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See detailHD 35155: the First Eclipsing Binary S Star (P=642 Days)
Jorissen, A.; Mayor, M.; Manfroid, Jean ULg et al

in Information Bulletin on Variable Stars (1992), 3730

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See detailHD 45314: a new γ Cassiopeiae analog among Oe stars
Rauw, Grégor ULg; Nazé, Yaël ULg; Spano, M. et al

in Astronomy and Astrophysics (2013), 555

Context. Oe stars possibly form an extension to higher temperatures of the Be phenomenon, but it is still unclear whether these stars have disks. <BR /> Aims: X-ray spectra could provide hints for ... [more ▼]

Context. Oe stars possibly form an extension to higher temperatures of the Be phenomenon, but it is still unclear whether these stars have disks. <BR /> Aims: X-ray spectra could provide hints for interactions of the star with a putative surrounding disk. <BR /> Methods: We obtained XMM-Newton observations of two Oe stars, HD 45314 and HD 60848. Spectra and light curves were extracted and analysed. Optical spectra were also obtained to support the X-ray observations. <BR /> Results: We find that both stars display very different X-ray properties. Whilst HD 60848 has an X-ray spectrum and emission level typical for its spectral type, HD 45314 displays a very hard X-ray emission, dominated by a thermal plasma with kT ~ 21 keV. Furthermore, HD 45314 displays count rate variations by a factor 2 on timescales of ~ 10[SUP]3[/SUP] s and a high log (L[SUB]X[/SUB]/L[SUB]bol[/SUB]) = -6.10 ± 0.03. <BR /> Conclusions: The X-ray properties of HD 45314 indicate that this star is a new member of the class of γ Cas analogs, the first one among the original category of Oe stars. Based on observations collected with XMM-Newton, an ESA Science Mission with instruments and contributions directly funded by ESA Member States and the USA (NASA), and observations collected at the European Southern Observatory (La Silla, Chile) and the Observatoire de Haute Provence (France). [less ▲]

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See detailHD 45677 est-elle une étoile variable ?
Swings, Jean-Pierre ULg; Swings, Polydore ULg

in Astronomy and Astrophysics (1972), 17(1), 142-145

Whereas HD 45677 has faded by approximately one magnitude since 1969, the amplitude of variation in photographic magnitude between 1899 and 1969 has always been smaller than 0.3 mag.

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See detailHD 65949: Rosetta Stone or Red Herring
Cowley, C. R.; Hubrig, S.; Palmeri, P. et al

in Monthly Notices of the Royal Astronomical Society (2010), 405

HD 65949 is a late B star with exceptionally strong Hg II λ3984, but it is not a typical HgMn star. The Re II spectrum is of extraordinary strength. Abundances or upper limits are derived here for 58 ... [more ▼]

HD 65949 is a late B star with exceptionally strong Hg II λ3984, but it is not a typical HgMn star. The Re II spectrum is of extraordinary strength. Abundances or upper limits are derived here for 58 elements based on a model with Teff = 13 100K and log(g) = 4.0. Even-Z elements through nickel show minor deviations from solar abundances. Anomalies among the odd-Z elements through copper are mostly small. Beyond the iron peak, a huge scatter is found. Enormous enhancements are found for the elements rhenium through mercury (Z = 75–80). We note the presence of Th III in the spectrum. The abundance pattern of the heaviest elements resembles the N = 126 r-process peak of solar material, though not in detail. An odd-Z anomaly appears at the triplet (Zr Nb Mo), and there is a large abundance jump between Xe (Z = 54) and Ba (Z = 56). These are signatures of chemical fractionation. We find a significant correlation of the abundance excesses with second ionization potentials for elements withZ > 30. If this is not a red herring (false lead), it indicates the relevance of photospheric or near-photospheric processes. Large excesses (4–6 dex) require diffusion from deeper layers with the elements passing through a number of ionization stages. That would make the correlation with second ionization potential puzzling. We explore a model with mass accretion of exotic material followed by the more commonly accepted differentiation by diffusion. That model leads to a number of predictions which challenge future work. New observations confirm the orbital elements of Gieseking and Karimie, apart from the systemic velocity, which has increased. Likely primary and secondary masses are near 3.3 and 1.6 M , with a separation of ca. 0.25 au. New atomic structure calculations are presented in two appendices. These include partition functions for the first through third spectra of Ru, Re and Os, as well as oscillator strengths in the Re II spectrum. [less ▲]

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See detailHD 85037 nouvelle variable à éclipses probable
Renson, Pierre ULg; Heck, A.

in Information Bulletin on Variable Stars (1983), 2298

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See detailHD 97658 and its super-Earth
Van Grootel, Valérie ULg; Gillon, Michaël ULg; Valencia, D. et al

in European Physical Journal Web of Conferences (2015, September 01)

Super-Earths transiting nearby bright stars are key objects that simultaneously allow for accurate measurements of both their mass and radius, providing essential constraints on their internal composition ... [more ▼]

Super-Earths transiting nearby bright stars are key objects that simultaneously allow for accurate measurements of both their mass and radius, providing essential constraints on their internal composition. We present the confirmation, based on Spitzer observations, that the super-Earth HD 97658 b transits its host star. HD 97658 is a low-mass (M*=0.77+-0.05 Msun) K1 dwarf, as determined from the Hipparcos parallax and stellar evolution modeling. To constrain the planet parameters, we carry out Bayesian global analyses of Keck-HIRES radial velocities, and MOST and Spitzer photometry. HD 97658 b is a massive (Mp=7.55 +0.83,-0.79 Mearth) and large (Rp = 2.247 +0.098,-0.095 Rearth at 4.5 microns) super-Earth. We investigate the possible internal compositions for HD 97658 b. Our results indicate a large rocky component, by at least 60% by mass, and very little H-He components, at most 2% by mass. We also discuss how future asteroseismic observations can improve the knowledge of the HD 97658 system, in particular by constraining its age. [less ▲]

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See detailHD 97658 and its super-Earth. Spitzer & MOST transit analysis and modeling of the host star
Van Grootel, Valérie ULg; Gillon, Michaël ULg; Valencia, D. et al

Conference (2014, July)

Super-Earths transiting nearby bright stars are key objects that simultaneously allow for accurate measurements of both their mass and radius, providing essential constraints on their internal composition ... [more ▼]

Super-Earths transiting nearby bright stars are key objects that simultaneously allow for accurate measurements of both their mass and radius, providing essential constraints on their internal composition. We present here the confirmation, based on Spitzer transit observations, that the super-Earth HD 97658 b transits its host star. HD 97658 is a low-mass ($M_*=0.77\pm0.05\,M_{\odot}$) K1 dwarf, as determined from the Hipparcos parallax and stellar evolution modeling. To constrain the planet parameters, we carry out Bayesian global analyses of Keck-HIRES radial velocities, and MOST and Spitzer photometry. HD 97658 b is a massive ($M_P=7.55^{+0.83}_{-0.79} M_{\oplus}$) and large ($R_{P} = 2.247^{+0.098}_{-0.095} R_{\oplus}$ at 4.5 $\mu$m) super-Earth. We investigate the possible internal compositions for HD 97658 b. Our results indicate a large rocky component, by at least 60% by mass, and very little H-He components, at most 2% by mass. We also discuss how future asteroseismic observations can improve the knowledge of the HD 97658 system, in particular by constraining its age. Orbiting a bright host star, HD 97658 b will be a key target for coming space missions TESS, CHEOPS, PLATO, and also JWST, to characterize thoroughly its structure and atmosphere. [less ▲]

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See detailHD 97658 and its super-Earth: Spitzer transit analysis and seismic modeling of the host star
Van Grootel, Valérie ULg; Gillon, Michaël ULg; Valencia, Diana et al

Conference (2013, December)

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See detailHD160529 - a New Galactic Luminous Blue Variable
Sterken, C.; Gosset, Eric ULg; Juttner, A. et al

in Astronomy and Astrophysics (1991), 247

The galactic early-type A hypergiant HD 160529 has been photometrically monitored in the Strömgren system during the past 18 years. HD 160529 has become fainter in the optical range by 0.5 mag during the ... [more ▼]

The galactic early-type A hypergiant HD 160529 has been photometrically monitored in the Strömgren system during the past 18 years. HD 160529 has become fainter in the optical range by 0.5 mag during the past eight years. In addition, pulsation-like variations with a quasi-period of 57 days and with a peak-to-peak amplitude of about 0.1 mag in b and y were found. The fading was not completely monotonous a fall of at least 0.2 mag in b and y within about 40 days around JD2446500 is particularly remarkable. This jump is accompanied by a change in the temperature-sensitive c[SUB]1[/SUB] index of about -0.14 mag. HD 160529 has become visually fainter and hotter during the past eight years, thus becoming a new case of a galactic Luminous Blue Variable (LBV). Model calculations on the basis of the photometry and previously published as well as new spectroscopic observations have shown HD 160529 to be a close counterpart of R 110, a recently discovered LBV in the LMC. From this comparison an absolute magnitude of M[SUB]V[/SUB] = -8.9 and a distance of 2.5 kpc is derived. The stellar parameters characterising the maximum state are estimated to be T[SUB]eff[/SUB] ≍ 8000 K, log g ≍ 0.55, R ≍ 330 R[SUB]sun[/SUB], from which the mass is estimated to be only M ≍ 13 M[SUB]sun[/SUB]. From the Hα profile a lower limit of the mass-loss rate of HD 160529 was calculated, which is about 10 times higher than that of R 110; this could be a consequence of the higher metallicity of the galactic LBV. The low mass of HD 160529 makes this luminous blue star a good candidate for a post-RSG (red supergiant phase) object, providing some evidence that (as sometimes argued) low metallicity is not a necessary prerequisite for evolution of massive stars backward to higher temperatures. [less ▲]

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See detailHD160529: a new galactic Luminous Blue Variable
Stahl, O.; Sterken, C.; Gosset, Eric ULg et al

(1992)

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See detailHD46407 - the First Eclipsing Binary Barium Star
Jorissen, A.; Manfroid, Jean ULg; Sterken, C.

in Evolutionary Processes in Interacting Binary Stars (1992)

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See detailHDA cycloadditions of 1-diethoxyphosphonyl-1,3-butadiene with nitroso heterodienophiles: a computational investigation
Monbaliu, Jean-Christophe ULg; Dive, Georges ULg; Marchand-Brynaert, Jacqueline et al

in Journal of Molecular Structure : Theochem (2010), 959

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See detailThe HDAC inhibitor panobinostat (LBH589) inhibits mesothelioma and lung cancer cells in vitro and in vivo with particular efficacy for small cell lung cancer
Crisanti, Cecilia; Wallace, Africa; Kapoor, Veena et al

in Molecular Cancer Therapeutics (2009), 8(8), 2221-2231

Lung cancer is the leading cause of cancer deaths in the United States. Current therapies are inadequate. Histone deacetylase inhibitors (HDACi) are a recently developed class of anticancer agents that ... [more ▼]

Lung cancer is the leading cause of cancer deaths in the United States. Current therapies are inadequate. Histone deacetylase inhibitors (HDACi) are a recently developed class of anticancer agents that cause increased acetylation of core histones and nonhistone proteins leading to modulation of gene expression and protein activityin - volved in cancer cell growth and survival pathways. We examined the efficacyof the HDACi panobinostat (LBH589) in a wide range of lung cancers and mesotheliomas. Panobinostat was cytotoxic in almost all 37 cancer cell lines tested. IC50 and LD50 values were in the low nmol/L range (4–470 nmol/L; median, 20 nmol/L). Small cell lung cancer (SCLC) cell lines were among the most sensitive lines, with LD50 values consistently <25 nmol/L. In lung cancer and mesothelioma animal models, panobinostat significantlyde creased tumor growth byan average of 62% when compared with vehicle control. Panobinostat was equallye ffective in immunocompetent and severe combined immunodeficiencymic e, indicating that the inhibition of tumor growth by panobinostat was not due to direct immunologic effects.Panobinostat was, however, particularlyeffective in SCLC xenografts, and the addition of the chemotherapyag ent etoposide augmented antitumor effects. Protein analysis of treated tumor biopsies revealed elevated amounts of cell cycle regulators such as p21 and proapoptosis factors, such as caspase 3 and 7 and cleaved poly[ADP-ribose] polymerase, coupled with decreased levels of antiapoptotic factors such as Bcl-2 and Bcl-XL. These studies together suggest that panobinostat maybe a useful adjunct in the treatment of thoracic malignancies, especiallySCLC. [less ▲]

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See detailHDAC4 represses p21(WAF1/Cip1) expression in human cancer cells through a Sp1-dependent, p53-independent mechanism.
Mottet, Denis ULg; Pirotte, Sophie ULg; Lamour, Virginie ULg et al

in Oncogene (2009), 28(2), 243-56

Cancer cells have complex, unique characteristics that distinguish them from normal cells, such as increased growth rates and evasion of anti-proliferative signals. Global inhibition of class I and II ... [more ▼]

Cancer cells have complex, unique characteristics that distinguish them from normal cells, such as increased growth rates and evasion of anti-proliferative signals. Global inhibition of class I and II histone deacetylases (HDACs) stops cancer cell proliferation in vitro and has proven effective against cancer in clinical trials, at least in part, through transcriptional reactivation of the p21(WAF1/Cip1)gene. The HDACs that regulate p21(WAF1/Cip1) are not fully identified. Using small interfering RNAs, we found that HDAC4 participates in the repression of p21(WAF1/Cip1) through Sp1/Sp3-, but not p53-binding sites. HDAC4 interacts with Sp1, binds and reduces histone H3 acetylation at the Sp1/Sp3 binding site-rich p21(WAF1/Cip1) proximal promoter, suggesting a key role for Sp1 in HDAC4-mediated repression of p21(WAF1/Cip1). Induction of p21(WAF1/Cip1) mediated by silencing of HDAC4 arrested cancer cell growth in vitro and inhibited tumor growth in an in vivo human glioblastoma model. Thus, HDAC4 could be a useful target for new anti-cancer therapies based on selective inhibition of specific HDACs. [less ▲]

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See detailHDAC5 depletion Decreases NDUFB5 Subunit of Mitochondrial Complex- I leading to Glucose-dependent Metabolic Reprogrammation
Hendrick, Elodie ULg; Matheus, Nicolas ULg; Peixoto, Paul ULg et al

Poster (2013, December 05)

Introduction : 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 ... [more ▼]

Introduction : 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. Aims : The goal of this study is to further understand the molecular mechanisms of action of HDAC5 in cancer cells. Methods and results : Screening transcriptomic study demonstrated that HDAC5 depletion induces a down-regulation of NDUFB5, a subunit of the complex I of the mitochondrial respiratory chain through modulation of mRNA stability. HDAC5 depletion-induced NDUFB5 downregulation causes a significant increase of ROS production and induces uncoupled mitochondrial respiration. In addition, this HDAC5 depletion-induced mitochondrial dysfunction provokes metabolic adaptation associated with increased importance of 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. Conclusions : Our study demonstrated for the first time that specific HDAC5 inhibition induces alteration of NDUFB5 gene expression by altering mRNA stability 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. [less ▲]

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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 ULg; Peixoto, Paul ULg; Polese, Catherine ULg 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 ▲]

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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 ULg; Peixoto, Paul ULg; Polese, Catherine ULg et al

Poster (2015, February 11)

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: 31 (9 ULg)
See detailHDAC5 Depletion in Cancer Cells Induces an Oxidative Stress and Leads to a Metabolic Reprogramming toward Glucose and Glutamine Metabolism
Hendrick, Elodie ULg; Peixoto, Paul ULg; Polese, Catherine ULg 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: 15 (3 ULg)
See detailHDAC5 Depletion in Cancer Cells Induces an Oxidative Stress and Leads to a Metabolic Reprogramming toward Glucose and Glutamine Metabolism
Hendrick, Elodie ULg; Peixoto, Paul ULg; Polese, Catherine ULg 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: 20 (0 ULg)