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Suberoylanilide hydroxamic acid saha

Manufactured by Selleck Chemicals
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About the product

Suberoylanilide hydroxamic acid (SAHA) is a synthetic compound used in laboratory research. It functions as a histone deacetylase (HDAC) inhibitor, which can potentially influence gene expression and cellular processes.

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Spelling variants (same manufacturer)

Suberoylanilide hydroxamic acid - 10 citations

Similar products (other manufacturers)

Suberoylanilide hydroxamic acid (SAHA) (by Merck Group) - 46 citations Suberoylanilide hydroxamic acid (SAHA) (by Cayman Chemical) - 39 citations Suberoylanilide hydroxamic acid (by Merck Group) - 36 citations Suberoylanilide hydroxamic acid (by Cayman Chemical) - 26 citations Suberoylanilide hydroxamic acid (SAHA) (by Cayman Biochemical) - 3 citations Suberoylanilide hydroxamic acid (SAHA (by Chemietek) - 3 citations Suberoylanilide Hydroxamic Acid (SAHA, (by Santa Cruz Biotechnology) - 3 citations Suberoylanilide hydroxamic acid (by Alexis Biochemicals) - 3 citations Suberoylanilide hydroxamic acid (by Aton Pharma) - 3 citations Suberoylanilide hydroxamic acid (vorinostat; SAHA) (by Cayman Chemical) - 3 citations

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18 protocols using «suberoylanilide hydroxamic acid saha»

1

Cell Viability Assay with Epigenetic Drugs

2024
Cell viability assays were performed with four to six different cell lines. Cell numbers were optimized for 80% confluency in 96- or 384-well plates, respectively. Drugs targeting different epigenetic modifiers (trametinib (LKT), decitabine (Sigma-Aldrich), JQ1 (Cayman), suberoylanilide hydroxamic acid (SAHA) (Selleckchem), mocetinostat (Selleckchem) dissolved in dimethyl sulfoxide (DMSO) (Sigma-Aldrich) were printed in the indicated logarithmic concentration ranges using the D300e Digital Dispenser (Tecan). The DMSO concentration in each well was adjusted to the highest value on the plate which was set to < 0.1% of the assay volume. Sealed plates were frozen at − 80 °C until use.
Cells were detached by 0.05% trypsin—ethylenediamine tetraacetic acid (EDTA) (1x) (Thermo Fisher Scientific) and recovered by centrifugation. Optimized cell numbers for 80% confluency at the end of experiment were seeded with the Multidrop Combi Dispenser (Thermo Fisher Scientific) onto the pre-printed plates and incubated at 37°C and 5% CO2.
Cell viability was determined using the CellTiter-Glo® Luminescent Cell Viability Assay (Promega) according to manufacturer’s instruction. The luminescence signal was measured with a Tecan Spark® 10 M multiplate reader (Tecan) for 500 ms.
Data were normalized to the signal of DMSO treated cells. IC50 determination was performed using the Graph Pad Prims v. 7.03 ‘log (inhibitor) vs. response (three parameters)’ equation.
Synergism was analyzed by applying the Loewe [43 (link)] method implemented in Combenefit v. 2.02 [44 (link)].
Godfrey L.K., Forster J., Liffers S.T., Schröder C., Köster J., Henschel L., Ludwig K.U., Lähnemann D., Trajkovic-Arsic M., Behrens D., Scarpa A., Lawlor R.T., Witzke K.E., Sitek B., Johnsen S.A., Rahmann S., Horsthemke B., Zeschnigk M, & Siveke J.T. (2024). Pancreatic cancer acquires resistance to MAPK pathway inhibition by clonal expansion and adaptive DNA hypermethylation. Clinical Epigenetics, 16, 13.
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2

Exploring Epigenetic and Signaling Modulators

2023
Using dimethylsulfoxide (DMSO) treated cells as controls, cells were treated with Temsirolimus (TEMS, #50-811-7, Fisher Scientific, Pittsburgh, PA) at a final concentration of 2μM, as described in our prior work (17 (link)). Likewise, as earlier described (24 (link)), 5-Azacytidine (AZA, #S1782, Selleck Chemicals, Houston, TX) was utilized at a final concentration of 1μM while Suberoylanilide hydroxamic acid (SAHA, #S1047, Selleck Chemicals, Houston, TX) was utilized at a final concentration of 50μM. Lysophosphatidic acid (LPA, as a sodium salt in chloroform, #857130C, Avanti Polar Lipids, Alabaster, AL) was utilized at a final dose of 10μM, as previously described (17 (link)). D-erythro-Sphingosine-1-Phosphate (S1P, #860492, Avanti Polar Lipids, Alabaster, AL) was utilized at a final concentration of 250nM. Deferoxamine mesylate (DFO, #D9533, Sigma-Aldrich, St. Louis, MO) was utilized at a final concentration of 10μM, as described in our earlier work (25 (link)).
Chhabra R., Guergues J., Wohlfahrt J., Rockfield S., Espinoza Gonzalez P., Rego S., Park M.A., Berglund A.E., Stevens SM J.r, & Nanjundan M. (2023). Deregulated expression of the 14q32 miRNA cluster in clear cell renal cancer cells. Frontiers in Oncology, 13, 1048419.
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3

Generation of Latent HIV-1 Infected Haploid Cell Lines

2021
We used a strategy described previously (56 (link), 57 (link)) to generate latent HIV-1 infected KBM7 haploid cell lines. Minimal HIV-1 (LTR-GFP, HIV-1-658) (65 (link)) virus was produced by transfection of 293T cells in 15-cm culture dishes using polyethylenimine (PEI) (Sigma-Aldrich) with a mixture of 6.8 μg p658, 2 μg vesicular stomatitis virus G (VSVG), and 4.5 μg Gag-Pol plasmids. Haploid KBM7 cells were infected with HIV-1-derived virus at low MOI such that approximately 5 to 10% of cells became productively infected as determined by GFP expression. Five days after infection, the GFP-negative cell population harboring uninfected and potentially latently infected cells was sorted by flow cytometry-activated cell sorting (FACS) and stimulated with 350 nM suberoylanilide hydroxamic acid (SAHA) (Selleck Chem), and 5 ng/μl TNF-α (Sigma-Aldrich). Twenty-four hours poststimulation, GFP-positive cells were single cell sorted by FACS into 96-well plates. Clones were expanded and characterized for their basal GFP expression and their potential for reactivation. From the clonal cell lines generated, Hap-Lat was selected for low background and relative high reactivation upon stimulation (GFP negative under basal conditions but able to be induced to express GFP upon activation).
Röling M., Mollapour Sisakht M., Ne E., Moulos P., Crespo R., Stoszko M., De Crignis E., Bodmer H., Kan T.W., Akbarzadeh M., Harokopos V., Hatzis P., Palstra R.J, & Mahmoudi T. (2021). A Two-Color Haploid Genetic Screen Identifies Novel Host Factors Involved in HIV-1 Latency. mBio, 12(6), e02980-21.
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4

HDAC Inhibitors Effect on RSTS LCLs

2021
Lymphoblastoid cell lines (LCLs) from eight different RSTS patients (four carrying CREBBP mutations and four carrying EP300 mutations, listed in Table S1) [20 (link),51 (link),52 (link),53 (link)] and seven healthy donors were obtained in collaboration with the Gaslini Genetic Bank service (Telethon Network of Genetic Biobanks); their use was approved by Ethics Committee of Università degli Studi di Milano (Comitato Etico number 99/20, 17 November 2020). Cells were maintained in RPMI 1640 culture medium supplemented with L-glutamine (Euroclone, Pero, Italy), 20% fetal bovine serum (Euroclone, Pero, Italy), and penicillin/streptomycin (Euroclone, Pero, Italy), and cultured in an incubator with 5% CO2 at 37 °C.
LCLs were exposed to four different HDAC inhibitors: Trichostatin A (TSA) (sc-3511, Santa Cruz Biotechnology, Dallas, TX, USA), Suberoylanilide hydroxamic acid (SAHA) (MK0683, Selleckchem, Houston, TX, USA), Valproic acid (VPA) (P4543, Sigma Aldrich, St. Louis, MO, USA), and Sodium Butyrate (NaB) (B5887, Sigma-Aldrich, St. Louis, MO, USA). We tested three different concentrations for each HDACi (Table S2) [54 (link),55 (link),56 (link),57 (link),58 (link),59 (link)] and selected the maximum dose and timing of exposure, ensuring acceptable LCLs survival (data not shown). Cells were incubated with vehicles (H2O or DMSO) at the maximum time (24 h), TSA 2 µM for 2 h, SAHA 2 µM for 24 h, VPA 2 mM for 24 h, or NaB 5 mM for 24 h as suggested from the literature (Table S2). Data were normalized on untreated cells and in vehicles for accounting for proliferation rate differences in basal condition between HD and RSTS lines.
Di Fede E., Ottaviano E., Grazioli P., Ceccarani C., Galeone A., Parodi C., Colombo E.A., Bassanini G., Fazio G., Severgnini M., Milani D., Verduci E., Vaccari T., Massa V., Borghi E, & Gervasini C. (2021). Insights into the Role of the Microbiota and of Short-Chain Fatty Acids in Rubinstein–Taybi Syndrome. International Journal of Molecular Sciences, 22(7), 3621.
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5

Apoptosis Induction in Cancer Cells

2020
Doxorubicin (Dox, HY‐15142; MedChem Express, Monmouth Junction, NJ, USA), etoposide (HY‐13629; MedChem Express), nutlin‐3a (SC4368; Beyotime, Shanghai, China), MG132 (S1748; Beyotime), cycloheximide (CHX, 2112S; CST, Beverly, MA, USA), suberoylanilide hydroxamic acid (SAHA, S1047; Selleck Chemicals, Houston, TX, USA) were used. PBS was used as vehicle control for Dox, and DMSO as control for etoposide, nutlin‐3a, SAHA, CHX, and MG132.
Zhang L., Yang J., Luo Y., Liu F., Yuan Y, & Zhuang S. (2020). A p53/lnc‐Ip53 Negative Feedback Loop Regulates Tumor Growth and Chemoresistance. Advanced Science, 7(21), 2001364.
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Top 5 protocols citing «suberoylanilide hydroxamic acid saha»

1

SAHA Compound Preparation and Dosage

Suberoylanilide hydroxamic acid (SAHA) (clinically known as Vorinostat [57 (link), 64 (link)]) (Selleckchem, Houston, TX) was dissolved in 100% ethanol to obtain a 10mM stock. Final working concentration used was 0.8uM.
Kasar S., Underbayev C., Yuan Y., Hanlon M., Aly S., Chang V., Batish M., Gavrilova T., Badiane F., Degheidy H., Marti G, & Raveche E. (2013). Therapeutic Implications of Activation of the Host Gene (Dleu2) Promoter for miR-15a/16-1 in Chronic Lymphocytic Leukemia (CLL). Oncogene, 33(25), 3307-3315.
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2

SAHA Compound Preparation and Dosage

Suberoylanilide hydroxamic acid (SAHA) (clinically known as Vorinostat [57 (link), 64 (link)]) (Selleckchem, Houston, TX) was dissolved in 100% ethanol to obtain a 10mM stock. Final working concentration used was 0.8uM.
Kasar S., Underbayev C., Yuan Y., Hanlon M., Aly S., Chang V., Batish M., Gavrilova T., Badiane F., Degheidy H., Marti G, & Raveche E. (2013). Therapeutic Implications of Activation of the Host Gene (Dleu2) Promoter for miR-15a/16-1 in Chronic Lymphocytic Leukemia (CLL). Oncogene, 33(25), 3307-3315.
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3

Cytotoxicity and Cell Cycle Assay of Luteolin

Cell culture and MTT assay. Human cell lines with known invasive ability, including HCT116 human colon carcinoma cells, MDA-MB-231 human breast carcinoma cells, A549 human lung carcinoma cells, PC-3 human prostatic carcinoma cells and ES-2 human ovarian clear cell adenocarcinoma cells, and B16-F10 murine melanoma cells were purchased from the Cell Bank of Type Culture Collection of the Chinese Academy of Sciences. B16-F10 cells were cultured in DMEM-high glucose (Gibco; Thermo Fisher Scientific, Inc.) and all other cells were cultured in RPMI-1640 medium (Gibco; Thermo Fisher Scientific, Inc.). All cell cultures were supplemented with 10% (v/v) fetal bovine serum (Gibco; Thermo Fisher Scientific, Inc.) and 2 mM L-glutamine, and cells were incubated in a humidified incubator with 5% CO 2 at 37˚C.
Cell viability was assessed using a MTT assay. Briefly, 5,000 HCT116, MDA-MB-231, A549, PC-3 or ES-2 cells/well were plated in a 96-well plate and incubated in a humidified incubator with 5% CO 2 at 37˚C, allowed to adhere for 4 h, then treated with different concentrations of luteolin (1.562, 3.125, 6.25,12.5, 25, 50, 100, 250 an 500 mM) (Shanghai Aladdin Bio-Chem Technology Co., Ltd.). Suberoylanilide hydroxamic acid (SAHA) (catalog no. S1047; Selleck Chemicals) was used as a positive control. After 48 h, 0.5% MTT solution was added to each well and incubated for 4 h. DMSO was then added to dissolve the formazan, and the optical density was measured at 570 nm using an EnSpire plate reader (PerkinElmer, Inc.).
Cell cycle analysis. MDA-MB-231 cells were seeded in 6-well plates at a density of 4x10 5 /well. Following incubation overnight, cells were treated with 3, 10 or 30 µM Luteolin dissolved in DMSO solution in a humidified incubator with 5% CO 2 at 37˚C. Control wells were treated with equal volumes of DMSO. Following 48 h of treatment, cells were harvested and fixed with 70% (v/v) ethanol/phosphate buffer at 4˚C overnight. The cells were washed with PBS twice and incubated with DNase-free RNase A (Beijing Solarbio Science & Technology, Co., Ltd.) at a concentration of 1 mg/ml for 30 min, then stained with propidium iodide (PI; 50 µg/ml; Beijing Solarbio Science & Technology, Co., Ltd.) for 30 min at room temperature in the dark. The DNA content was measured using a flow cytometer (FACS Aria III; BD Biosciences) and analyzed using FlowJo V10 software (FlowJo LLC).
Feng J., Zheng T., Hou Z., Lv C., Xue A., Han T., Han B., Sun X, & Wei Y. (2020). Luteolin, an aryl hydrocarbon receptor ligand, suppresses tumor metastasis in vitro and in vivo. Oncology reports, 44(5).
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4

Investigating Synergistic Anti-Cancer Effects

Suberoylanilide hydroxamic acid (SAHA, vorinostat), LBH589 (panobinostat), MS275 (entinostat), lenalidomide (Len), pomalidomide (Pom) and bortezomib (BTZ) were purchased from Selleck Chemicals (Houston, TX, USA). HDAC6 inhibitor ACY1215 (ricolinostat) was obtained from ChemieTek (Indianapolis, IN, USA). Anti-acetylated α-tubulin antibody (Ab) and -cereblon Abs were purchased from Sigma (St. Louis, MO, USA). Anti-c-Myc, anti-acetylated lysine, anti-glyceraldehyde 3-phosphate dehydrogenase (GAPDH), anti-caspase-8, anti-caspase-9, anti-cleaved-caspase-3, anti-poly (ADP-ribose) polymerase (PARP), anti-X-linked inhibitor of apoptosis protein (XIAP), Bcl2, anti-cIAP2, anti-α-tubulin, phospho-STAT3, HDAC6, IKZF1, IKZF3 and IRF4 Abs were obtained from Cell Signaling Technology (Danvers, MA, USA). Anti-IKZF1 Abs were purchased from Cell Signaling Technology or R&D Systems (Minneapolis, MN, USA) Figure 4d. Human interleukin-6, insulin-like growth factor 1, vascular endothelial growth factor and tumor necrosis factor α were obtained from R&D Systems.
Hideshima T., Cottini F., Ohguchi H., Jakubikova J., Gorgun G., Mimura N., Tai Y.T., Munshi N.C., Richardson P.G, & Anderson K.C. (2015). Rational combination treatment with histone deacetylase inhibitors and immunomodulatory drugs in multiple myeloma. Blood Cancer Journal, 5(5), e312-.
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5

SAHA Otoprotection Against Noise Exposure

Mice were injected intraperitoneally with suberoylanilide hydroxamic acid (SAHA) (Selleckchem, TX), (100 mg/kg body weight) dissolved in DMSO (MilliporeSigma, MA), or with DMSO alone (vehicle) 3 days before exposure to noise and 2 h after the end of the noise exposure. The SAHA dosing amount was based on a previous publication using SAHA as an otoprotective agent, where the authors tried different dose concentrations of SAHA and reported a 100 mg/kg dose to be most efficacious without cytotoxicity [12 (link)]. Because studies vary in their dosing regimen for SAHA, the frequency of the dosing was based on the published literature with minor modifications [14 (link), 31 (link)].
Milon B., Mitra S., Song Y., Margulies Z., Casserly R., Drake V., Mong J.A., Depireux D.A, & Hertzano R. (2018). The impact of biological sex on the response to noise and otoprotective therapies against acoustic injury in mice. Biology of Sex Differences, 9, 12.
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