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See detailHDAC5 Depletion in Cancer Cells Induces an Oxidative Stress and Leads to a Metabolic Reprogramming toward Glucose and Glutamine Metabolism
Hendrick, Elodie ULiege; Peixoto, Paul ULiege; Polese, Catherine ULiege et al

Poster (2015, January 31)

Histone deacetylases (HDAC) is a family of eighteen enzymes, which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad-spectrum ... [more ▼]

Histone deacetylases (HDAC) is a family of eighteen enzymes, which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad-spectrum inhibitors of these enzymes such as SAHA can inhibit tumor growth both in vitro and in vivo and are currently used as anti-cancer agents in clinic. For many years, we are investigating the specific role of individual HDAC members in cancer biology and we have recently demonstrated that specific depletion of HDAC5 using siRNA technology reduced cancer cells proliferation and survival1 The goal of this study is to further understand the molecular mechanisms of action of HDAC5 in cancer cells. Screening transcriptomic study demonstrated that HDAC5 depletion induces a down-regulation of subunits of the complex I of the mitochondrial respiratory chain (NDUFB5-NDUFA3) as well as anti-oxydant proteins (Ferritin, Metalothionein,¿) through modulation of mRNA stability. Therefore, HDAC5 depletion causes a significant increase of ROS production inducing both apoptosis and mechanisms of mitochondria quality control (mitophagy and mitobiogenesis). This HDAC5 depletion-induced mitochondrial dysfunction provokes metabolic adaptation associated with increased importance of glucose and glutamine. Indeed, interference with both glucose and glutamine supply in HDAC5-depleted cancer cells significantly increases apoptotic cell death suggesting that glucose or glutamine deprivation might be combined to HDAC5 inhibition as a therapeutic strategy to kill cancer cells. Our study demonstrated for the first time that specific HDAC5 inhibition induces metabolic reprogramming and provides insight into a valuable experimental strategy for manipulation of specific HDAC5 inhibition and glucose metabolism in therapy against cancer. 1.Peixoto, P. et al. HDAC5 is required for maintenance of pericentric heterochromatin, and controls cell-cycle progression and survival of human cancer cells. Cell death and differentiation, 2012; 1-14. Presenting author e-mail: elodie.hendrick@student.ulg.ac.be [less ▲]

Detailed reference viewed: 40 (2 ULiège)
See detailHDAC5 Depletion in Cancer Cells Induces an Oxidative Stress and Leads to a Metabolic Reprogramming toward Glucose and Glutamine Metabolism
Hendrick, Elodie ULiege; Peixoto, Paul ULiege; Polese, Catherine ULiege et al

Poster (2015, January 27)

Histone deacetylases (HDAC) is a family of eighteen enzymes, which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad-spectrum ... [more ▼]

Histone deacetylases (HDAC) is a family of eighteen enzymes, which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad-spectrum inhibitors of these enzymes such as SAHA can inhibit tumor growth both in vitro and in vivo and are currently used as anti-cancer agents in clinic. For many years, we are investigating the specific role of individual HDAC members in cancer biology and we have recently demonstrated that specific depletion of HDAC5 using siRNA technology reduced cancer cells proliferation and survival1 The goal of this study is to further understand the molecular mechanisms of action of HDAC5 in cancer cells. Screening transcriptomic study demonstrated that HDAC5 depletion induces a down-regulation of subunits of the complex I of the mitochondrial respiratory chain (NDUFB5-NDUFA3) as well as anti-oxydant proteins (Ferritin, Metalothionein,¿) through modulation of mRNA stability. Therefore, HDAC5 depletion causes a significant increase of ROS production inducing both apoptosis and mechanisms of mitochondria quality control (mitophagy and mitobiogenesis). This HDAC5 depletion-induced mitochondrial dysfunction provokes metabolic adaptation associated with increased importance of glucose and glutamine. Indeed, interference with both glucose and glutamine supply in HDAC5-depleted cancer cells significantly increases apoptotic cell death suggesting that glucose or glutamine deprivation might be combined to HDAC5 inhibition as a therapeutic strategy to kill cancer cells. Our study demonstrated for the first time that specific HDAC5 inhibition induces metabolic reprogramming and provides insight into a valuable experimental strategy for manipulation of specific HDAC5 inhibition and glucose metabolism in therapy against cancer. 1.Peixoto, P. et al. HDAC5 is required for maintenance of pericentric heterochromatin, and controls cell-cycle progression and survival of human cancer cells. Cell death and differentiation, 2012; 1-14. Presenting author e-mail: elodie.hendrick@student.ulg.ac.be [less ▲]

Detailed reference viewed: 19 (2 ULiège)
See detailHDAC5 Depletion in Cancer Cells Induces an Oxidative Stress and Leads to a Metabolic Reprogramming toward Glucose and Glutamine Metabolism
Hendrick, Elodie ULiege; Peixoto, Paul ULiege; Polese, Catherine ULiege et al

Conference (2014, September 30)

Histone deacetylases (HDAC) is a family of eighteen enzymes, which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad-spectrum ... [more ▼]

Histone deacetylases (HDAC) is a family of eighteen enzymes, which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad-spectrum inhibitors of these enzymes such as SAHA can inhibit tumor growth both in vitro and in vivo and are currently used as anti-cancer agents in clinic. For many years, we are investigating the specific role of individual HDAC members in cancer biology and we have recently demonstrated that specific depletion of HDAC5 using siRNA technology reduced cancer cells proliferation and survival1 The goal of this study is to further understand the molecular mechanisms of action of HDAC5 in cancer cells. Screening transcriptomic study demonstrated that HDAC5 depletion induces a down-regulation of subunits of the complex I of the mitochondrial respiratory chain (NDUFB5-NDUFA3) as well as anti-oxydant proteins (Ferritin, Metalothionein,¿) through modulation of mRNA stability. Therefore, HDAC5 depletion causes a significant increase of ROS production inducing both apoptosis and mechanisms of mitochondria quality control (mitophagy and mitobiogenesis). This HDAC5 depletion-induced mitochondrial dysfunction provokes metabolic adaptation associated with increased importance of glycolysis and glucose. Indeed, interference with glucose supply in HDAC5-depleted cancer cells significantly increases apoptotic cell death suggesting that glucose deprivation might be combined to HDAC5 inhibition as a therapeutic strategy to kill cancer cells. Our study demonstrated for the first time that specific HDAC5 inhibition induces metabolic reprogramming and provides insight into a valuable experimental strategy for manipulation of specific HDAC5 inhibition and glucose metabolism in therapy against cancer. 1.Peixoto, P. et al. HDAC5 is required for maintenance of pericentric heterochromatin, and controls cell-cycle progression and survival of human cancer cells. Cell death and differentiation, 2012; 1-14. Presenting author e-mail: elodie.hendrick@student.ulg.ac.be [less ▲]

Detailed reference viewed: 24 (0 ULiège)
See detailHDAC5 Depletion in Cancer Cells Induces an Oxidative Stress and Leads to a Metabolic Reprogramming toward Glucose and Glutamine Metabolism
Hendrick, Elodie ULiege; Peixoto, Paul ULiege; Polese, Catherine ULiege et al

Poster (2014, September 25)

Histone deacetylases (HDAC) is a family of eighteen enzymes, which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad-spectrum ... [more ▼]

Histone deacetylases (HDAC) is a family of eighteen enzymes, which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad-spectrum inhibitors of these enzymes such as SAHA can inhibit tumor growth both in vitro and in vivo and are currently used as anti-cancer agents in clinic. For many years, we are investigating the specific role of individual HDAC members in cancer biology and we have recently demonstrated that specific depletion of HDAC5 using siRNA technology reduced cancer cells proliferation and survival1 The goal of this study is to further understand the molecular mechanisms of action of HDAC5 in cancer cells. Screening transcriptomic study demonstrated that HDAC5 depletion induces a down-regulation of subunits of the complex I of the mitochondrial respiratory chain (NDUFB5-NDUFA3) as well as anti-oxydant proteins (Ferritin, Metalothionein,¿) through modulation of mRNA stability. Therefore, HDAC5 depletion causes a significant increase of ROS production inducing both apoptosis and mechanisms of mitochondria quality control (mitophagy and mitobiogenesis). This HDAC5 depletion-induced mitochondrial dysfunction provokes metabolic adaptation associated with increased importance of glycolysis and glucose. Indeed, interference with glucose supply in HDAC5-depleted cancer cells significantly increases apoptotic cell death suggesting that glucose deprivation might be combined to HDAC5 inhibition as a therapeutic strategy to kill cancer cells. Our study demonstrated for the first time that specific HDAC5 inhibition induces metabolic reprogramming and provides insight into a valuable experimental strategy for manipulation of specific HDAC5 inhibition and glucose metabolism in therapy against cancer. 1.Peixoto, P. et al. HDAC5 is required for maintenance of pericentric heterochromatin, and controls cell-cycle progression and survival of human cancer cells. Cell death and differentiation, 2012; 1-14. Presenting author e-mail: elodie.hendrick@student.ulg.ac.be [less ▲]

Detailed reference viewed: 27 (0 ULiège)
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See detailHDAC5 depletion modulates heterochromatin plasticity and triggers programmed cell death of human cancer cells
Peixoto, P; Castronovo, V; Matheus, N et al

Poster (2012)

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See detailHDAC5 is required for maintenance of pericentric heterochromatin, and controls cell-cycle progression and survival of human cancer cells
Peixoto, Paul ULiege; Castronovo, Vincenzo ULiege; Matheus, Nicolas ULiege et al

in Cell Death & Differentiation (2012)

Histone deacetylases (HDACs) form a family of enzymes, which have fundamental roles in the epigenetic regulation of gene expression and contribute to the growth, differentiation, and apoptosis of cancer ... [more ▼]

Histone deacetylases (HDACs) form a family of enzymes, which have fundamental roles in the epigenetic regulation of gene expression and contribute to the growth, differentiation, and apoptosis of cancer cells. In this study, we further investigated the biological function of HDAC5 in cancer cells. We found HDAC5 is associated with actively replicating pericentric heterochromatin during late S phase. We demonstrated that specific depletion of HDAC5 by RNA interference resulted in profound changes in the heterochromatin structure and slowed down ongoing replication forks. This defect in heterochromatin maintenance and assembly are sensed by DNA damage checkpoint pathways, which triggered cancer cells to autophagy and apoptosis, and arrested their growth both in vitro and in vivo. Finally, we also demonstrated that HDAC5 depletion led to enhanced sensitivity of DNA to DNA-damaging agents, suggesting that heterochromatin de-condensation induced by histone HDAC5 silencing may enhance the efficacy of cytotoxic agents that act by targeting DNA in vitro. Together, these results highlighted for the first time an unrecognized link between HDAC5 and the maintenance/assembly of heterochromatin structure, and demonstrated that its specific inhibition might contribute to increase the efficacy of DNA alteration-based cancer therapies in clinic. [less ▲]

Detailed reference viewed: 108 (45 ULiège)
See detailHDAC6 Inhibition compensates for the transport deficit in Huntington’s Disease by increasing tubulin acetylation
Godin, Juliette ULiege; Dompierre; Charrin, Bénédicte C. et al

Conference (2008, March)

Detailed reference viewed: 9 (1 ULiège)
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See detailHDAC7 inhibition resets STAT3 tumorigenic activity in human glioblastoma independently of EGFR and PTEN: new opportunities for selected targeted therapies
Peixoto, Paul; Blomme, Arnaud; Costanza, Brunella ULiege et al

in Oncogene (2016)

To date, the mutational status of EGFR and PTEN has been shown as relevant for favoring pro- or anti-tumor functions of STAT3 in human glioblastoma multiforme (GBM). We have screened genomic data from 154 ... [more ▼]

To date, the mutational status of EGFR and PTEN has been shown as relevant for favoring pro- or anti-tumor functions of STAT3 in human glioblastoma multiforme (GBM). We have screened genomic data from 154 patients and have identified a strong positive correlation between STAT3 and HDAC7 expression. In the current work we show the existence of a subpopulation of patients overexpressing HDAC7 and STAT3 that has particularly poor clinical outcome. Surprisingly, the somatic mutation rate of both STAT3 and HDAC7 was insignificant in GBM comparing with EGFR, PTEN or TP53. Depletion of HDAC7 in a range of GBM cells induced the expression of tyrosine kinase JAK1 and the tumor suppressor AKAP12. Both proteins synergistically sustained the activity of STAT3 by inducing its phosphorylation (JAK1) and protein expression (AKAP12). In absence of HDAC7, activated STAT3 was responsible for significant imbalance of secreted pro-/anti-angiogenic factors. This inhibited the migration and sprouting of endothelial cells in paracrine fashion in vitro as well as angiogenesis in vivo. In a murine model of GBM, induced HDAC7-silencing decreased the tumor burden by threefold. The current data show for the first time that silencing HDAC7 can reset the tumor suppressor activity of STAT3, independently of the EGFR/PTEN/TP53 background of the GBM. This effect could be exploited to overcome tumor heterogeneity and provide a new rationale behind the development of specific HDAC7 inhibitors for clinical use. [less ▲]

Detailed reference viewed: 55 (13 ULiège)
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See detailHDAC7, a thymus-specific class II histone deacetylase, regulates Nur77 transcription and TCR-mediated apoptosis.
Dequiedt, Franck ULiege; Kasler, Herbert; Fischle, Wolfgang et al

in Immunity (2003), 18(5), 687-98

We report that HDAC7, a class II histone deacetylase, is highly expressed in CD4(+)CD8(+) double-positive thymocytes. HDAC7 inhibits the expression of Nur77, an orphan receptor involved in apoptosis and ... [more ▼]

We report that HDAC7, a class II histone deacetylase, is highly expressed in CD4(+)CD8(+) double-positive thymocytes. HDAC7 inhibits the expression of Nur77, an orphan receptor involved in apoptosis and negative selection, via the transcription factor MEF2D. HDAC7 is exported from the nucleus during T cell receptor activation, leading to Nur77 expression. A triple HDAC7 mutant (S155A, S318A, S448A) is not exported from the nucleus in response to TCR activation and suppresses TCR-mediated apoptosis. Conversely, a fusion of HDAC7 to the transcriptional activator VP16 activates Nur77 expression. Inhibition of HDAC7 expression by RNA interference causes increased apoptosis in response to TCR activation. These observations define HDAC7 as a regulator of Nur77 and apoptosis in developing thymocytes. [less ▲]

Detailed reference viewed: 27 (8 ULiège)
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See detailHDAC8 is necessary for TGFß-induced myofibroblastic differenciation W. Glénisson, S.L. Tran, V. Castronovo, D. Waltregny
Glénisson, Wendy; Tran, Syv Li; Castronovo, Vincenzo ULiege et al

Conference (2004)

Detailed reference viewed: 19 (0 ULiège)
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See detailHDAC8 is required for myofibroblastic differentiation induced by TGFß
Glénisson, Wendy; Tran, Syv Li; Castronovo, Vincenzo ULiege et al

Conference (2004)

Detailed reference viewed: 14 (0 ULiège)
See detailHE 0435-1223 lensed QSO VRi light curves (Ricci+, 2011)
Ricci, Davide ULiege; Poels, Joël ULiege; Elyiv, Andrii ULiege et al

Textual, factual or bibliographical database (2011)

We present VRi photometric observations of the quadruply imaged quasar HE0435-1223, carried out with the Danish 1.54m telescope at the La Silla Observatory. Our aim was to monitor and study the magnitudes ... [more ▼]

We present VRi photometric observations of the quadruply imaged quasar HE0435-1223, carried out with the Danish 1.54m telescope at the La Silla Observatory. Our aim was to monitor and study the magnitudes and colors of each lensed component as a function of time. [less ▲]

Detailed reference viewed: 84 (29 ULiège)
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See detailHe and Si surface inhomogeneities of four Bp variable stars
Briquet, Maryline ULiege; Aerts, C.; Lüftinger, T. et al

in Astronomy and Astrophysics (2004), 413

We present ground-based multi-colour Geneva photometry and high-resolution spectra of four variable B-type stars: HD 105382, HD 131120, HD 138769 and HD 55522. All sets of data reveal monoperiodic stars ... [more ▼]

We present ground-based multi-colour Geneva photometry and high-resolution spectra of four variable B-type stars: HD 105382, HD 131120, HD 138769 and HD 55522. All sets of data reveal monoperiodic stars. A comparison of moment variations of two spectral lines, one silicon line and one helium line, allows us to exclude the pulsation model as being the cause of the observed variability of the four stars. We therefore delete the four stars from the list of candidate slowly pulsating B stars. We attribute the line-profile variations to non-homogeneous distributions of elements on the stellar surface and we derive abundance maps for both elements on the stellar surface by means of the Doppler Imaging technique. We confirm HD 131120 to be a He-weak star and we classify HD 105382, HD 138769 as new He-weak stars. HD 55522 has the solar helium abundance but the mean abundance value of He varies by 0.8 dex during the stellar rotation. For HD 131120 and HD 105382, helium is enhanced in regions of the stellar surface where silicon is depleted and depleted in regions where silicon is enhanced. Based on observations obtained with the Swiss photometric telescope and ESO's CAT/CES telescope, both situated at La Silla, Chile. Appendix A, Tables 1 and 2 and Figs. 9, 11, 13 are only available in electronic form at http://www.edpsciences.org [less ▲]

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See detailhe influence of transformational leadership on commitment: New underlying processes
Marique, Géraldine; Stinglhamber, Florence; Hanin, Dorothée et al

Poster (2012, April)

Detailed reference viewed: 115 (4 ULiège)
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See detailA He(I) Photoelectron Spectroscopic Study of the X2A"2state of NH3+ and ND3+. A Reanalysis and evidence for the Coriolis Coupling between the Bending nu2 and nu4 Modes.
Locht, Robert ULiege; Leyh, Bernard ULiege; Hottmann, K. et al

in Chemical Physics (1998), 233

In the He(I) photoelectron spectrum of NH3 and its isotopomer ND3 the complete vibrational structure of the X2A"2 state of NH3+ and ND3+ is examined in detail. Three vibrational progressions are ... [more ▼]

In the He(I) photoelectron spectrum of NH3 and its isotopomer ND3 the complete vibrational structure of the X2A"2 state of NH3+ and ND3+ is examined in detail. Three vibrational progressions are identified. The well-known strongest progression, already unambiguously assigned to the nu2 out-of-plane bending mode, is observed from v=0-17 in NH3+ and v=0-20 in ND3+. For NH3+ this vibration could be characterized not only by its energy hcomega2= 0.109+/-0.001 eV (or omega2= 878+/-7 cm-1) but also by its first anharmonicity constant hcomega22x22=-(16.2+/-1.2)10-4 eV (or omega22x22=-13.0+/-1.0 cm-1). The best fit of the experimental data required the introduction of a second anharmonicity constant, i.e. hcomega22y22= -(30.7+/-4.2)x10-6 eV (or omega22y22=-0.248+/-0.034 cm-1). The earlier reported weak progression assigned to the vibrational combination nu1+nnu2 transitions has been reexamined. Suitable handling of the data leads to two possible energies for the nu1 degenerate NH stretching vibrational normal mode, i.e. hcomega1 =0.306+/-0.006 eV or 0.422+/-0.005 eV. Several arguments are brought to favour the value of hcomega1=0.422 eV (or omega1=3404 cm-1). Finally a third weak progression, reported for the first time, is assigned to nu4+nnu2 transitions where the nu4 in-plane bending mode is optically forbidden. This vibrational normal mode is characterized by an energy hcomega4=0.186+/-0.010 eV (omega4=1500+/-80 cm-1). In agreement with the theoretical predictions, this transition becomes allowed through a strong Coriolis vibro-rotational coupling between the nu4 and the nu2 vibrational normal modes. The same measurements and the isotope effect on the molecular constants are investigated in ND3+ too. [less ▲]

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See detailThe He(I), Threshold photoelectron and Constant Ion State spectroscopy of Vinylchloride (C2H3Cl).
Locht, Robert ULiege; Leyh, Bernard ULiege; Hottmann, K. et al

in Chemical Physics (1997), 220

Using synchrotron radiation the threshold photoelectron (TPES) spectrum and constant ion state (CIS) spectroscopy of C2H3Cl are reported. For comparison, the He(I) photoelectron spectrum has also been ... [more ▼]

Using synchrotron radiation the threshold photoelectron (TPES) spectrum and constant ion state (CIS) spectroscopy of C2H3Cl are reported. For comparison, the He(I) photoelectron spectrum has also been measured and reexamined. The threshold photoelectron spectrum has been measured between 9.0 and 25.0 eV and the photon energy range of 9.9-12.0 eV has been investigated in detail. Many features have been identified and tentatively assigned with the help of the photoabsorption spectroscopic results. These data were compared with the well-resolved He(I) photoelectron spectrum. The fine structure observed in the two first ionic states is assigned to progressions belonging partially to previously unobserved vibration normal modes. State-selected CIS spectra have been recorded for the first vibronic states between 10.0 and 11.67 eV. They exhibit fine structure assigned to autoionization of Rydberg states. [less ▲]

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See detailHead shape disparity of the cod icefishes Trematominae (Notothenioidei, Teleostei)
Frederich, Bruno ULiege; Heindler, Franz M.; Dettai, Agnès et al

Poster (2016, December 16)

The suborder Notothenioidei (Teleostei) has undergone a remarkable adaptive radiation in the Southern Ocean. Within this suborder, the subfamily Trematominae is endemic to Antarctic waters and represents ... [more ▼]

The suborder Notothenioidei (Teleostei) has undergone a remarkable adaptive radiation in the Southern Ocean. Within this suborder, the subfamily Trematominae is endemic to Antarctic waters and represents a dominant component of the shelf fish fauna. After recent advances in molecular phylogenetics, 14 species of Trematomus are currently recognized (including Pagothenia and Cryothenia spp.) comprising both considerable morphological and ecological diversity. Here, we aim to illustrate the main axes of shape variation in Trematomus and explore the evolution of their morphology. A dataset of 96 specimens representing 10 species of Trematomus from the collection of the Natural History Museum of Paris was assembled, and landmark-based geometric morphometrics was applied to quantify head shape disparity. Regular regression analysis revealed significant interspecific allometry while a low percentage of shape variation was explained by size (R2 = 0.11; P < 0.001). Main shape variation across species was explored using a principal component (PC) analysis on shape variables. Two groups diverged along PC1: (1) T. bernacchii, T. hansoni, T. pennellii and T. tokarevi have short cephalic profiles with larger cheeks (lowest values along PC1); and (2) T. lepidorhinus, T. eulepidotus and T. newnesi show lengthened cephalic profiles with larger eyes (highest values along PC1). Trematomus scotti differed from all other species mainly along PC3 indicating more elongated cheeks. Phenogram based on Procrustes shape distances will be compared to molecular phylogenetic trees and morphometric data will be mapped onto phylogenetic trees in order to illustrate the mode of phenotypic diversification of Trematomus during evolution. [less ▲]

Detailed reference viewed: 48 (1 ULiège)