Relevant bibliographies by topics / Suberoylanilide Hydroxamic Acid (SAHA)

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Suberoylanilide Hydroxamic Acid (SAHA)'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Suberoylanilide Hydroxamic Acid (SAHA).'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Suberoylanilide Hydroxamic Acid (SAHA)"

1

Zhou, Hongyan, Sheng Jiang, Jianping Chen, and Shao Bo Su. "Suberoylanilide hydroxamic acid suppresses inflammation-induced neovascularization." Canadian Journal of Physiology and Pharmacology 92, no. 10 (October 2014): 879–85. http://dx.doi.org/10.1139/cjpp-2014-0117.

Full text
Abstract:
Histone deacetylases (HDACs) regulate gene transcription by modifying the acetylation of histone and nonhistone proteins. Deregulated expression of HDACs has been implicated in tumorigenesis and angiogenesis. In this study, we examined the effect of suberoylanilide hydroxamic acid (SAHA), a potent inhibitor of HDACs, on inflammatory corneal angiogenesis. In a mouse model of alkali-induced corneal neovascularization (CNV), topical application of SAHA to the injured corneas attenuated CNV. In addition, in vivo treatment with SAHA downregulated the expression of the pro-angiogenic factors vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), transforming growth factor beta 1 (TGFβ1), and epidermal growth factor (EGF), but upregulated the expression of the anti-angiogenic factors thrombospondin (TSP)-1, TSP-2, and ADAMTS-1 in the injured corneas. Furthermore, SAHA inhibited the expression of pro-angiogenic factors, migration, proliferation, and tube formation by human microvascular endothelial cells (HEMC-1) in vitro. These data indicate that SAHA has therapeutic potential for CNV.
APA, Harvard, Vancouver, ISO, and other styles
2

Cenik, Basar, Chantelle F. Sephton, Colleen M. Dewey, Xunde Xian, Shuguang Wei, Kimberley Yu, Wenze Niu, et al. "Suberoylanilide Hydroxamic Acid (Vorinostat) Up-regulates Progranulin Transcription." Journal of Biological Chemistry 286, no. 18 (March 23, 2011): 16101–8. http://dx.doi.org/10.1074/jbc.m110.193433.

Full text
Abstract:
Progranulin (GRN) haploinsufficiency is a frequent cause of familial frontotemporal dementia, a currently untreatable progressive neurodegenerative disease. By chemical library screening, we identified suberoylanilide hydroxamic acid (SAHA), a Food and Drug Administration-approved histone deacetylase inhibitor, as an enhancer of GRN expression. SAHA dose-dependently increased GRN mRNA and protein levels in cultured cells and restored near-normal GRN expression in haploinsufficient cells from human subjects. Although elevation of secreted progranulin levels through a post-transcriptional mechanism has recently been reported, this is, to the best of our knowledge, the first report of a small molecule enhancer of progranulin transcription. SAHA has demonstrated therapeutic potential in other neurodegenerative diseases and thus holds promise as a first generation drug for the prevention and treatment of frontotemporal dementia.
APA, Harvard, Vancouver, ISO, and other styles
3

Kim, M. J., H. J. Oh, G. A. Kim, H. N. Suh, Y. K. Jo, Y. B. Choi, D. H. Kim, H. J. Han, and B. C. Lee. "36 EFFECT OF SUBEROYLANILIDE HYDROXAMIC ACID TREATED DONOR CELLS ON DOG CLONING." Reproduction, Fertility and Development 27, no. 1 (2015): 110. http://dx.doi.org/10.1071/rdv27n1ab36.

Full text
Abstract:
Although dog cloning technology has been applied to conservation of endangered canids, propagation of elite dogs and production of transgenic dogs, the efficiency of cloning is still very low. To help overcome this problem, we evaluated the effect of treating donor cells with suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor (HDACi), on dog cloning efficiency. Relative mRNA expression of the bax1, bcl2, and Dnmt1 in fibroblasts treated with different concentrations (0, 1, 10, 50 μM) of SAHA and durations (0, 20, 44 h) were assessed using real-time polymerase chain reaction. After determining an optimum concentration and duration, histone acetylation levels (H3K9, H4K5/K8/K12/K16) of SAHA-treated cells were analysed using immunostaining. The SAHA-treated cells were used as donor cells for somatic cell nuclear transfer, and activated reconstructed embryos were transferred to recipients. Pregnancy diagnosis was performed by ultrasonography at least 29 days after the embryo transfer. All experiments were repeated more than 3 times and the data were analysed using Graph Prism software (GraphPad Software Inc., San Diego, CA, USA). An unpaired t-test was used to compare transcripts levels and fluorescence intensities. A chi-squared test was used to compare the implantation rates. The bax1/bcl2 ratio of the 1 μM SAHA group was similar to that of control but significantly increased in the 10 μM and 50 μM groups. Expression of Dnmt1 was decreased in the 1 μM SAHA group, and the 10 μM and 50 μM groups showed the lowest expression compared with the control group. Although the bax1/blc2 ratio was not affected by the SAHA treatment duration, 20-h treatment group showed significantly decreased Dnmt1 levels compared with control group. As a pan-HDAC inhibitor, 1 μM for 20 h of SAHA treatment significantly increased acetylation of H3K9, H4K5, H4K8, and H4K16. For control and SAHA groups, a total of 76 and 64 cloned embryos were produced and transferred to 7 and 5 recipients, respectively. Three fetuses were diagnosed in both groups but there was no significant difference in the pregnancy rate. In conclusion, although SAHA treatment as used in this study significantly decreased bax/bcl2 and Dnmt1 transcripts of donor nuclei, as well as increased H3 and H4 acetylation, it would not enough to increase in vivo developmental competence of cloned dog embryos.This study was supported by RDA (#PJ008975022014), IPET (#311062–04–3SB010), Research Institute for Veterinary Science and the BK21 plus program.
APA, Harvard, Vancouver, ISO, and other styles
4

Cao, Hua, Manfred Jung, and George Stamatoyannopoulos. "Hydroxamic Acids Derivatives Induce γ Globin Gene Expression in Vivo." Blood 104, no. 11 (November 16, 2004): 1224. http://dx.doi.org/10.1182/blood.v104.11.1224.1224.

Full text
Abstract:
Abstract We have previously shown that four hydroxamic acids: butyric and propionic hydroxamic acids, subericbishydroxamic acid (SBHA) and suberoylanilide hydroxamic acid (SAHA) are potent inhibitors of histone deacetylase and strong inducers of fetal hemoglobin expression in vitro (Exp Hematol.31:197, 2003). In the present study we tested their effect on fetal hemoglobin synthesis in vivo. Transgenic mice carrying the human μLCR Aγ construct continue to express the human γ gene in the adult stage of development ( γ/α mRNA ratio ~ 5%, Blood.77:1326, 1991). These mice were crossed to mice heterozygous for a thalassemia gene due to β globin gene deletion (PNAS.92:11608, 1995). The β thalassemia/μLCR Aγ mice represent an appropriate moderately anemic animal model for testing the effects of Hb F inducers. Compounds were administered subcutaneously with a mini-osmotic pump continuously for 7days in a high and a low concentration. Concentrations were: for butyric hydroxamic acid: 500mg/kg/day/100mg/kg/day; for propionic hydroxamic acid: 500mg/kg/day/100mg/kg/day; for SAHA: 100mg/kg/day/20mg/kg/day; and for SBHA: 200mg/kg/day/40mg/kg/day. Two test groups were studied. In group 1, 70μL mice blood was drawn every other day up to 20 days; in group 2, 70μL mice blood was drawn only on days 0 and 21. Reticulocytes and F reticulocytes were measured using flow cytometry, while γ globin gene expression was quantitated by RNase protection assay. Butyric and propionate hydroxamic acids increased reticulocytes by 70.52% (from 13.96% to 23.81%) and 172.52% (from 10.34% to 28.20%) respectively. There was only small increase in reticulocytes in the mice treated with SAHA (from 13.33% to 15.36%), SBHA (from 14.24% to 16.27%) and the PBS control (11.06% to 14.11%). All the compounds increased the level of γ mRNA: butyric hydroxamate by 53.07%; propionic hydroxamate by 40.05%; SAHA by 49.87%, and SBHA by 34.05%. These results suggest first that all the hydroxamic acid derivatives we used increase fetal hemoglobin in vivo in the thalassemia animal model; second butyric and propionic hydroxanic acids are in addition inducers of in vivo erythropoiesis.
APA, Harvard, Vancouver, ISO, and other styles
5

Kim, Da Som, Hong-Ki Min, Eun Kyung Kim, Seung Cheon Yang, Hyun Sik Na, Seon-Yeong Lee, Jeong-Won Choi, et al. "Suberoylanilide Hydroxamic Acid Attenuates Autoimmune Arthritis by Suppressing Th17 Cells through NR1D1 Inhibition." Mediators of Inflammation 2019 (October 24, 2019): 1–11. http://dx.doi.org/10.1155/2019/5648987.

Full text
Abstract:
Rheumatoid arthritis (RA) is a type of systemic autoimmune arthritis that causes joint inflammation and destruction. One of the pathological mechanisms of RA is known to involve histone acetylation. Although the histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) can attenuate arthritis in animal models of RA, the mechanism underlying this effect is poorly understood. This study was performed to examine whether SAHA has therapeutic potential in an animal model of RA and to investigate its mechanism of action. Collagen-induced arthritis (CIA) mice were orally administered SAHA daily for 8 weeks and examined for their arthritis score and incidence of arthritis. CD4+ T cell regulation following SAHA treatment was confirmed in splenocytes cultured under type 17 helper T (Th17) cell differentiation conditions. Clinical scores and the incidence of CIA were lower in mice in the SAHA treatment group compared to the controls. In addition, SAHA inhibited Th17 cell differentiation, as well as decreased expression of the Th17 cell-related transcription factors pSTAT3 Y705 and pSTAT3 S727. In vitro experiments showed that SAHA maintained regulatory T (Treg) cells but specifically reduced Th17 cells. The same results were obtained when mouse splenocytes were cultured under Treg cell differentiation conditions and then converted to Th17 cell differentiation conditions. In conclusion, SAHA was confirmed to specifically inhibit Th17 cell differentiation through nuclear receptor subfamily 1 group D member 1 (NR1D1), a factor associated with Th17 differentiation. The results of the present study suggested that SAHA can attenuate CIA development by inhibition of the Th17 population and maintenance of the Treg population through NR1D1 inhibition. Therefore, SAHA is a potential therapeutic candidate for RA.
APA, Harvard, Vancouver, ISO, and other styles
6

Yu, J., H. Wu, Z. Lin, K. Su, J. Zhang, F. Sun, X. Wang, C. Wen, H. Cao, and L. Hu. "Metabolic changes in rat serum after administration of suberoylanilide hydroxamic acid and discriminated by SVM." Human & Experimental Toxicology 36, no. 12 (January 13, 2017): 1286–94. http://dx.doi.org/10.1177/0960327116688067.

Full text
Abstract:
Suberoylanilide hydroxamic acid (SAHA) exerts marked anticancer effects via promotion of apoptosis, cell cycle arrest, and prevention of oncogene expression. In this study, serum metabolomics and artificial intelligence recognition were used to investigate SAHA toxicity. Forty rats (220 ± 20 g) were randomly divided into control and three SAHA groups (low, medium, and high); the experimental groups were treated with 12.3, 24.5, or 49.0 mg kg−1 SAHA once a day via intragastric administration. After 7 days, blood samples from the four groups were collected and analyzed by gas chromatography–mass spectrometry, and pathological changes in the liver were examined using microscopy. The results showed that increased levels of urea, oleic acid, and glutaconic acid were the most significant indicators of toxicity. Octadecanoic acid, pentadecanoic acid, glycerol, propanoic acid, and uric acid levels were lower in the high SAHA group. Microscopic observation revealed no obvious damage to the liver. Based on these data, a support vector machine (SVM) discrimination model was established that recognized the metabolic changes in the three SAHA groups and the control group with 100% accuracy. In conclusion, the main toxicity caused by SAHA was due to excessive metabolism of saturated fatty acids, which could be recognized by an SVM model.
APA, Harvard, Vancouver, ISO, and other styles
7

Kawamata, Norihiko, John Chen, and H. Phillip Koeffler. "Suberoylanilide hydroxamic acid (SAHA; vorinostat) suppresses translation of cyclin D1 in mantle cell lymphoma cells." Blood 110, no. 7 (October 1, 2007): 2667–73. http://dx.doi.org/10.1182/blood-2005-11-026344.

Full text
Abstract:
Mantle cell lymphoma (MCL) has a chromosomal translocation resulting in the expression of the cyclin D1 gene driven by the powerful enhancer of the immunoglobulin heavy chain gene, leading to uncontrolled, overexpressed cyclin D1 protein. We showed that suberoylanilide hydroxamic acid (SAHA; vorinostat), one of the histone deacetylase inhibitors derived from hydroxamic acid, caused a dramatic decrease (90%) in protein levels of cyclin D1 after 8-hour exposure to SAHA (5 μM) in MCL lines (SP49, SP53, Jeko1). mRNA levels and protein stability of cyclin D1 were minimally affected by SAHA over 8 hours. In contrast, metabolic labeling assays showed that SAHA decreased incorporation of [35S]methionine into cyclin D1 protein. The drug also decreased levels of phosphorylated Akt, mammalian target of Rapamycin (mTOR), and eukaryotic translation initiation factor 4E binding protein (eIF4E-BP) and lowered the cap site binding activity of eIF4E in the MCL cells. In vitro phosphatidyl inositol (PI) kinase assay demonstrated that SAHA directly inhibited kinase activity of PI 3′ kinase. Taken together, SAHA caused a rapid decrease of cyclin D1 in MCL by blocking the translation of cyclin D1 by inhibiting the phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR/eIF4E-BP pathway, probably by PI3K inhibition.
APA, Harvard, Vancouver, ISO, and other styles
8

Ekou, Lynda, Tchirioua Ekou, Javier Garcia, Isabelle Opalinski, and Jean Pierre Gesson. "Design and Synthesis of Small Molecules Based on a Substructural Analysis of the Histone Deacetylase Inhibitors TSA and SAHA." E-Journal of Chemistry 8, no. 3 (2011): 1394–400. http://dx.doi.org/10.1155/2011/403129.

Full text
Abstract:
Inhibitors of histone deacetylases (HDACs) are patent inducers of differentiation and bear considerable potential as drugs for chemoprevention and treatment of cancer. In this paper, we have investigated three synthetic, inhibitors A1a,b, A2a. Analogue hybrid trichostatine A (TSA), suberoylanilide hydroxamic acid SAHA, in order to seek new histone deacetylases (HDACs) inhibitors.
APA, Harvard, Vancouver, ISO, and other styles
9

Qin, Yu, Xuejiao Zhao, and Yong Fang. "PP242 Synergizes With Suberoylanilide Hydroxamic Acid to Inhibit Growth of Ovarian Cancer Cells." International Journal of Gynecologic Cancer 24, no. 8 (October 2014): 1373–80. http://dx.doi.org/10.1097/igc.0000000000000238.

Full text
Abstract:
ObjectivesOverexpression of histone deacetylases and activation of the phosphatidylinositol 3-kinase/mammalian target of rapamycin pathway are common aberrations in ovarian cancer. For this reason, simultaneous inhibition of such targets is a rational therapeutic strategy to treat patients with ovarian cancer. This study aimed to investigate the biological effect of the histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), in combination with the dual mTOR complex 1 and mTOR complex 2 inhibitor, PP242, against ovarian cancer cells.Materials and MethodsThe effects of SAHA and PP242 on the growth of SKOV3 and A2780 cells were examined using Cell Counting Kit-8. The apoptosis was analyzed through flow cytometry, and the expression of apoptosis-related proteins was investigated through Western blotting. Induction of autophagy was determined through fluorescence microscopy using a stably transfected green fluorescent protein/microtubule-associated protein light chain 3 construct to visualize autophagosome formation. The expression of autophagy-related proteins was determined through Western blot analysis. The effect of SAHA and PP242 on the growth of ovarian cancer was also examined in an orthotopic ovarian cancer model.ResultsThe combination of SAHA and PP242 significantly inhibited cell proliferation and synergistically increased apoptosis and autophagy compared with each agent alone in vitro. In vivo, this combination exhibited greater inhibition on tumor growth than monotreatments did and it significantly prolonged the survival time of the mice.ConclusionsThese results suggest that the combination of SAHA and PP242 may lead to a novel strategy in treating patients with ovarian cancer.
APA, Harvard, Vancouver, ISO, and other styles
10

Wang, Wenwen, Min Yan, Qiuhong Ji, Jinbiao Lu, Yuhua Ji, and Juling Ji. "Suberoylanilide hydroxamic acid suppresses hepatic stellate cells activation by HMGB1 dependent reduction of NF-κB1." PeerJ 3 (November 3, 2015): e1362. http://dx.doi.org/10.7717/peerj.1362.

Full text
Abstract:
Hepatic stellate cells (HSCs) activation is essential to the pathogenesis of liver fibrosis. Exploring drugs targeting HSC activation is a promising anti-fibrotic strategy. In the present study, we found suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor, prominently suppressed the activation phenotype of a human hepatic stellate cell line—LX2. The production of collagen type I andα-smooth muscle actin (α-SMA) as well as the proliferation and migration of LX2 cells were significantly reduced by SAHA treatment. To determine the molecular mechanisms underlying this suppression, genome wild gene regulation by SAHA was determined by Affymetrix 1.0 human cDNA array. Upon SAHA treatment, the abundance of 331 genes was up-regulated and 173 genes was down-regulated in LX2 cells. Bioinformatic analyses of these altered genes highlighted the high mobility group box 1 (HMGB1) pathway was one of the most relevant pathways that contributed to SAHA induced suppression of HSCs activation. Further studies demonstrated the increased acetylation of intracellular HMGB1 in SAHA treated HSCs, and this increasing is most likely to be responsible for SAHA induced down-regulation of nuclear factor kappa B1 (NF-κB1) and is one of the main underlying mechanisms for the therapeutic effect of SAHA for liver fibrosis.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Suberoylanilide Hydroxamic Acid (SAHA)"

1

Nikkhah, Mehdi. "Identification of Cell Biomechanical Signatures Using Three Dimensional Isotropic Microstructures." Diss., Virginia Tech, 2010. http://hdl.handle.net/10919/77278.

Full text
Abstract:
Micro and nanofabrication technologies have been used extensively in many biomedical and biological applications. Integration of MEMS technology and biology (BioMEMS) enables precise control of the cellular microenvironments and offers high throughput systems. The focus of this research was to develop three dimensional (3-D) isotropic microstructures for comprehensive analysis on cell-substrate interactions. The aim was to investigate whether the normal and cancerous cells differentially respond to their underlying substrate and whether the differential response of the cells leads to a novel label-free technique to distinguish between normal and cancerous cells. Three different generations of 3-D isotropic microstructures comprised of curved surfaces were developed using a single-mask, single-etch step process. Our experimental model included HS68 normal human fibroblasts, MCF10A normal human breast epithelial cells and MDA-MB-231 metastatic human breast cancer cells. Primary findings on the first generation of silicon substrates demonstrated a distinct adhesion and growth behavior in HS68 and MDA-MB-231 cells. MDA-MB-231 cells deformed while the fibroblasts stretched and elongated their cytoskeleton on the curved surfaces. Unlike fibroblasts, MDA-MB-231 cells mainly trapped and localized inside the deep microchambers. Detailed investigations on cytoskeletal organization, adhesion pattern and morphology of the cells on the second generation of the silicon substrates demonstrated that cytoskeletal prestress and microtubules organization in HS68 cells, cell-cell junction and cell-substrate adhesion strength in MCF10A cells, and deformability of MDA-MB-231 cells (obtained by using AFM technique) affect their behavior inside the etched cavities. Treatment of MDA-MB-231 cells with experimental breast cancer drug, SAHA, on the second generation of substrates, significantly altered the cells morphology, cytoarchitecture and adhesion pattern inside the 3-D microstructures. Third generation of silicon substrates was developed for comprehensive analysis on behavior of MDA-MB-231 and MCF10A cells in a co-culture system in response to SAHA drug. Formation of colonies of both cell types was evident inside the cavities within a few hours after seeding the cells on the chips. SAHA selectively altered the morphology and cytoarchitecture in MDA-MB-231 cells. Most importantly, the majority of MDA-MB-231 cells stretched inside the etched cavities, while the adhesion pattern of MCF10A cells remained unaltered. In the last part of this dissertation, using AFM analysis, we showed that the growth medium composition has a pronounced effect on cell elasticity. Our findings demonstrated that the proposed isotropic silicon microstructures have potential applications in development of biosensor platforms for cell segregation as well as conducting fundamental biological studies.
Ph. D.
APA, Harvard, Vancouver, ISO, and other styles
2

Siyoucef, Souhila Safia. "Implication des facteurs épigénétiques dans l'épileptogenèse et les déficits cognitifs associés à l'épilepsie du lobe temporal." Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM5064.

Full text
Abstract:
L'épilepsie du lobe temporal (ELT) est la forme la plus fréquente de l'épilepsie chez l'adulte. Elle se traduit par des crises spontanées et récurrentes, qui sont résistantes à tout traitement dans 90% des cas. Une agression initiale du cerveau (traumatisme crânien, méningite, convulsions fébriles etc.), est souvent à l'origine de la transformation d'un cerveau « sain » en cerveau épileptique. L'ensemble des processus responsables de cette transition s'appelle l'épileptogenèse. Pouvoir bloquer et/ou retarder l'épileptogenèse chez les patients à risque est une question de santé majeure. En plus des crises, l'ELT soulève d'autres questions. Elle est souvent associée à des déficits cognitifs, qui sont la conséquence de la réorganisation des circuits neuronaux. Ces déficits pourraient être traités de façon indépendante de l'épilepsie elle-même. Le projet de recherche de cette thèse s'inscrit dans ce cadre général
Temporal Lobe Epilepsy (TLE) is the most common form of epilepsy in adults. It translates into spontaneous and recurrent seizures, which are resistant to any treatment in 90% of cases. An initial brain insult (head injury, meningitis, febrile seizures etc.), is often the cause of the transformation of a "healthy" brain into an epileptic one. The process responsible for this transition is called epileptogenesis. Blocking and/or delaying epileptogenesis in at-risk patients is a key issue for public health. In addition to the seizures, TLE raises other problems. It is often associated with cognitive deficits, which are the result of the reorganization of neuronal circuits. These deficits may be treated independently of epilepsy itself. The work presented here fits into this general framework
APA, Harvard, Vancouver, ISO, and other styles
3

Sha, De-Yuan, and 沙德媛. "Suberoylanilide Hydroxamic Acid (SAHA) induced growth arrest and apoptosis in oral cancer cells." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/96988248837165394695.

Full text
Abstract:
碩士
臺灣大學
口腔生物科學研究所
95
Oral cancer is the fourth leading cause of cancer-related deaths in male population in Taiwan. Despite recent advances in radiotherapy and chemotherapy, the survival of patients with oral cancer has not improved significantly. Continued investigation of new chemotherapeutic agents is thus needed. Our recent studies have shown that histone deacetylase 2 (HDAC2) is overexpressed in 70% of oral cancer specimens. Furthermore, recent studies have shown that inhibitors of HDACs (HDACIs) possess antitumor activity and are well tolerated, supporting the idea that their use might develop as a specific strategy for cancer treatment. In this study, we investigated the effects and mechanisms of suberoylanilide hydroxamic acid (SAHA, one of the most potent HDAC inhibitors) on OSCC cell lines SAS and Ca9-22. Here, we demonstrated that SAHA induces apoptosis in human oral cancer cell lines SAS and Ca9-22 as evidenced by nuclear condensation, TUNEL labeling and cleavage of PARP. Apoptosis induced by SAHA was both time- and dose-dependent; however, the mechanisms are different in these two cells. In SAS cells, SAHA treatment induced DR5, FAS/FASL, FADD, caspase-8, -9 activation and Bid cleavage. In addition, SAHA treatment induced reactive oxygen species (ROS) production as detected by H2DCFDA fluorescence. Pretreatment of cells with N-acetyl cysteine (NAC) reduced the up-regulation of DR5, FAS, FADD and completely inhibited SAHA-induced apoptosis. These results indicated that ROS was an important mechanism for SAHA-induced apoptosis in SAS cells. SAHA-induced apoptosis was also completely inhibited in the presence of caspase 8 or caspase 9 inhibitors (Z-LEHD-FMK, Z-IETD-FMK). Taking together, SAHA induced apoptosis via subsequent induction of ROS, DR5, FADD, FAS/FASL, caspase-8 activation, Bid cleavage and then activation of mitochondrial pathway. In Ca9-22 cells, SAHA induced Bax protein expression, caspase 9 activation. In addition, we found SAHA down-regulated the expression of Bcl-2. Treatment caspase 9 inhibitor (Z-IETD-FMK) decreased SAHA induced apoptosis and the result was not more effective when both of caspase 8 and capase 9 inhibitors were treated. These data showed that SAHA-induced apoptosis by activating intrinsic- apoptosis pathway. We further evaluated the potential combinative effect of TRAIL and SAHA in OSCC cell lines. Compared with either TRAIL (20ng/ml) or SAHA (1
APA, Harvard, Vancouver, ISO, and other styles
4

Siddiquey, Mohammed Nure Alam. "Anti-tumor effects of suberoylanilide hydroxamic acid on Epstein-Barr virus-associated T cell and natural killer cell lymphoma." Thesis, 2014. http://hdl.handle.net/2237/20975.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Rzeczkowska, Paulina Agnieszka. "Regulation of the Timing of Puberty: Exploration of the Role of Epigenetics." Thesis, 2012. http://hdl.handle.net/1807/32622.

Full text
Abstract:
Pubertal timing displays wide, normally distributed variation in a healthy population of sexually maturing adolescents. However, like many complex traits, factors contributing to the variation are not well understood. Epigenetic regulation may contribute to some of the population variation. The role that epigenetics, specifically DNA methylation and histone acetylation, may play in regulating pubertal timing was investigated in C57BL/6 female mice: investigating whether population variation in pubertal timing among inbred mice could be explained by environmental factors; whether perturbing the epigenome using a histone deacetylase inhibitor or methyl-donor would alter pubertal timing; and examining genome-wide methylation patterns in hypothalami of early versus late maturing mice. Results demonstrate that measurable micro-environmental factors have only negligible effects on pubertal timing; pubertal timing was significantly altered by administration of epigenetic modifying agents; differences in methylation patterns are subtle. This initial evidence supports the involvement of epigenetic mechanisms in regulating pubertal timing.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Suberoylanilide Hydroxamic Acid (SAHA)"

1

Ganai, Shabir Ahmad. "HDAC Inhibitors Entinostat and Suberoylanilide Hydroxamic Acid (SAHA): The Ray of Hope for Cancer Therapy." In Molecular Life Sciences, 495–510. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-1531-2_503.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Ganai, Shabir Ahmad. "HDAC Inhibitors Entinostat and Suberoylanilide Hydroxamic Acid (SAHA): The Ray of Hope for Cancer Therapy." In Molecular Life Sciences, 1–16. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6436-5_503-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

"SAHA (suberoylanilide hydroxamic acid)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1753. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_14996.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

"Suberoylanilide Hydroxamic Acid." In Encyclopedia of Cancer, 4388. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_102207.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

"Suberoylanilide Hydroxamic Acid." In Encyclopedia of Cancer, 3552. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_5549.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Suberoylanilide Hydroxamic Acid (SAHA)"

1

Nikkhah, Mehdi, Jeannine S. Strobl, and Masoud Agah. "Study the Effect of Anticancer Drugs on Human Breast Cancer Cells Using Three Dimensional Silicon Microstructures." In ASME 2008 International Mechanical Engineering Congress and Exposition. ASMEDC, 2008. http://dx.doi.org/10.1115/imece2008-66680.

Full text
Abstract:
In this paper we report development of three dimensional silicon microenvironments in order to test the morphological changes and adhesion properties of human breast cancer cells after treatment with different anticancer drugs such as Trichostatin A (TSA), suberoylanilide hydroxamic acid (SAHA) and Scriptaid. Our results indicate that the cancer cells reorganize their cytoskeleton structure after treatment with TSA and Scriptaid. However, SAHA does not change the behavior of the cells inside the three dimensional microstructures while TSA and Scriptaid evoked striking changes in the cells morphology. TSA and Scriptaid drugs cause the cells to stretch inside the isotropic microchambers to avoid contact with curved sidewalls in contrast to their originally rounded shape. The proposed microstructures can be used to evaluate mechanical properties and the pathological grade of various cancer cell lines after different conditions i.e. drug exposure.
APA, Harvard, Vancouver, ISO, and other styles
2

Strobl, Jeannine S., Mehdi Nikkhah, Robert Rhoades, and Masoud Agah. "Effects of an Experimental Drug, Suberoylanilide Hydroxamic Acid (SAHA), on Attachment, Spreading, and Stiffness of Human Breast Cancer Cells on Silicon Substrates." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13037.

Full text
Abstract:
We are investigating silicon-based platforms for detection and analysis of breast cancer cells. Attachment and spreading of MDA-MB-231 human metastatic breast cancer cells was compared to that of non-tumorigenic human breast epithelial cells, MCF-10A, and the impact of SAHA (Vorinostat), a histone deacetylase (HDAC) inhibitor, on cell behaviors was ascertained. Our results showed the cancer cells attached to flat silicon and PECVD nitride-coated silicon more efficiently than non-cancer cells, and preferential cancer cell attachment was enhanced by SAHA. Fluorescent immunohistochemistry (IHC) revealed that SAHA stimulated actin stress fiber formation and focal adhesion to the substrates; atomic force microscopy (AFM) showed SAHA increased the cancer cell stiffness. Collectively, SAHA-induced biomechanical changes altered the cell morphology and mode of attachment to flat silicon and to three-dimensional silicon microstructures. This is the first report of the use of AFM to characterize the biomechanical effects of a HDAC inhibitor in cancer cells.
APA, Harvard, Vancouver, ISO, and other styles
3

Cheng, Hsuen-Tsen, and Wen-Chun Hung. "Abstract A9: The HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) inhibits vascular endothelial growth factor C-induced lymphangiogenesis." In Abstracts: AACR International Conference on Translational Cancer Medicine-- Jul 11-14, 2010; San Francisco, CA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcmusa10-a9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

McCormick, David L., Thomas L. Horn, William D. Johnson, Ronald A. Lubet, and Vernon E. Steele. "Abstract 1858: Inhibition of oral carcinogenesis in rats by the histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA)." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1858.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Kim, Soyeon, Tae Min Kim, Se-Hoon Lee, Dong-Wan Kim, and Dae Seog Heo. "Abstract 3500: Histone deacetylator (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA) sensitizes squamous carcinoma cells of lung to pemetrexed." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3500.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Khatua, Soumen, Joya Chandra, Miriam M. Morrell, Heather B. Meador, David I. Sandberg, Jeffrey Weinberg, Greg Fuller, et al. "Abstract CT113: A Phase I study of Suberoylanilide Hydroxamic Acid (SAHA) with Temsirolimus in children with newly diagnosed or progressive diffuse intrinsic pontine glioma (DIPG)." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-ct113.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Khatua, Soumen, Joya Chandra, Miriam M. Morrell, Heather B. Meador, David I. Sandberg, Jeffrey Weinberg, Greg Fuller, et al. "Abstract CT113: A Phase I study of Suberoylanilide Hydroxamic Acid (SAHA) with Temsirolimus in children with newly diagnosed or progressive diffuse intrinsic pontine glioma (DIPG)." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-ct113.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Santos, Javier V., Alex Vara, Craig Thomas, Medhi Wangpaichitr, Min You, Niramol Savaraj, and Dao M. Nguyen. "Abstract 3489: Profound cytotoxicity of the histone deacetylase inhibitor SAHA (Suberoylanilide Hydroxamic Acid) and TRAIL (Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand) combination in malignant pleural mesothelioma." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3489.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Chen, Fang-Hsin, Ching-Fang Yu, and Ji-Hong Hong. "Abstract 5844: Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, improved radiosensitivity of human hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5844.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Robertson, F., W. Woodward, W. Bornmann, A. Player, Z. Ye, and M. Cristofanilli. "The pan-HDAC Inhibitor Suberoylanilide Hydroxamic Acid Targets Self Renewal of Breast Cancer Stem Cells." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-3141.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Suberoylanilide Hydroxamic Acid (SAHA)' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography