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1. Comparative roadmaps of reprogramming and oncogenic transformation identify Bcl11b and Atoh8 as broad regulators of cellular plasticity

Author

Huyghe, A., Furlan, G., Schroeder, J., Cascales, E., Trajkova, A., Ruel, M., Stüder, F., Larcombe, M., Yang Sun, Y. Bo, Mugnier, F., De Matteo, L., Baygin, A., Wang, J., Yu, Y., Rama, N., Gibert, B., Kielbassa, J., Tonon, L., Wajda, P., Gadot, N., Brevet, M., Siouda, M., Mulligan, P., Dante, R., Liu, P., Gronemeyer, H., Mendoza-Parra, M., Polo, J. M., and Lavial, F.

Published
2022
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5. Comparative roadmaps of reprogramming and oncogenic transformation identify Bcl11b and Atoh8 as broad regulators of cellular plasticity

Author

Huyghe, A, Furlan, G, Schroeder, J, Cascales, E, Trajkova, A, Ruel, M, Studer, F, Larcombe, M, Yang Sun, YB, Mugnier, F, De Matteo, L, Baygin, A, Wang, J, Yu, Y, Rama, N, Gibert, B, Kielbassa, J, Tonon, L, Wajda, P, Gadot, N, Brevet, M, Siouda, M, Mulligan, P, Dante, R, Liu, P, Gronemeyer, H, Mendoza-Parra, M, Polo, JM, Lavial, F, Huyghe, A, Furlan, G, Schroeder, J, Cascales, E, Trajkova, A, Ruel, M, Studer, F, Larcombe, M, Yang Sun, YB, Mugnier, F, De Matteo, L, Baygin, A, Wang, J, Yu, Y, Rama, N, Gibert, B, Kielbassa, J, Tonon, L, Wajda, P, Gadot, N, Brevet, M, Siouda, M, Mulligan, P, Dante, R, Liu, P, Gronemeyer, H, Mendoza-Parra, M, Polo, JM, and Lavial, F

Abstract

Coordinated changes of cellular plasticity and identity are critical for pluripotent reprogramming and oncogenic transformation. However, the sequences of events that orchestrate these intermingled modifications have never been comparatively dissected. Here, we deconvolute the cellular trajectories of reprogramming (via Oct4/Sox2/Klf4/c-Myc) and transformation (via Ras/c-Myc) at the single-cell resolution and reveal how the two processes intersect before they bifurcate. This approach led us to identify the transcription factor Bcl11b as a broad-range regulator of cell fate changes, as well as a pertinent marker to capture early cellular intermediates that emerge simultaneously during reprogramming and transformation. Multiomics characterization of these intermediates unveiled a c-Myc/Atoh8/Sfrp1 regulatory axis that constrains reprogramming, transformation and transdifferentiation. Mechanistically, we found that Atoh8 restrains cellular plasticity, independent of cellular identity, by binding a specific enhancer network. This study provides insights into the partitioned control of cellular plasticity and identity for both regenerative and cancer biology.

Published
2022

11. The comprehensive roadmaps of reprogramming and transformation unveiled antagonistic roles for bHLH transcription factors in the control of cellular plasticity

Author

Huyghe, A., primary, Furlan, G., additional, Schroeder, J., additional, Stüder, J., additional, Mugnier, F., additional, De Matteo, L., additional, Wang, J., additional, Yu, Y., additional, Rama, N., additional, Gibert, B., additional, Wajda, P., additional, Goddard, I., additional, Gadot, N., additional, Brevet, M., additional, Siouda, M., additional, Mulligan, P., additional, Dante, R., additional, Liu, P., additional, Gronemeyer, H., additional, Mendoza-Parra, M., additional, Polo, J., additional, and Lavial, F., additional

Published
2020
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16. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Author

Galluzzi, L, Vitale, I, Aaronson, SA, Abrams, JM, Adam, D, Agostinis, P, Alnemri, ES, Altucci, L, Amelio, I, Andrews, DW, Annicchiarico-Petruzzelli, M, Antonov, AV, Arama, E, Baehrecke, EH, Barlev, NA, Bazan, NG, Bernassola, F, Bertrand, MJM, Bianchi, K, Blagosklonny, MV, Blomgren, K, Borner, C, Boya, P, Brenner, C, Campanella, M, Candi, E, Carmona-Gutierrez, D, Cecconi, F, Chan, FK-M, Chandel, NS, Cheng, EH, Chipuk, JE, Cidlowski, JA, Ciechanover, A, Cohen, GM, Conrad, M, Cubillos-Ruiz, JR, Czabotar, PE, D'Angiolella, V, Dawson, TM, Dawson, VL, De laurenzi, V, De Maria, R, Debatin, K-M, DeBerardinis, RJ, Deshmukh, M, Di Daniele, N, Di Virgilio, F, Dixit, VM, Dixon, SJ, Duckett, CS, Dynlacht, BD, El-Deiry, WS, Elrod, JW, Fimia, GM, Fulda, S, Garcia-Saez, AJ, Garg, AD, Garrido, C, Gavathiotis, E, Golstein, P, Gottlieb, E, Green, DR, Greene, LA, Gronemeyer, H, Gross, A, Hajnoczky, G, Hardwick, JM, Harris, IS, Hengartner, MO, Hetz, C, Ichijo, H, Jaattela, M, Joseph, B, Jost, PJ, Juin, PP, Kaiser, WJ, Karin, M, Kaufmann, T, Kepp, O, Kimchi, A, Kitsis, RN, Klionsky, DJ, Knight, RA, Kumar, S, Lee, SW, Lemasters, JJ, Levine, B, Linkermann, A, Lipton, SA, Lockshin, RA, Lopez-Otin, C, Lowe, SW, Luedde, T, Lugli, E, MacFarlane, M, Madeo, F, Malewicz, M, Malorni, W, Manic, G, Marine, J-C, Martin, SJ, Martinou, J-C, Medema, JP, Mehlen, P, Meier, P, Melino, S, Miao, EA, Molkentin, JD, Moll, UM, Munoz-Pinedo, C, Nagata, S, Nunez, G, Oberst, A, Oren, M, Overholtzer, M, Pagano, M, Panaretakis, T, Pasparakis, M, Penninger, JM, Pereira, DM, Pervaiz, S, Peter, ME, Piacentini, M, Pinton, P, Prehn, JHM, Puthalakath, H, Rabinovich, GA, Rehm, M, Rizzuto, R, Rodrigues, CMP, Rubinsztein, DC, Rudel, T, Ryan, KM, Sayan, E, Scorrano, L, Shao, F, Shi, Y, Silke, J, Simon, H-U, Sistigu, A, Stockwell, BR, Strasser, A, Szabadkai, G, Tait, SWG, Tang, D, Tavernarakis, N, Thorburn, A, Tsujimoto, Y, Turk, B, Vanden Berghe, T, Vandenabeele, P, Heiden, MGV, Villunger, A, Virgin, HW, Vousden, KH, Vucic, D, Wagner, EF, Walczak, H, Wallach, D, Wang, Y, Wells, JA, Wood, W, Yuan, J, Zakeri, Z, Zhivotovsky, B, Zitvogel, L, Melino, G, Kroemer, G, Galluzzi, L, Vitale, I, Aaronson, SA, Abrams, JM, Adam, D, Agostinis, P, Alnemri, ES, Altucci, L, Amelio, I, Andrews, DW, Annicchiarico-Petruzzelli, M, Antonov, AV, Arama, E, Baehrecke, EH, Barlev, NA, Bazan, NG, Bernassola, F, Bertrand, MJM, Bianchi, K, Blagosklonny, MV, Blomgren, K, Borner, C, Boya, P, Brenner, C, Campanella, M, Candi, E, Carmona-Gutierrez, D, Cecconi, F, Chan, FK-M, Chandel, NS, Cheng, EH, Chipuk, JE, Cidlowski, JA, Ciechanover, A, Cohen, GM, Conrad, M, Cubillos-Ruiz, JR, Czabotar, PE, D'Angiolella, V, Dawson, TM, Dawson, VL, De laurenzi, V, De Maria, R, Debatin, K-M, DeBerardinis, RJ, Deshmukh, M, Di Daniele, N, Di Virgilio, F, Dixit, VM, Dixon, SJ, Duckett, CS, Dynlacht, BD, El-Deiry, WS, Elrod, JW, Fimia, GM, Fulda, S, Garcia-Saez, AJ, Garg, AD, Garrido, C, Gavathiotis, E, Golstein, P, Gottlieb, E, Green, DR, Greene, LA, Gronemeyer, H, Gross, A, Hajnoczky, G, Hardwick, JM, Harris, IS, Hengartner, MO, Hetz, C, Ichijo, H, Jaattela, M, Joseph, B, Jost, PJ, Juin, PP, Kaiser, WJ, Karin, M, Kaufmann, T, Kepp, O, Kimchi, A, Kitsis, RN, Klionsky, DJ, Knight, RA, Kumar, S, Lee, SW, Lemasters, JJ, Levine, B, Linkermann, A, Lipton, SA, Lockshin, RA, Lopez-Otin, C, Lowe, SW, Luedde, T, Lugli, E, MacFarlane, M, Madeo, F, Malewicz, M, Malorni, W, Manic, G, Marine, J-C, Martin, SJ, Martinou, J-C, Medema, JP, Mehlen, P, Meier, P, Melino, S, Miao, EA, Molkentin, JD, Moll, UM, Munoz-Pinedo, C, Nagata, S, Nunez, G, Oberst, A, Oren, M, Overholtzer, M, Pagano, M, Panaretakis, T, Pasparakis, M, Penninger, JM, Pereira, DM, Pervaiz, S, Peter, ME, Piacentini, M, Pinton, P, Prehn, JHM, Puthalakath, H, Rabinovich, GA, Rehm, M, Rizzuto, R, Rodrigues, CMP, Rubinsztein, DC, Rudel, T, Ryan, KM, Sayan, E, Scorrano, L, Shao, F, Shi, Y, Silke, J, Simon, H-U, Sistigu, A, Stockwell, BR, Strasser, A, Szabadkai, G, Tait, SWG, Tang, D, Tavernarakis, N, Thorburn, A, Tsujimoto, Y, Turk, B, Vanden Berghe, T, Vandenabeele, P, Heiden, MGV, Villunger, A, Virgin, HW, Vousden, KH, Vucic, D, Wagner, EF, Walczak, H, Wallach, D, Wang, Y, Wells, JA, Wood, W, Yuan, J, Zakeri, Z, Zhivotovsky, B, Zitvogel, L, Melino, G, and Kroemer, G

Abstract

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

Published
2018

19. HDACs class II selective inhibition alters nuclear receptor dependent differentiation

Author

NEBBIOSO, Angela, DELL'AVERSANA C, BUGGE AK, SARNO R, VALENTE S, ROTILI D, MANZO F, TETI D, MANDRUP S, CIANA P, MAGGI AC, MAI A, GRONEMEYER H, ALTUCCI, Lucia, Nebbioso, Angela, Dell'Aversana, C, Bugge, Ak, Sarno, R, Valente, S, Rotili, D, Manzo, F, Teti, D, Mandrup, S, Ciana, P, Maggi, Ac, Mai, A, Gronemeyer, H, and Altucci, Lucia

Subjects
Differentiation, Epigenetic, HDACs
Abstract

Epigenetic deregulation contributes to diseases including cancer, neurodegeneration, osteodystrophy, cardiovascular defects, and obesity. For this reason, several inhibitors for histone deacetylases (HDACs) are being validated as novel anti-cancer drugs in clinical studies and display important anti-proliferative activities. While most inhibitors act on both class I, II, and IV HDACs, evidence is accumulating that class I is directly involved in regulation of cell growth and death, whereas class II members regulate differentiation processes, such as muscle and neuronal differentiation. Here, we show that the novel class II-selective inhibitor MC1568 interferes with the RAR- and peroxisome proliferator-activated receptor γ (PPARγ)-mediated differentiation-inducing signaling pathways. In F9 cells, this inhibitor specifically blocks endodermal differentiation despite not affecting retinoic acid-induced maturation of promyelocytic NB4 cells. In 3T3-L1 cells, MC1568 attenuates PPARγ-induced adipogenesis, while the class I-selective MS275 blocked adipogenesis completely thus revealing a different mode of action and/or target profile of the two classes of HDACs. Using in vivo reporting PPRE-Luc mice, we find that MC1568 impairs PPARγ signaling mostly in the heart and adipose tissues. These results illustrate how HDAC functions can be dissected by selective inhibitors.

Published
2010

23. Retinoids & TRAIL

Author

ALTUCCI, Lucia, GRONEMEYER H., LITWACK G., Altucci, Lucia, and Gronemeyer, H.

Published
2004

31. Essential versus accessory aspects of cell death: Recommendations of the NCCD 2015

Author

Galluzzi, L., Bravo-San Pedro, J. M., Vitale, Ilio, Aaronson, S. A., Abrams, J. M., Adam, D., Alnemri, E. S., Altucci, L., Andrews, D., Annicchiarico-Petruzzelli, M., Baehrecke, E. H., Bazan, N. G., Bertrand, M. J., Bianchi, K., Blagosklonny, M. V., Blomgren, K., Borner, C., Bredesen, D. E., Brenner, C., Campanella, M., Candi, E., Cecconi, F., Chan, F. K., Chandel, N. S., Cheng, E. H., Chipuk, J. E., Cidlowski, J. A., Ciechanover, A., Dawson, T. M., Dawson, V. L., De Laurenzi, V., De Maria Marchiano, Ruggero, Debatin, K. -M., Di Daniele, N., Dixit, V. M., Dynlacht, B. D., El-Deiry, W. S., Fimia, G. M., Flavell, R. A., Fulda, S., Garrido, C., Gougeon, M. -L., Green, D. R., Gronemeyer, H., Hajnoczky, G., Hardwick, J. M., Hengartner, M. O., Ichijo, H., Joseph, B., Jost, P. J., Kaufmann, T., Kepp, O., Klionsky, D. J., Knight, R. A., Kumar, S., Lemasters, J. J., Levine, B., Linkermann, A., Lipton, S. A., Lockshin, R. A., López-Otín, C., Lugli, E., Madeo, F., Malorni, W., Marine, J. -C., Martin, S. J., Martinou, J. -C., Medema, Jan Paul, Meier, P., Melino, S., Mizushima, N., Moll, U., Muñoz-Pinedo, C., Nuñez, G., Oberst, A., Panaretakis, T., Penninger, J. M., Peter, M. E., Piacentini, M., Calzavara Pinton, Piergiacomo, Prehn, J. H., Puthalakath, H., Rabinovich, G. A., Ravichandran, K. S., Rizzuto, R., Rodrigues, C. M., Rubinsztein, D. C., Rudel, T., Shi, Y., Simon, H. -U., Stockwell, B. R., Szabadkai, G., Tait, S. W., Tang, H. L., Tavernarakis, N., Tsujimoto, Y., Vanden Berghe, T., Vandenabeele, P., Villunger, A., Wagner, E. F., Walczak, H., White, E., Wood, W. G., Yuan, J., Zakeri, Z., Zhivotovsky, B., Melino, G., Kroemer, G., Vitale, I., De Maria Marchiano, R. (ORCID:0000-0003-2255-0583), Medema, J. P., Calzavara Pinton, P., Galluzzi, L., Bravo-San Pedro, J. M., Vitale, Ilio, Aaronson, S. A., Abrams, J. M., Adam, D., Alnemri, E. S., Altucci, L., Andrews, D., Annicchiarico-Petruzzelli, M., Baehrecke, E. H., Bazan, N. G., Bertrand, M. J., Bianchi, K., Blagosklonny, M. V., Blomgren, K., Borner, C., Bredesen, D. E., Brenner, C., Campanella, M., Candi, E., Cecconi, F., Chan, F. K., Chandel, N. S., Cheng, E. H., Chipuk, J. E., Cidlowski, J. A., Ciechanover, A., Dawson, T. M., Dawson, V. L., De Laurenzi, V., De Maria Marchiano, Ruggero, Debatin, K. -M., Di Daniele, N., Dixit, V. M., Dynlacht, B. D., El-Deiry, W. S., Fimia, G. M., Flavell, R. A., Fulda, S., Garrido, C., Gougeon, M. -L., Green, D. R., Gronemeyer, H., Hajnoczky, G., Hardwick, J. M., Hengartner, M. O., Ichijo, H., Joseph, B., Jost, P. J., Kaufmann, T., Kepp, O., Klionsky, D. J., Knight, R. A., Kumar, S., Lemasters, J. J., Levine, B., Linkermann, A., Lipton, S. A., Lockshin, R. A., López-Otín, C., Lugli, E., Madeo, F., Malorni, W., Marine, J. -C., Martin, S. J., Martinou, J. -C., Medema, Jan Paul, Meier, P., Melino, S., Mizushima, N., Moll, U., Muñoz-Pinedo, C., Nuñez, G., Oberst, A., Panaretakis, T., Penninger, J. M., Peter, M. E., Piacentini, M., Calzavara Pinton, Piergiacomo, Prehn, J. H., Puthalakath, H., Rabinovich, G. A., Ravichandran, K. S., Rizzuto, R., Rodrigues, C. M., Rubinsztein, D. C., Rudel, T., Shi, Y., Simon, H. -U., Stockwell, B. R., Szabadkai, G., Tait, S. W., Tang, H. L., Tavernarakis, N., Tsujimoto, Y., Vanden Berghe, T., Vandenabeele, P., Villunger, A., Wagner, E. F., Walczak, H., White, E., Wood, W. G., Yuan, J., Zakeri, Z., Zhivotovsky, B., Melino, G., Kroemer, G., Vitale, I., De Maria Marchiano, R. (ORCID:0000-0003-2255-0583), Medema, J. P., and Calzavara Pinton, P.

Abstract

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as 'accidental cell death' (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. 'Regulated cell death' (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.

Published
2015

34. Rexinoid-triggered differentiation and tumor-selective apoptosis of AML by protein kinase A-mediated de-subordination of RXR

Author

Altucci, L., Rossin, A., Hirsch, O., Nebbioso, A., Vitoux, D., Wilhelm, E., Guidez, F., Simone M., De, E.M., Schiavone, Grimwade, D., Zelent, A., de Thé, H., Gronemeyer, H., Pathologie et virologie moléculaire (PVM (UMR_7151)), and Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Published
2005

35. Plasminogen activator urokinase expression reveals TRAIL responsiveness and supports fractional survival of cancer cells

Author

University of Helsinki, Institute for Molecular Medicine Finland (FIMM), Pavet, V., Shlyakhtina, Y., He, T., Ceschin, D. G., Kohonen, P., Perala, M., Kallioniemi, O., Gronemeyer, H., University of Helsinki, Institute for Molecular Medicine Finland (FIMM), Pavet, V., Shlyakhtina, Y., He, T., Ceschin, D. G., Kohonen, P., Perala, M., Kallioniemi, O., and Gronemeyer, H.

Published
2014

36. Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Author

Galluzzi, L, Bravo-San Pedro, Jm, Vitale, I, Aaronson, Sa, Abrams, Jm, Adam, D, Alnemri, E, Altucci, L, Andrews, D, Annicchiarico-Petruzzelli, M, Baehrecke, Eh, Bazan, Ng, Bertrand, Mj, Bianchi, K, Blagosklonny, Mv, Blomgren, K, Borner, C, Bredesen, De, Brenner, C, Campanella, M, Candi, E, Cecconi, F, Chan, Fk, Chandel, N, Cheng, Eh, Chipuk, Je, Cidlowski, Ja, Ciechanover, A, Dawson, Tm, Dawson, Vl, De Laurenzi, V, De Maria Marchiano, Ruggero, Debatin, Km, Di Daniele, N, Dixit, Vm, Dynlacht, Bd, El-Deiry, W, Fimia, Gm, Flavell, Ra, Fulda, S, Garrido, C, Gougeon, Ml, Green, Dr, Gronemeyer, H, Hajnoczky, G, Hardwick, Jm, Hengartner, Mo, Ichijo, H, Joseph, B, Jost, Pj, Kaufmann, T, Kepp, O, Klionsky, Dj, Knight, Ra, Kumar, S, Lemasters, Jj, Levine, B, Linkermann, A, Lipton, Sa, Lockshin, Ra, López-Otín, C, Lugli, E, Madeo, F, Malorni, W, Marine, Jc, Martin, Sj, Martinou, Jc, Medema, Jan Paul, Meier, P, Melino, S, Mizushima, N, Moll, U, Muñoz-Pinedo, C, Nuñez, G, Oberst, A, Panaretakis, T, Penninger, Jm, Peter, Me, Piacentini, M, Calzavara Pinton, Piergiacomo, Prehn, Jh, Puthalakath, H, Rabinovich, Ga, Ravichandran, K, Rizzuto, R, Rodrigues, Cm, Rubinsztein, Dc, Rudel, T, Shi, Y, Simon, Hu, Stockwell, Br, Szabadkai, G, Tait, Sw, Tang, Hl, Tavernarakis, N, Tsujimoto, Y, Vanden Berghe, T, Vandenabeele, P, Villunger, A, Wagner, Ef, Walczak, H, White, E, Wood, Wg, Yuan, J, Zakeri, Z, Zhivotovsky, B, Melino, G, Kroemer, G., De Maria Marchiano R (ORCID:0000-0003-2255-0583), Medema JP, Calzavara Pinton P, Galluzzi, L, Bravo-San Pedro, Jm, Vitale, I, Aaronson, Sa, Abrams, Jm, Adam, D, Alnemri, E, Altucci, L, Andrews, D, Annicchiarico-Petruzzelli, M, Baehrecke, Eh, Bazan, Ng, Bertrand, Mj, Bianchi, K, Blagosklonny, Mv, Blomgren, K, Borner, C, Bredesen, De, Brenner, C, Campanella, M, Candi, E, Cecconi, F, Chan, Fk, Chandel, N, Cheng, Eh, Chipuk, Je, Cidlowski, Ja, Ciechanover, A, Dawson, Tm, Dawson, Vl, De Laurenzi, V, De Maria Marchiano, Ruggero, Debatin, Km, Di Daniele, N, Dixit, Vm, Dynlacht, Bd, El-Deiry, W, Fimia, Gm, Flavell, Ra, Fulda, S, Garrido, C, Gougeon, Ml, Green, Dr, Gronemeyer, H, Hajnoczky, G, Hardwick, Jm, Hengartner, Mo, Ichijo, H, Joseph, B, Jost, Pj, Kaufmann, T, Kepp, O, Klionsky, Dj, Knight, Ra, Kumar, S, Lemasters, Jj, Levine, B, Linkermann, A, Lipton, Sa, Lockshin, Ra, López-Otín, C, Lugli, E, Madeo, F, Malorni, W, Marine, Jc, Martin, Sj, Martinou, Jc, Medema, Jan Paul, Meier, P, Melino, S, Mizushima, N, Moll, U, Muñoz-Pinedo, C, Nuñez, G, Oberst, A, Panaretakis, T, Penninger, Jm, Peter, Me, Piacentini, M, Calzavara Pinton, Piergiacomo, Prehn, Jh, Puthalakath, H, Rabinovich, Ga, Ravichandran, K, Rizzuto, R, Rodrigues, Cm, Rubinsztein, Dc, Rudel, T, Shi, Y, Simon, Hu, Stockwell, Br, Szabadkai, G, Tait, Sw, Tang, Hl, Tavernarakis, N, Tsujimoto, Y, Vanden Berghe, T, Vandenabeele, P, Villunger, A, Wagner, Ef, Walczak, H, White, E, Wood, Wg, Yuan, J, Zakeri, Z, Zhivotovsky, B, Melino, G, Kroemer, G., De Maria Marchiano R (ORCID:0000-0003-2255-0583), Medema JP, and Calzavara Pinton P

Abstract

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as 'accidental cell death' (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. 'Regulated cell death' (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.

Published
2014

38. Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Author

Galluzzi, L, primary, Bravo-San Pedro, J M, additional, Vitale, I, additional, Aaronson, S A, additional, Abrams, J M, additional, Adam, D, additional, Alnemri, E S, additional, Altucci, L, additional, Andrews, D, additional, Annicchiarico-Petruzzelli, M, additional, Baehrecke, E H, additional, Bazan, N G, additional, Bertrand, M J, additional, Bianchi, K, additional, Blagosklonny, M V, additional, Blomgren, K, additional, Borner, C, additional, Bredesen, D E, additional, Brenner, C, additional, Campanella, M, additional, Candi, E, additional, Cecconi, F, additional, Chan, F K, additional, Chandel, N S, additional, Cheng, E H, additional, Chipuk, J E, additional, Cidlowski, J A, additional, Ciechanover, A, additional, Dawson, T M, additional, Dawson, V L, additional, De Laurenzi, V, additional, De Maria, R, additional, Debatin, K-M, additional, Di Daniele, N, additional, Dixit, V M, additional, Dynlacht, B D, additional, El-Deiry, W S, additional, Fimia, G M, additional, Flavell, R A, additional, Fulda, S, additional, Garrido, C, additional, Gougeon, M-L, additional, Green, D R, additional, Gronemeyer, H, additional, Hajnoczky, G, additional, Hardwick, J M, additional, Hengartner, M O, additional, Ichijo, H, additional, Joseph, B, additional, Jost, P J, additional, Kaufmann, T, additional, Kepp, O, additional, Klionsky, D J, additional, Knight, R A, additional, Kumar, S, additional, Lemasters, J J, additional, Levine, B, additional, Linkermann, A, additional, Lipton, S A, additional, Lockshin, R A, additional, López-Otín, C, additional, Lugli, E, additional, Madeo, F, additional, Malorni, W, additional, Marine, J-C, additional, Martin, S J, additional, Martinou, J-C, additional, Medema, J P, additional, Meier, P, additional, Melino, S, additional, Mizushima, N, additional, Moll, U, additional, Muñoz-Pinedo, C, additional, Nuñez, G, additional, Oberst, A, additional, Panaretakis, T, additional, Penninger, J M, additional, Peter, M E, additional, Piacentini, M, additional, Pinton, P, additional, Prehn, J H, additional, Puthalakath, H, additional, Rabinovich, G A, additional, Ravichandran, K S, additional, Rizzuto, R, additional, Rodrigues, C M, additional, Rubinsztein, D C, additional, Rudel, T, additional, Shi, Y, additional, Simon, H-U, additional, Stockwell, B R, additional, Szabadkai, G, additional, Tait, S W, additional, Tang, H L, additional, Tavernarakis, N, additional, Tsujimoto, Y, additional, Vanden Berghe, T, additional, Vandenabeele, P, additional, Villunger, A, additional, Wagner, E F, additional, Walczak, H, additional, White, E, additional, Wood, W G, additional, Yuan, J, additional, Zakeri, Z, additional, Zhivotovsky, B, additional, Melino, G, additional, and Kroemer, G, additional

Published
2014
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40. Indole-Derived Psammaplin A Analogues as Epigenetic Modulators with Multiple Inhibitory Activities

Author

Pereira, R., Benedetti, R., Pérez-Rodríguez, S., Nebbioso, A., García-Rodríguez, J., Carafa, V., Stuhldreier, M., Conte, M., Rodríguez-Barrios, F., Stunnenberg, H.G., Gronemeyer, H., Altucci, L., Lera, Á.R. de, Pereira, R., Benedetti, R., Pérez-Rodríguez, S., Nebbioso, A., García-Rodríguez, J., Carafa, V., Stuhldreier, M., Conte, M., Rodríguez-Barrios, F., Stunnenberg, H.G., Gronemeyer, H., Altucci, L., and Lera, Á.R. de

Abstract

Item does not contain fulltext

Published
2012

41. Death receptor pathway activation and increase of ROS production by the triple epigenetic inhibitor, UVI5008

Author

Nebbioso, A., Pereira, R., Khanwalkar, H., Matarese, F., Garcia-Rodriguez, J., Miceli, M., Logie, C., Kedinger, V., Ferrara, F., Stunnenberg, H.G., Lera, A.R. de, Gronemeyer, H., Altucci, L., Nebbioso, A., Pereira, R., Khanwalkar, H., Matarese, F., Garcia-Rodriguez, J., Miceli, M., Logie, C., Kedinger, V., Ferrara, F., Stunnenberg, H.G., Lera, A.R. de, Gronemeyer, H., and Altucci, L.

Abstract

Item does not contain fulltext

Published
2011

42. Multivalent DR5 peptides activate the TRAIL death pathway and exert tumoricidal activity.

Author

Pavet, V., Beyrath, J.D., Pardin, C., Morizot, A., Lechner, M.C., Briand, J.P., Wendland, M., Maison, W., Fournel, S., Micheau, O., Guichard, G., Gronemeyer, H., Pavet, V., Beyrath, J.D., Pardin, C., Morizot, A., Lechner, M.C., Briand, J.P., Wendland, M., Maison, W., Fournel, S., Micheau, O., Guichard, G., and Gronemeyer, H.

Abstract

Item does not contain fulltext, Ongoing clinical trials are exploring anticancer approaches based on signaling by TRAIL, a ligand for the cell death receptors DR4 and DR5. In this study, we report on the selective apoptotic effects of multivalent DR5 binding peptides (TRAIL(mim/DR5)) on cancer cells in vitro and in vivo. Surface plasmon resonance revealed up to several thousand-fold increased affinities of TRAIL(mim/DR5)-receptor complexes on generation of divalent and trivalent molecules, the latter of which was achieved with a conformationally restricted adamantane core. Notably, only multivalent molecules triggered a substantial DR5-dependent apoptotic response in vitro. In tumor models derived from human embryonic kidney cells or primary foreskin fibroblasts, TRAIL(mim/DR5) peptides exerted a cancer cell-selective action that could synergize with resveratrol in a manner independent of p53. In a xenograft model of human colon cancer, a divalent TRAIL(mim/DR5) peptide inhibited tumor growth. Our results offer a proof-of-principle for the development of synthetic small molecules to trigger the TRAIL apoptosis pathway for cancer therapy.

Published
2010

43. Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes

Author

Galluzzi, L., Aaronson, S. A., Abrams, J., Alnemri, E. S., Andrews, D. W., Baehrecke, E. H., Bazan, N. G., Blagosklonny, M. V., Blomgren, K., Borner, C., Bredesen, D. E., Brenner, C., Castedo, M., Cidlowski, J. A., Ciechanover, A., Cohen, G. M., De Laurenzi, V., De Maria Marchiano, Ruggero, Deshmukh, M., Dynlacht, B. D., El-Deiry, W. S., Flavell, R. A., Fulda, S., Garrido, C., Golstein, P., Gougeon, M. -L., Green, D. R., Gronemeyer, H., Hajnóczky, G., Hardwick, J. M., Hengartner, M. O., Ichijo, H., Jäättelä, M., Kepp, O., Kimchi, A., Klionsky, D. J., Knight, R. A., Kornbluth, S., Kumar, S., Levine, B., Lipton, S. A., Lugli, E., Madeo, F., Malorni, W., Marine, J. -C. W., Martin, S. J., Medema, Jan Paul, Mehlen, P., Melino, G., Moll, U. M., Morselli, E., Nagata, S., Nicholson, D. W., Nicotera, P., Nuñez, G., Oren, M., Penninger, J., Pervaiz, S., Peter, M. E., Piacentini, M., Prehn, J. H. M., Puthalakath, H., Rabinovich, G. A., Rizzuto, R., Rodrigues, C. M. P., Rubinsztein, D. C., Rudel, T., Scorrano, L., Simon, H. -U., Steller, H., Tschopp, J., Tsujimoto, Y., Vandenabeele, P., Vitale, Ilio, Vousden, K. H., Youle, R. J., Yuan, J., Zhivotovsky, B., Kroemer, G., De Maria Marchiano, R. (ORCID:0000-0003-2255-0583), Medema, J. P., Vitale, I., Galluzzi, L., Aaronson, S. A., Abrams, J., Alnemri, E. S., Andrews, D. W., Baehrecke, E. H., Bazan, N. G., Blagosklonny, M. V., Blomgren, K., Borner, C., Bredesen, D. E., Brenner, C., Castedo, M., Cidlowski, J. A., Ciechanover, A., Cohen, G. M., De Laurenzi, V., De Maria Marchiano, Ruggero, Deshmukh, M., Dynlacht, B. D., El-Deiry, W. S., Flavell, R. A., Fulda, S., Garrido, C., Golstein, P., Gougeon, M. -L., Green, D. R., Gronemeyer, H., Hajnóczky, G., Hardwick, J. M., Hengartner, M. O., Ichijo, H., Jäättelä, M., Kepp, O., Kimchi, A., Klionsky, D. J., Knight, R. A., Kornbluth, S., Kumar, S., Levine, B., Lipton, S. A., Lugli, E., Madeo, F., Malorni, W., Marine, J. -C. W., Martin, S. J., Medema, Jan Paul, Mehlen, P., Melino, G., Moll, U. M., Morselli, E., Nagata, S., Nicholson, D. W., Nicotera, P., Nuñez, G., Oren, M., Penninger, J., Pervaiz, S., Peter, M. E., Piacentini, M., Prehn, J. H. M., Puthalakath, H., Rabinovich, G. A., Rizzuto, R., Rodrigues, C. M. P., Rubinsztein, D. C., Rudel, T., Scorrano, L., Simon, H. -U., Steller, H., Tschopp, J., Tsujimoto, Y., Vandenabeele, P., Vitale, Ilio, Vousden, K. H., Youle, R. J., Yuan, J., Zhivotovsky, B., Kroemer, G., De Maria Marchiano, R. (ORCID:0000-0003-2255-0583), Medema, J. P., and Vitale, I.

Abstract

Cell death is essential for a plethora of physiological processes, and its deregulation characterizes numerous human diseases. Thus, the in-depth investigation of cell death and its mechanisms constitutes a formidable challenge for fundamental and applied biomedical research, and has tremendous implications for the development of novel therapeutic strategies. It is, therefore, of utmost importance to standardize the experimental procedures that identify dying and dead cells in cell cultures and/or in tissues, from model organisms and/or humans, in healthy and/or pathological scenarios. Thus far, dozens of methods have been proposed to quantify cell death-related parameters. However, no guidelines exist regarding their use and interpretation, and nobody has thoroughly annotated the experimental settings for which each of these techniques is most appropriate. Here, we provide a nonexhaustive comparison of methods to detect cell death with apoptotic or nonapoptotic morphologies, their advantages and pitfalls. These guidelines are intended for investigators who study cell death, as well as for reviewers who need to constructively critique scientific reports that deal with cellular demise. Given the difficulties in determining the exact number of cells that have passed the point-of-no-return of the signaling cascades leading to cell death, we emphasize the importance of performing multiple, methodologically unrelated assays to quantify dying and dead cells.

Published
2009

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