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Apicidin

Manufactured by Merck Group
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Sourced in United States, Germany

Apicidin is a laboratory product manufactured by Merck Group. It is a histone deacetylase (HDAC) inhibitor, a class of compounds that can be used to study cellular processes and biochemical pathways.

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Lab products found in correlation

Fetal bovine serum (fbs), by Thermo Fisher Scientific (6 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (4 mentions) Trichostatin a, by Merck Group (4 mentions) Droxinostat, by Selleck Chemicals (4 mentions) Unc0638, by Merck Group (3 mentions) Ms 275, by Selleck Chemicals (3 mentions) Mc1568, by Merck Group (3 mentions) Puromycin, by InvivoGen (3 mentions) Cycloheximide (chx), by Merck Group (3 mentions) Paclitaxel, by Selleck Chemicals (2 mentions) Mgcd0103, by Selleck Chemicals (2 mentions) Doxirubicin, by Selleck Chemicals (2 mentions) Mc1568, by Selleck Chemicals (2 mentions) Mc1575, by Merck Group (2 mentions) Gsk126, by Cayman Chemical (2 mentions) 5 fluorouracil, by Merck Group (2 mentions) Sirtinol, by Merck Group (2 mentions) Jib 04, by Merck Group (2 mentions) Gsk lsd1, by Merck Group (2 mentions) Mithramycin a, by Merck Group (2 mentions)

32 protocols using apicidin

1

NIH3T3 Cell Culture and Compound Treatment

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NIH3T3 cells were cultured in Dulbecco’s modified Eagle’s medium (Gibco, USA) supplemented with 10% fetal bovine serum (Gibco, USA) and 1% penicillin/streptomycin (Gibco, USA). Cells were incubated at 37 °C in a humidified 5% CO2 incubator. Cells were treated with 1 μM UNC0638 (Sigma, USA) or 2 μM apicidin (Sigma, USA) for 96 or 48 h, respectively, and compound-containing media was refreshed every 24 h.
Kang J.G., Park J.S., Ko J.H, & Kim Y.S. (2019). Regulation of gene expression by altered promoter methylation using a CRISPR/Cas9-mediated epigenetic editing system. Scientific Reports, 9, 11960.
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2

Breast Cancer and Leukemia Cell Lines

Cited 2 times
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MCF7 and T47D ER+, and BT-20 and MDA-MB-231 ER- human breast cancer, and K562 leukemia cells were obtained from commercial sources; the American Type Culture Collection (ATCC), USA. The chemicals Doxorubicin hydrochloride (DOX; Pfizer), Tamoxifen (TAM; Cayman Chemical), phenformin (Sigma), Trichostatin A (TSA; Sigma), estradiol (Cayman Chemical), Apicidin (Sigma), and Troglitazone (TRG; Calbiochem) were acquired from the indicated providers. All treatment compounds were reconstituted in dimethylsulfoxide (DMSO) except metformin (Sigma), which was reconstituted in molecular-grade water (Hyclone). The HDACi assay and in vitro hypoxia experiments were conducted as previously described [14 (link)]. MCF7 and K562 parental cells were selected for drug resistance according to our published methods [14 (link), 15 (link)].
Davies G., Lobanova L., Dawicki W., Groot G., Gordon J.R., Bowen M., Harkness T, & Arnason T. (2017). Metformin inhibits the development, and promotes the resensitization, of treatment-resistant breast cancer. PLoS ONE, 12(12), e0187191.
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3

Autophagy Inhibitor and Cell Viability

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A specific autophagy inhibitor chloroquine (CQ; 50 µM; Sigma-Aldrich; Merck KGaA) was co-treated with apicidin (Sigma-Aldrich; Merck KGaA) in AT-84 cells for 24 h at 37°C. Following treatment, cell proliferation was measured using a trypan blue exclusion assay. The trypan blue exclusion assay was based on the capability of viable cells to exclude the dye. After 5 min of treatment of cells with 0.4% trypan blue (Sigma-Aldrich; Merck KGaA) at room temperature, they were loaded into a hemocytometer and counted for the dye uptake. The number of viable cells was calculated as the percentage of the total cell population.
, & Ahn M.Y. (2018). HDAC inhibitor apicidin suppresses murine oral squamous cell carcinoma cell growth in vitro and in vivo via inhibiting HDAC8 expression. Oncology Letters, 16(5), 6552-6560.
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4

Evaluating Short-Term Drug Effects on Cell Growth

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To assess effect of short-term drug pretreatment on 2D/3D growth, cells are plated in six-well plates and allowed to recover for 24 h. At this point, drug-containing media was added to each well. After 24 h of treatment, cells were then were plated for mammospheres or 2D proliferation assays. 2D proliferation was determined after 3 days by viable cell counts, and assessed as a percentage of the DMSO control. All treatments were carried out in triplicate, and repeated a minimum of three times. The error bars represent the standard error of the mean of the three replicates. The small molecule drugs that are used to treat the cells for various experiments are: TSA (Selleck) Doxirubicin (Selleck), Paclitaxel (Selleck), 5-Fluorouracil (Sigma), SAHA (Selleck), GSK126 (Cayman Chem), MS275 (Selleck), MGCD0103 (Selleck), MC1568 (Selleck), MC1575 (Gift of Dr. Antonello Mai), Apicidin (Sigma), Droxinostat (Selleck). All drugs are prepared in DMSO, which was used as vehicle control in each assay.
Witt A.E., Lee C.W., Lee T.I., Azzam D.J., Wang B., Caslini C., Petrocca F., Grosso J., Jones M., Cohick E.B., Gropper A.B., Wahlestedt C., Richardson A.L., Shiekhattar R., Young R.A, & Ince T.A. (2016). Identification of a cancer stem cell-specific function for the histone deacetylases, HDAC1 and HDAC7, in breast and ovarian cancer. Oncogene, 36(12), 1707-1720.
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5

Small Molecule Inhibition Screening

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For all small molecule inhibition studies, the drug was added on the day of encapsulation and replaced with each subsequent media change. The inhibitors used were GSK 126 (100 nM, Fisher Scientific), UNC 0638 (250 nM, Sigma), JIB-04 (1 μM, Sigma), GSK-J4 (10 μM, Abcam), GSK-LSD1 (100 nM, Sigma), Sirtinol (50 μM, Sigma), apicidin (1 μM, Sigma), mithramycin A (50 nM, Sigma), LY294002 (20 μM, Sigma) and SAHA (1 μM, Sigma). All drugs were dissolved in DMSO and diluted in basal medium before adding to the culture medium. DMSO alone was added to the culture medium as a vehicle control.
Stowers R.S., Shcherbina A., Israeli J., Gruber J.J., Chang J., Nam S., Rabiee A., Teruel M.N., Snyder M.P., Kundaje A, & Chaudhuri O. (2019). Matrix stiffness induces a tumorigenic phenotype in mammary epithelium through changes in chromatin accessibility. Nature biomedical engineering, 3(12), 1009-1019.
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6

Culturing Atxn3-WT and Atxn3-KO Mouse MEFs

Cited 1 time
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The MEFs from both Atxn3-WT and Atxn3-KO mice [27 (link)] were maintained in DMEM with 10% FBS, 1% Non-essential Amino Acids solution and 1% penicillin/streptomycin at 37° C and 5% CO2. Where needed, cells were treated with Trichostatin A (1μM; Calbiochem), Apicidin (0.1μg/ml; Sigma-Aldrich) or DMSO (Sigma-Aldrich).
Zeng L., Zhang D., McLoughlin H.S., Zalon A.J., Aravind L, & Paulson H.L. (2018). Loss of the Spinocerebellar Ataxia type 3 disease protein ATXN3 alters transcription of multiple signal transduction pathways. PLoS ONE, 13(9), e0204438.
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7

Analyzing Treg Precursor Cell Differentiation

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Sorted Treg precursor cells (CD4+Foxp3GFP–CD25+) were seeded into 96-well plates in the presence of medium alone or medium containing rmIL-2 (50U/ml). In another set of experiments, cells were treated with 100 nM Trichostatin A (Sigma, St. Louis, MO), 800 nM Apicidin (Sigma, St. Louis, MO), or DMSO (0.2%) and rmIL-22. 24 hrs later, cells were analyzed by flow cytometry.
Yi Z., Lin W.W., Stunz L.L, & Bishop G.A. (2014). The adaptor molecule TRAF3 restrains the lineage determination of thymic regulatory T cells by modulating interleukin-2 receptor signaling. Nature immunology, 15(9), 866-874.
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8

In Vitro Bradyzoite Differentiation Assay

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For in vitro bradyzoite differentiation assays, HFF were seeded in 6-W plates and infected with 10^6 tachyzoites. After 24 h, the medium was replaced and supplemented with 40 nM of the histone deacetylase inhibitor apicidin (Sigma-Aldrich) in order to promote bradyzoite differentiation(Bougdour et al., 2009 (link); Boyle et al., 2006 (link)). After 24 h for the untreated or 72 h for the apicidin-treated, parasites were released with a 23-G needle, lyzed in 1x Laemmli buffer (Bio-Rad) containing 10 % 2-mercaptoethanol (Bio-Rad) and heated for 5 min at 70°C. Total cell lysates were forced through a 29-G needle, separated by electrophoresis on 15 % polyacrylamide gels and transferred to nitrocellulose membranes. Immunologic detection was performed using purified rabbit anti-SIINFEKL antisera (custom-made, Biotem, Grenoble) and mouse anti-GRA1 (Biotem) followed by horseradish peroxidase-conjugated antibodies (Promega). Peroxidase activity was visualized by chemiluminescence and quantified using a ChemiDoc XRS+ system (Bio-Rad).
Salvioni A., Belloy M., Lebourg A., Bassot E., Cantaloube-Ferrieu V., Vasseur V., Blanié S., Liblau R.S., Suberbielle E., Robey E.A, & Blanchard N. (2019). Robust control of a brain-persisting parasite through MHC I presentation by infected neurons. Cell reports, 27(11), 3254-3268.e8.
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9

Culturing and Stimulating Trichomonas vaginalis

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The T016 strain of T. vaginalis57 (link) was axenically subcultivated at 37 °C in Diamond’s trypticase–yeast extract–maltose (TYM) medium with 10% heat-inactivated horse serum (Gibco) and 0.5% penicillin/streptomycin (Gibco). T. vaginalis cells were stimulated with 70 nM apicidin (Sigma) or 1μM TSA (Sigma) for 4 hours for RNA-seq and ChIP-seq. Iron-rich medium and iron-restricted medium were supplemented with 250 μM ammonium iron (II) sulfate (Sigma) and 50 μM 2′-2-bipyridyl (Sigma), respectively.
Song M.J., Kim M., Choi Y., Yi M.H., Kim J., Park S.J., Yong T.S, & Kim H.P. (2017). Epigenome mapping highlights chromatin-mediated gene regulation in the protozoan parasite Trichomonas vaginalis. Scientific Reports, 7, 45365.
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10

Immortalized Bone Marrow-Derived MSCs

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Human bone marrow-derived MSC immortalized by the introduction of telomerase were kindly provided by Professor Yeon-Soo Kim (Inje University, Inje, South Korea). MSCs were cultured in Dulbecco's Modified Eagle's Medium (DMEM) with 10% fetal bovine serum and 1% penicillin/streptomycin (Gibco, USA). Cells were grown at 37°C in a humidified atmosphere of 95% air and 5% CO2, and the medium was changed every 3 days. Apicidin was purchased from Sigma-Aldrich (St Louis, MO, USA).
Cho D.I., Kang W.S., Hong M.H., Kang H.J., Kim M.R., Kim M.C., Kim Y.S, & Ahn Y. (2017). The optimization of cell therapy by combinational application with apicidin-treated mesenchymal stem cells after myocardial infarction. Oncotarget, 8(27), 44281-44294.
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