Española Contra el Cáncer, Principado de Asturias, European Commission, Instituto de Salud Carlos III, Agence Nationale de la Recherche (France), Ligue Nationale contre le Cancer (France), Association de la Recherche Contre le Cancer (France), Cancéropôle Île-de-France, Chancellerie des Universités de Paris, Fondation pour la Recherche Médicale, European Research Area Network on Cardiovascular Diseases, Institut National du Cancer (France), Fondation Leducq, Université de Paris, Biotechnology and Biological Sciences Research Council (UK), European Research Council, Ministerio de Economía y Competitividad (España), Generalitat de Catalunya, Chondronasiou, Dafni, Gill, Diljeet, Mosteiro, Lluc, Urdinguio, Rocío G., Berenguer-Llergo, Antonio, Aguilera,Mònica, Durand, Sylvère, Aprahamian, Fanny, Nirmalathasan, Nitharsshini, Abad, Maria, Martin-Herranz, Daniel E., Stephan-Otto Attolini, Camille, Prats, Neus, Kroemer, Guido, Fraga, Mario F., Reik, Wolf, and Serrano, Manuel

Abstract

The expression of the pluripotency factors OCT4, SOX2, KLF4, and MYC (OSKM) can convert somatic differentiated cells into pluripotent stem cells in a process known as reprogramming. Notably, partial and reversible reprogramming does not change cell identity but can reverse markers of aging in cells, improve the capacity of aged mice to repair tissue injuries, and extend longevity in progeroid mice. However, little is known about the mechanisms involved. Here, we have studied changes in the DNA methylome, transcriptome, and metabolome in naturally aged mice subject to a single period of transient OSKM expression. We found that this is sufficient to reverse DNA methylation changes that occur upon aging in the pancreas, liver, spleen, and blood. Similarly, we observed reversion of transcriptional changes, especially regarding biological processes known to change during aging. Finally, some serum metabolites and biomarkers altered with aging were also restored to young levels upon transient reprogramming. These observations indicate that a single period of OSKM expression can drive epigenetic, transcriptomic, and metabolomic changes toward a younger configuration in multiple tissues and in the serum.

Published
2022

21. Functional patient-derived organoid screenings identify MCLA-158 as a therapeutic EGFR x LGR5 bispecific antibody with efficacy in epithelial tumors

Author

CMM, Cancer, Hubrecht Institute with UMC, Herpers, Bram, Eppink, Berina, James, Mark I., Cortina, Carme, Cañellas-Socias, Adrià, Boj, Sylvia F., Hernando-Momblona, Xavier, Glodzik, Dominik, Roovers, Rob C., van de Wetering, Marc, Bartelink-Clements, Carina, Zondag-van der Zande, Vanessa, Mateos, Jara García, Yan, Kuan, Salinaro, Lucia, Basmeleh, Abdul, Fatrai, Szabolcs, Maussang, David, Lammerts van Bueren, Jeroen J., Chicote, Irene, Serna, Garazi, Cabellos, Laia, Ramírez, Lorena, Nuciforo, Paolo, Salazar, Ramon, Santos, Cristina, Villanueva, Alberto, Stephan-Otto Attolini, Camille, Sancho, Elena, Palmer, Hector G., Tabernero, Josep, Stratton, Michael R., de Kruif, John, Logtenberg, Ton, Clevers, Hans, Price, Leo S., Vries, Robert G.J., Batlle, Eduard, Throsby, Mark, CMM, Cancer, Hubrecht Institute with UMC, Herpers, Bram, Eppink, Berina, James, Mark I., Cortina, Carme, Cañellas-Socias, Adrià, Boj, Sylvia F., Hernando-Momblona, Xavier, Glodzik, Dominik, Roovers, Rob C., van de Wetering, Marc, Bartelink-Clements, Carina, Zondag-van der Zande, Vanessa, Mateos, Jara García, Yan, Kuan, Salinaro, Lucia, Basmeleh, Abdul, Fatrai, Szabolcs, Maussang, David, Lammerts van Bueren, Jeroen J., Chicote, Irene, Serna, Garazi, Cabellos, Laia, Ramírez, Lorena, Nuciforo, Paolo, Salazar, Ramon, Santos, Cristina, Villanueva, Alberto, Stephan-Otto Attolini, Camille, Sancho, Elena, Palmer, Hector G., Tabernero, Josep, Stratton, Michael R., de Kruif, John, Logtenberg, Ton, Clevers, Hans, Price, Leo S., Vries, Robert G.J., Batlle, Eduard, and Throsby, Mark

Published
2022

22. Multi‐omic rejuvenation of naturally aged tissues by a single cycle of transient reprogramming

Author

Chondronasiou, Dafni, primary, Gill, Diljeet, additional, Mosteiro, Lluc, additional, Urdinguio, Rocio G., additional, Berenguer‐Llergo, Antonio, additional, Aguilera, Mònica, additional, Durand, Sylvere, additional, Aprahamian, Fanny, additional, Nirmalathasan, Nitharsshini, additional, Abad, Maria, additional, Martin‐Herranz, Daniel E., additional, Stephan‐Otto Attolini, Camille, additional, Prats, Neus, additional, Kroemer, Guido, additional, Fraga, Mario F., additional, Reik, Wolf, additional, and Serrano, Manuel, additional

Published
2022
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24. Publisher Correction: MSK1 regulates luminal cell differentiation and metastatic dormancy in ER+ breast cancer

Author

Gawrzak, Sylwia, Rinaldi, Lorenzo, Gregorio, Sara, Arenas, Enrique J., Salvador, Fernando, Urosevic, Jelena, Figueras-Puig, Cristina, Rojo, Federico, del Barco Barrantes, Ivan, Cejalvo, Juan Miguel, Palafox, Marta, Guiu, Marc, Berenguer-Llergo, Antonio, Symeonidi, Aikaterini, Bellmunt, Anna, Kalafatovic, Daniela, Arnal-Estapé, Anna, Fernández, Esther, Müllauer, Barbara, Groeneveld, Rianne, Slobodnyuk, Konstantin, Stephan-Otto Attolini, Camille, Saura, Cristina, Arribas, Joaquín, Cortes, Javier, Rovira, Ana, Muñoz, Montse, Lluch, Ana, Serra, Violeta, Albanell, Joan, Prat, Aleix, Nebreda, Angel R., Benitah, Salvador Aznar, and Gomis, Roger R.

Published
2018
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26. Changes in glucagon‐like peptide 1 and 2 levels in people with obesity after a diet‐induced weight‐loss intervention are related to a specific microbiota signature: A prospective cohort study

Author

Instituto de Salud Carlos III, Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), Generalitat Valenciana, European Commission, Rodríguez-Peña, M-Mar, Astiarraga, Brenno, Seco, Jesús, Ceperuelo-Mallafré, Victoria, Caballé, Adrià, Pérez-Brocal, Vicente, Stephan‐Otto Attolini, Camille, Moya, Andrés, Llauradó, Gemma, Megía, Ana, Pellitero, Silvia, Vilarrasa, Núria, Fernández‐Veledo, Sonia, Vendrell, Joan, Instituto de Salud Carlos III, Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), Generalitat Valenciana, European Commission, Rodríguez-Peña, M-Mar, Astiarraga, Brenno, Seco, Jesús, Ceperuelo-Mallafré, Victoria, Caballé, Adrià, Pérez-Brocal, Vicente, Stephan‐Otto Attolini, Camille, Moya, Andrés, Llauradó, Gemma, Megía, Ana, Pellitero, Silvia, Vilarrasa, Núria, Fernández‐Veledo, Sonia, and Vendrell, Joan

Published
2021

27. Stability of imprinting and differentiation capacity in naïve human cells induced by chemical inhibition of CDK8 and CDK19

Author

Asociación Española Contra el Cáncer, Principado de Asturias, Instituto de Salud Carlos III, European Commission, Obra Social Cajastur, Fundación General CSIC, Liberbank, European Research Council, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Generalitat de Catalunya, Fundación la Caixa, Bernad, Raquel, Lynch, Cian J., Urdinguio, Rocío G., Stephan-Otto Attolini, Camille, Fraga, Mario F., Serrano, Manuel, Asociación Española Contra el Cáncer, Principado de Asturias, Instituto de Salud Carlos III, European Commission, Obra Social Cajastur, Fundación General CSIC, Liberbank, European Research Council, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Generalitat de Catalunya, Fundación la Caixa, Bernad, Raquel, Lynch, Cian J., Urdinguio, Rocío G., Stephan-Otto Attolini, Camille, Fraga, Mario F., and Serrano, Manuel

Abstract

Pluripotent stem cells can be stabilized in vitro at different developmental states by the use of specific chemicals and soluble factors. The naïve and primed states are the best characterized pluripotency states. Naïve pluripotent stem cells (PSCs) correspond to the early pre-implantation blastocyst and, in mice, constitute the optimal starting state for subsequent developmental applications. However, the stabilization of human naïve PSCs remains challenging because, after short-term culture, most current methods result in karyotypic abnormalities, aberrant DNA methylation patterns, loss of imprinting and severely compromised developmental potency. We have recently developed a novel method to induce and stabilize naïve human PSCs that consists in the simple addition of a chemical inhibitor for the closely related CDK8 and CDK19 kinases (CDK8/19i). Long-term cultured CDK8/19i-naïve human PSCs preserve their normal karyotype and do not show widespread DNA demethylation. Here, we investigate the long-term stability of allele-specific methylation at imprinted loci and the differentiation potency of CDK8/19i-naïve human PSCs. We report that long-term cultured CDK8/19i-naïve human PSCs retain the imprinting profile of their parental primed cells, and imprints are further retained upon differentiation in the context of teratoma formation. We have also tested the capacity of long-term cultured CDK8/19i-naïve human PSCs to differentiate into primordial germ cell (PGC)-like cells (PGCLCs) and trophoblast stem cells (TSCs), two cell types that are accessible from the naïve state. Interestingly, long-term cultured CDK8/19i-naïve human PSCs differentiated into PGCLCs with a similar efficiency to their primed counterparts. Also, long-term cultured CDK8/19i-naïve human PSCs were able to differentiate into TSCs, a transition that was not possible for primed PSCs. We conclude that inhibition of CDK8/19 stabilizes human PSCs in a functional naïve state that preserves imprinting and

Published
2021

30. Blimp-1 mediates tracheal lumen maturation in drosophila melanogaster

Author

Generalitat de Catalunya, Ministerio de Economía y Competitividad (España), Consejo Superior de Investigaciones Científicas (España), Institute for Research in Biomedicine (Spain), La Caixa, Stephan-Otto Attolini, Camille [0000-0001-8045-320X], Araújo, Sofia J. [0000-0002-4749-8913], Öztürk-Çolak, Arzu, Stephan-Otto Attolini, Camille, Casanova, Jordi, Araújo, Sofia J., Generalitat de Catalunya, Ministerio de Economía y Competitividad (España), Consejo Superior de Investigaciones Científicas (España), Institute for Research in Biomedicine (Spain), La Caixa, Stephan-Otto Attolini, Camille [0000-0001-8045-320X], Araújo, Sofia J. [0000-0002-4749-8913], Öztürk-Çolak, Arzu, Stephan-Otto Attolini, Camille, Casanova, Jordi, and Araújo, Sofia J.

Abstract

The specification of tissue identity during embryonic development requires precise spatio-temporal coordination of gene expression. Many transcription factors required for the development of organs have been identified and their expression patterns are known; however, the mechanisms through which they coordinate gene expression in time remain poorly understood. Here, we show that hormone-induced transcription factor Blimp-1 participates in the temporal coordination of tubulogenesis in Drosophila melanogaster by regulating the expression of many genes involved in tube maturation. In particular, we demonstrate that Blimp-1 regulates the expression of genes involved in chitin deposition and F-actin organization. We show that Blimp-1 is involved in the temporal control of lumen maturation by regulating the beginning of chitin deposition. We also report that Blimp-1 represses a variety of genes involved in tracheal maturation. Finally, we reveal that the kinase Btk29A serves as a link between Blimp-1 transcriptional repression and apical extracellular matrix organization.

Published
2018

31. Global hyperactivation of enhancers stabilizes human and mouse naive pluripotency through inhibition of CDK8/19 mediator kinases

Author

Leverhulme Trust, Wellcome Trust, Generalitat de Catalunya, European Research Council, Fondation pour la Recherche Médicale, European Commission, Agence Nationale de la Recherche (France), Université de Lyon, Ministerio de Economía y Competitividad (España), Centro Nacional de Investigaciones Oncológicas (España), Institut National du Cancer (France), Ligue Nationale contre le Cancer (France), Asociación Española Contra el Cáncer, Ministerio de Ciencia, Innovación y Universidades (España), Instituto de Salud Carlos III, Agencia Estatal de Investigación (España), Principado de Asturias, Liberbank, Obra Social Cajastur, Banco Santander, Fundación Botín, Fundación la Caixa, Lynch, Cian J., Bernad, Raquel, Martínez-Val, Ana, Shahbazi, Marta N., Nóbrega-Pereira, Sandrina, Calvo, Isabel, Blanco-Aparicio, Carmen, Tarantino, Carolina, Garreta, Elena, Richart-Ginés, Laia, Alcazar, Noelia, Graña-Castro, Osvaldo, Gómez-López, Gonzalo, Aksoy, Irene, Muñoz-Martín, Maribel, Martinez, Sonia, Ortega, Sagrario, Prieto, Susana, Simboeck, Elisabeth, Camasses, Alain, Stephan-Otto Attolini, Camille, Fernández, Agustín F., Sierra, Marta I., Fraga, Mario F., Pastor, Joaquín, Fisher, Daniel, Montserrat, Núria, Savatier, Pierre, Muñoz, Javier, Zernicka-Goetz, Magdalena, Serrano, Manuel, Leverhulme Trust, Wellcome Trust, Generalitat de Catalunya, European Research Council, Fondation pour la Recherche Médicale, European Commission, Agence Nationale de la Recherche (France), Université de Lyon, Ministerio de Economía y Competitividad (España), Centro Nacional de Investigaciones Oncológicas (España), Institut National du Cancer (France), Ligue Nationale contre le Cancer (France), Asociación Española Contra el Cáncer, Ministerio de Ciencia, Innovación y Universidades (España), Instituto de Salud Carlos III, Agencia Estatal de Investigación (España), Principado de Asturias, Liberbank, Obra Social Cajastur, Banco Santander, Fundación Botín, Fundación la Caixa, Lynch, Cian J., Bernad, Raquel, Martínez-Val, Ana, Shahbazi, Marta N., Nóbrega-Pereira, Sandrina, Calvo, Isabel, Blanco-Aparicio, Carmen, Tarantino, Carolina, Garreta, Elena, Richart-Ginés, Laia, Alcazar, Noelia, Graña-Castro, Osvaldo, Gómez-López, Gonzalo, Aksoy, Irene, Muñoz-Martín, Maribel, Martinez, Sonia, Ortega, Sagrario, Prieto, Susana, Simboeck, Elisabeth, Camasses, Alain, Stephan-Otto Attolini, Camille, Fernández, Agustín F., Sierra, Marta I., Fraga, Mario F., Pastor, Joaquín, Fisher, Daniel, Montserrat, Núria, Savatier, Pierre, Muñoz, Javier, Zernicka-Goetz, Magdalena, and Serrano, Manuel

Abstract

Pluripotent stem cells (PSCs) transition between cell states in vitro, reflecting developmental changes in the early embryo. PSCs can be stabilized in the naive state by blocking extracellular differentiation stimuli, particularly FGF–MEK signalling. Here, we report that multiple features of the naive state in human and mouse PSCs can be recapitulated without affecting FGF–MEK signalling or global DNA methylation. Mechanistically, chemical inhibition of CDK8 and CDK19 (hereafter CDK8/19) kinases removes their ability to repress the Mediator complex at enhancers. CDK8/19 inhibition therefore increases Mediator-driven recruitment of RNA polymerase II (RNA Pol II) to promoters and enhancers. This efficiently stabilizes the naive transcriptional program and confers resistance to enhancer perturbation by BRD4 inhibition. Moreover, naive pluripotency during embryonic development coincides with a reduction in CDK8/19. We conclude that global hyperactivation of enhancers drives naive pluripotency, and this can be achieved in vitro by inhibiting CDK8/19 kinase activity. These principles may apply to other contexts of cellular plasticity.

Published
2020

32. Differential Distribution of the wlaN and cgtB Genes, Associated with Guillain-Barré Syndrome, in Campylobacter jejuni Isolates from Humans, Broiler Chickens, and Wild Birds

Author

Guirado, Pedro, primary, Paytubi, Sonia, additional, Miró, Elisenda, additional, Iglesias-Torrens, Yaidelis, additional, Navarro, Ferran, additional, Cerdà-Cuéllar, Marta, additional, Stephan-Otto Attolini, Camille, additional, Balsalobre, Carlos, additional, and Madrid, Cristina, additional

Published
2020
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33. 12 Grand Challenges in Single-Cell Data Science

Author

Laehnemann, David, primary, Köster, Johannes, additional, Szczurek, Ewa, additional, McCarthy, Davis J, additional, Hicks, Stephanie C, additional, Robinson, Mark D, additional, Vallejos, Catalina A, additional, Beerenwinkel, Niko, additional, Campbell, Kieran R, additional, Mahfouz, Ahmed, additional, Pinello, Luca, additional, Skums, Pavel, additional, Stamatakis, Alexandros, additional, Stephan-Otto Attolini, Camille, additional, Aparicio, Samuel, additional, Baaijens, Jasmijn, additional, Balvert, Marleen, additional, de Barbanson, Buys, additional, Cappuccio, Antonio, additional, Corleone, Giacomo, additional, Dutilh, Bas E, additional, Florescu, Maria, additional, Guryev, Victor, additional, Holmer, Rens, additional, Jahn, Katharina, additional, Jessurun Lobo, Thamar, additional, Keizer, Emma M, additional, Khatri, Indu, additional, Kiełbasa, Szymon M, additional, Korbel, Jan O, additional, Kozlov, Alexey M, additional, Kuo, Tzu-Hao, additional, Lelieveldt, Boudewijn PF, additional, Mandoiu, Ion I, additional, Marioni, John C, additional, Marschall, Tobias, additional, Mölder, Felix, additional, Niknejad, Amir, additional, Rączkowski, Łukasz, additional, Reinders, Marcel, additional, de Ridder, Jeroen, additional, Saliba, Antoine-Emmanuel, additional, Somarakis, Antonios, additional, Stegle, Oliver, additional, Theis, Fabian J, additional, Yang, Huan, additional, Zelikovsky, Alex, additional, McHardy, Alice C, additional, Raphael, Benjamin J, additional, Shah, Sohrab P, additional, and Schönhuth, Alexander, additional

Published
2019
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41. The transcription factor GATA6 enables self-renewal of colon adenoma stem cells by repressing BMP gene expression

Author

Whissell, Gavin, primary, Montagni, Elisa, additional, Martinelli, Paola, additional, Hernando-Momblona, Xavier, additional, Sevillano, Marta, additional, Jung, Peter, additional, Cortina, Carme, additional, Calon, Alexandre, additional, Abuli, Anna, additional, Castells, Antoni, additional, Castellvi-Bel, Sergi, additional, Nacht, Ana Silvina, additional, Sancho, Elena, additional, Stephan-Otto Attolini, Camille, additional, Vicent, Guillermo P., additional, Real, Francisco X., additional, and Batlle, Eduard, additional

Published
2014
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43. CelloS: a Multi-level Approach to Evolutionary Dynamics

Author

Stephan-Otto Attolini, Camille, Stadler, Peter F., Flamm, Christoph, Stephan-Otto Attolini, Camille, Stadler, Peter F., and Flamm, Christoph

Abstract

We study the evolution of simple cells that are equipped with a genome, a rudimentary gene regulation network at transcription level and two classes of functional genes: motion effectors allow the cell to move in response to nutrient gradients while nutrient importers are required to actually feed from the environment. The model is inspired by the protist Naegleria gruberi which can switch between a feeding and dividing amoeboid state and a mobile agellate state depending on environmental conditions. Simulation results demonstrate how selection in a variable environment affects the gene number and effciency so that the cells can rapidly switch from one expression regime to the other depending on the external conditions.

Published
2005

44. MSK1 regulates luminal cell differentiation and metastatic dormancy in ER+breast cancer

Author

Gawrzak, Sylwia, Rinaldi, Lorenzo, Gregorio, Sara, Arenas, Enrique, Salvador, Fernando, Urosevic, Jelena, Figueras-Puig, Cristina, Rojo, Federico, del Barco Barrantes, Ivan, Cejalvo, Juan, Palafox, Marta, Guiu, Marc, Berenguer-Llergo, Antonio, Symeonidi, Aikaterini, Bellmunt, Anna, Kalafatovic, Daniela, Arnal-Estapé, Anna, Fernández, Esther, Müllauer, Barbara, Groeneveld, Rianne, Slobodnyuk, Konstantin, Stephan-Otto Attolini, Camille, Saura, Cristina, Arribas, Joaquín, Cortes, Javier, Rovira, Ana, Muñoz, Montse, Lluch, Ana, Serra, Violeta, Albanell, Joan, Prat, Aleix, Nebreda, Angel, Benitah, Salvador, and Gomis, Roger

Abstract

For many patients with breast cancer, symptomatic bone metastases appear after years of latency. How micrometastatic lesions remain dormant and undetectable before initiating colonization is unclear. Here, we describe a mechanism involved in bone metastatic latency of oestrogen receptor-positive (ER+) breast cancer. Using an in vivo genome-wide short hairpin RNA screening, we identified the kinase MSK1 as an important regulator of metastatic dormancy in breast cancer. In patients with ER+breast cancer, low MSK1 expression associates with early metastasis. We show that MSK1 downregulation impairs the differentiation of breast cancer cells, increasing their bone homing and growth capacities. MSK1 controls the expression of genes required for luminal cell differentiation, including the GATA3 and FOXA1 transcription factors, by modulating their promoter chromatin status. Our results indicate that MSK1 prevents metastatic progression of ER+breast cancer, suggesting that stratifying patients with breast cancer as high or low risk for early relapse based on MSK1 expression could improve prognosis. Gawrzak et al. show that MSK1 regulates bone metastatic dormancy of ER+breast cancer. MSK1 affects histone modifications at luminal transcription factor promoters to prevent cell differentiation and bone homing.

Published
2018
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46. Iro/IRX transcription factors negatively regulate Dpp/ TGF-β pathway activity during intestinal tumorigenesis.

Author

Martorell, Òscar, Barriga, Francisco M, Merlos‐Suárez, Anna, Stephan‐Otto Attolini, Camille, Casanova, Jordi, Batlle, Eduard, Sancho, Elena, and Casali, Andreu

Abstract

Activating mutations in Wnt and EGFR/Ras signaling pathways are common in colorectal cancer ( CRC). Remarkably, clonal co-activation of these pathways in the adult Drosophila midgut induces 'tumor-like' overgrowths. Here, we show that, in these clones and in CRC cell lines, Dpp/ TGF-β acts as a tumor suppressor. Moreover, we discover that the Iroquois/IRX-family-protein Mirror downregulates the transcription of core components of the Dpp pathway, reducing its tumor suppressor activity. We also show that this genetic interaction is conserved in human CRC cells, where the Iro/IRX proteins IRX3 and IRX5 diminish the response to TGF-β. IRX3 and IRX5 are upregulated in human adenomas, and their levels correlate inversely with the gene expression signature of response to TGF-β. In addition, Irx5 expression confers a growth advantage in the presence of TGF-β, but is selected against in its absence. Together, our results identify a set of Iro/IRX proteins as conserved negative regulators of Dpp/ TGF-β activity. We propose that during the characteristic adenoma-to-carcinoma transition of human CRC, the activity of IRX proteins could reduce the sensitivity to the cytostatic effect of TGF-β, conferring a growth advantage to tumor cells prior to the acquisition of mutations in TGF-β pathway components. [ABSTRACT FROM AUTHOR]

Published
2014
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47. NEUTRAL NETWORKS OF INTERACTING RNA SECONDARY STRUCTURES.

Author

STEPHAN-OTTO ATTOLINI, CAMILLE and STADLER, PETER F.

Subjects
*RNA, *NUCLEIC acids, *RIBOSE, *GENETIC mutation, *MOLECULES
Abstract

RNA molecules interact by forming inter-molecular base pairs that compete with the intra-molecular base pairs of their secondary structures. We investigate the patterns of neutral mutations in RNAs whose function is the interaction with other RNAs, i.e. the co-folding with one or more other RNA molecules. We find that (i) the degree of neutrality is much smaller in interacting RNAs compared to RNAs that just have to coform to a single externally prescribed target structure, and (ii) strengthening this contraint to the conservation of the co-folded structure with two or more partners essentially eliminates neutrality. It follows that RNAs whose function depends on the formation of a specific interaction complex with a target RNA molecule will evolve much more slowly than RNAs with a function depending only on their own structure. [ABSTRACT FROM AUTHOR]

Published
2005
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48. Publisher Correction: MSK1 regulates luminal cell differentiation and metastatic dormancy in ER+breast cancer

Author

Gawrzak, Sylwia, Rinaldi, Lorenzo, Gregorio, Sara, Arenas, Enrique, Salvador, Fernando, Urosevic, Jelena, Figueras-Puig, Cristina, Rojo, Federico, Barco Barrantes, Ivan, Cejalvo, Juan, Palafox, Marta, Guiu, Marc, Berenguer-Llergo, Antonio, Symeonidi, Aikaterini, Bellmunt, Anna, Kalafatovic, Daniela, Arnal-Estapé, Anna, Fernández, Esther, Müllauer, Barbara, Groeneveld, Rianne, Slobodnyuk, Konstantin, Stephan-Otto Attolini, Camille, Saura, Cristina, Arribas, Joaquín, Cortes, Javier, Rovira, Ana, Muñoz, Montse, Lluch, Ana, Serra, Violeta, Albanell, Joan, Prat, Aleix, Nebreda, Angel, Benitah, Salvador, and Gomis, Roger

Abstract

In the version of this Article originally published, the boxes framing the two plots in Fig. 1g were misaligned from the axes due to a technical error. This has now been corrected in all versions of the Article.

Published
2018
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49. Blimp-1 Mediates Tracheal Lumen Maturation in Drosophila melanogaster

Author

Camille Stephan-Otto Attolini, Sofia J. Araújo, Arzu Öztürk-Çolak, Jordi Casanova, Generalitat de Catalunya, Ministerio de Economía y Competitividad (España), Consejo Superior de Investigaciones Científicas (España), Institute for Research in Biomedicine (Spain), La Caixa, Stephan-Otto Attolini, Camille, Araújo, Sofia J., Stephan-Otto Attolini, Camille [0000-0001-8045-320X], and Araújo, Sofia J. [0000-0002-4749-8913]

Subjects
0301 basic medicine, Btk29A, Chitin, Biology, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Gene expression, Genetics, Gene, Transcription factor, Kinase, Embryogenesis, AECM, biology.organism_classification, Blimp-1, Cell biology, Trachea, 030104 developmental biology, chemistry, Drosophila, Drosophila melanogaster, Developmental biology, 030217 neurology & neurosurgery, Extracellular matrix organization
Abstract

The specification of tissue identity during embryonic development requires precise spatio-temporal coordination of gene expression. Many transcription factors required for the development of organs have been identified and their expression patterns are known; however, the mechanisms through which they coordinate gene expression in time remain poorly understood. Here, we show that hormone-induced transcription factor Blimp-1 participates in the temporal coordination of tubulogenesis in Drosophila melanogaster by regulating the expression of many genes involved in tube maturation. In particular, we demonstrate that Blimp-1 regulates the expression of genes involved in chitin deposition and F-actin organization. We show that Blimp-1 is involved in the temporal control of lumen maturation by regulating the beginning of chitin deposition. We also report that Blimp-1 represses a variety of genes involved in tracheal maturation. Finally, we reveal that the kinase Btk29A serves as a link between Blimp-1 transcriptional repression and apical extracellular matrix organization., S.J.A. was a Ramon y Cajal Researcher (RYC-2007-00417); A.O. was the recipient of an IRB-La Caixa fellowship. This work was supported by grants from the Generalitat de Catalunya and the Spanish Ministerio de Ciencia e Innovación (BFU2009-07629).

Published
2018
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50. Multi-omic rejuvenation of naturally aged tissues by a single cycle of transient reprogramming

Author

Dafni Chondronasiou, Diljeet Gill, Lluc Mosteiro, Rocio G. Urdinguio, Antonio Berenguer‐Llergo, Mònica Aguilera, Sylvere Durand, Fanny Aprahamian, Nitharsshini Nirmalathasan, Maria Abad, Daniel E. Martin‐Herranz, Camille Stephan‐Otto Attolini, Neus Prats, Guido Kroemer, Mario F. Fraga, Wolf Reik, Manuel Serrano, Gill, Diljeet [0000-0002-5725-2466], Mosteiro, Lluc [0000-0003-4041-9706], Urdinguio, Rocio G [0000-0003-2736-5758], Berenguer-Llergo, Antonio [0000-0002-3742-8161], Aguilera, Mònica [0000-0003-0763-7947], Abad, Maria [0000-0002-1462-2498], Martin-Herranz, Daniel E [0000-0002-2285-3317], Stephan-Otto Attolini, Camille [0000-0001-8045-320X], Prats, Neus [0000-0001-5653-7390], Fraga, Mario F [0000-0001-8450-2603], Reik, Wolf [0000-0003-0216-9881], Serrano, Manuel [0000-0001-7177-9312], Apollo - University of Cambridge Repository, Institut Català de la Salut, [Chondronasiou D, Berenguer-Llergo A, Aguilera M] Institute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain. [Gill D] Epigenetics Programme, Babraham Institute, Cambridge, UK. [Mosteiro L] Genentech, San Francisco, USA. [Urdinguio RG] Cancer Epigenetics and Nanomedicine Laboratory, Nanomaterials and Nanotechnology Research Center (CINN CSIC), Oviedo, Spain. Health Research Institute of Asturias (ISPA), Oviedo, Spain. Institute of Oncology of Asturias (IUOPA), University of Oviedo, Oviedo, Spain. Department of Organisms and Systems Biology (BOS), University of Oviedo, Oviedo, Spain. CIBER of Rare Diseases (CIBERER), Oviedo, Spain. [Abad M] Vall d'Hebron Institute of Oncology (VHIO), Barcelona, Spain, Vall d'Hebron Barcelona Hospital Campus, Fundación 'la Caixa', Fundación Científica Asociación Española Contra el Cáncer, Principado de Asturias, European Commission, Instituto de Salud Carlos III, Agence Nationale de la Recherche (France), Ligue Nationale contre le Cancer (France), Association de la Recherche Contre le Cancer (France), Cancéropôle Île-de-France, Chancellerie des Universités de Paris, Fondation pour la Recherche Médicale, European Research Area Network on Cardiovascular Diseases, Institut National du Cancer (France), Fondation Leducq, Université de Paris, Biotechnology and Biological Sciences Research Council (UK), European Research Council, Ministerio de Economía y Competitividad (España), and Generalitat de Catalunya

Subjects
Aging, transcriptomic clocks, Induced Pluripotent Stem Cells, epigenetic clocks, Yamanaka, RESEARCH ARTICLES, RESEARCH ARTICLE, Epigenome, Mice, Envelliment, Genetic Phenomena [PHENOMENA AND PROCESSES], Animals, Rejuvenation, Ratolins, aging, reprogramming, Cell Differentiation, Cell Biology, DNA Methylation, pluripotency, Cellular Reprogramming, Epigenètica, fenómenos genéticos [FENÓMENOS Y PROCESOS], OSKM, Epigenetics, sense organs, Cèl·lules - Envelliment, Cèl·lules mare
Abstract

The expression of the pluripotency factors OCT4, SOX2, KLF4, and MYC (OSKM) can convert somatic differentiated cells into pluripotent stem cells in a process known as reprogramming. Notably, partial and reversible reprogramming does not change cell identity but can reverse markers of aging in cells, improve the capacity of aged mice to repair tissue injuries, and extend longevity in progeroid mice. However, little is known about the mechanisms involved. Here, we have studied changes in the DNA methylome, transcriptome, and metabolome in naturally aged mice subject to a single period of transient OSKM expression. We found that this is sufficient to reverse DNA methylation changes that occur upon aging in the pancreas, liver, spleen, and blood. Similarly, we observed reversion of transcriptional changes, especially regarding biological processes known to change during aging. Finally, some serum metabolites and biomarkers altered with aging were also restored to young levels upon transient reprogramming. These observations indicate that a single period of OSKM expression can drive epigenetic, transcriptomic, and metabolomic changes toward a younger configuration in multiple tissues and in the serum., D.C. was recipient of a fellowship from “laCaixa” Foundation. Work in the laboratory of M.F.F. was funded by Fundación Científica Asociación Española Contra el Cáncer (AECC) (PROYE18061FER), the Asturias Government (PCTI) co-funding 2018- 2022/FEDER (IDI/2018/146), the Health Institute Carlos III (Plan Nacional de I+D+I) co-funding FEDER (PI18/01527). Work in the laboratory of G.K. was supported by the Ligue contre le Cancer (équipe labellisée); Agence National de la Recherche (ANR)—Projets blancs; ANR under the frame of E-Rare-2, the ERA-Net for Research on Rare Diseases; AMMICa US23/CNRS UMS3655; Association pour la recherche sur le cancer (ARC); Association “Ruban Rose”; Cancéropôle Ile-de-France; Chancelerie des universités de Paris (Legs Poix), Fondation pour la Recherche Médicale (FRM); a donation by Elior; European Research Area Network on Cardiovascular Diseases (ERA-CVD, MINOTAUR); Gustave Roussy Odyssea, the European Union Horizon 2020 Project Oncobiome; Fondation Carrefour; High-end Foreign Expert Program in China (GDW20171100085), Institut National du Cancer (INCa); Inserm (HTE); Institut Universitaire de France; LeDucq Foundation; the LabEx Immuno-Oncology (ANR-18-IDEX-0001); the RHU Torino Lumière; the Seerave Foundation; the SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE); and the SIRIC Cancer Research and Personalized Medicine (CARPEM). This study contributes to the IdEx Université de Paris ANR-18-IDEX-0001. Work in the laboratory of W.R. was funded by the Biotechnology and Biological Sciences Research Council (BBS/E/B/000C0425). Work in the laboratory of M.S. was funded by the IRB, and by grants from Spanish Ministry of Economy co-funded by European Regional Development Fund (ERDF) (SAF2013-48256-R), European Research Council (ERC-2014-AdG/669622), Secretaria d'Universitats i Recerca del Departament d'Empresa i Coneixement of Catalonia (Grup de Recerca consolidat 2017 SGR 282) and “laCaixa” Foundation.

Published
2022

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