Etoposide

Manufactured by Merck Group

Sourced in United States, Germany, United Kingdom, Japan, France, China, Italy, Canada, Switzerland, Belgium, Macao, Portugal, Poland

Etoposide is a chemotherapeutic agent used in the treatment of various types of cancer. It is a topoisomerase inhibitor that disrupts the process of DNA replication, leading to cell death. Etoposide is available as a solution for intravenous administration.

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Lab products found in correlation

Cisplatin, by Merck Group (110 mentions) Doxorubicin, by Merck Group (108 mentions) Dimethyl sulfoxide (dmso), by Merck Group (55 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (54 mentions) Camptothecin, by Merck Group (49 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (35 mentions) Paclitaxel, by Merck Group (34 mentions) Cycloheximide (chx), by Merck Group (33 mentions) Mg132, by Merck Group (27 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (27 mentions) Staurosporine, by Merck Group (26 mentions) Gemcitabine, by Merck Group (23 mentions) 5 fluorouracil, by Merck Group (22 mentions) Lipofectamine 2000, by Thermo Fisher Scientific (21 mentions) Actinomycin d, by Merck Group (21 mentions) Hydroxyurea, by Merck Group (20 mentions) Vincristine, by Merck Group (19 mentions) Propidium iodide, by Merck Group (19 mentions) Mitomycin c, by Merck Group (17 mentions) Rapamycin, by Merck Group (17 mentions)

848 protocols using etoposide

Cell Viability Assay with Sorafenib and Etoposide

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For the cell viability assays, the cells were seeded in 96-well plates at a density of 5000 cells/well (100 μL total volume/well) and were grown for 24 h. The cells were then washed with sterile phosphate-buffered saline and maintained in low-glucose (5.56 mM) DMEM supplemented with 10% FBS with/without sodium pyruvate (1 mM, Thermo Fisher Scientific, Waltham, MA, USA) for 24 h before adding the sorafenib (LC Laboratories, Woburn, MA, USA) or etoposide (Sigma-Aldrich, Saint Louis, MO, USA). The cells were treated with different concentrations of sorafenib or etoposide, and the controls were treated with vehicle (DMSO, Sigma-Aldrich). After 24-h treatment, WST-1 solution (DoGenBio, Seoul, South Korea) was added to the cells for 1–2 h, and the absorbance at 450 nm was then measured using a VICTORTMX3 Multilabel Plate Reader (PerkinElmer Inc., Waltham, MA, USA).

Kim D., Hwang C.Y, & Cho K.H. (2024). The fitness trade-off between growth and stress resistance determines the phenotypic landscape. BMC Biology, 22, 62.

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Cytotoxic Drug Preparation Protocol

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carboplatin (cat. no. C2538, Sigma), vincristine (cat. no. V8879, Sigma), and etoposide (cat. no. E1383, Sigma) were diluted to indicated concentrations with distilled water (carboplatin), methanol (vincristine), or DMSO (etoposide) for further experiments.

Jo D.H., Lee K., Kim J.H., Jun H.O., Kim Y., Cho Y.L., Yu Y.S., Min J.K, & Kim J.H. (2017). L1 increases adhesion-mediated proliferation and chemoresistance of retinoblastoma. Oncotarget, 8(9), 15441-15452.

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Comparative DNA Damage Response in MEFs and CHO Cells

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MEFs were generated from
B10^k.Rag1^−/− and
NOD^k.Rag1^−/−mice and
were treated with 5 μM etoposide (Sigma-Aldrich) for 1 h. MEFs were
allowed to recover for 15 h before fixation and staining with Alexa Fluor
647–conjugated antibody to phosphorylated H2A.X (Ser139; clone 2F3,
Biolegend) for flow cytometry.
CHO cells and Xrcc4^−/− CHO
cells were a kind gift from P. Jeggo (University of Sussex). Xrcc4 expression
vectors were constructed with the B10 or NOD allele of Xrcc4(or GFP control), preceded by a chicken β-actin intron
and followed by a sequence encoding GFP linked to the Xrcc4 C terminus via a T2A
peptide, under the control of the chicken β-actin promoter and CMV
enhancer. Xrcc4^−/− CHO cells were
transfected using Lipofectamine 3000 (Invitrogen), followed by treatment with 5
μM etoposide (Sigma-Aldrich) for 1 h, and cells were allowed to recover
for 15 h. Cell sorting was performed for GFP⁺ CHO cells on a
FACS Aria II (Becton Dickinson). GFP⁺ cells were stained with
the Zombie Aqua Fixable Viability kit (Biolegend) before fixation and staining
with Alexa Fluor 647–conjugated antibody to phosphorylated H2A.X
(Ser139; clone 2F3, Biolegend) and propidium iodide (eBioscience) for flow
cytometry analysis.

Dooley J., Tian L., Schonefeldt S., Delghingaro-Augusto V., Garcia-Perez J.E., Pasciuto E., Di Marino D., Carr E.J., Oskolkov N., Lyssenko V., Franckaert D., Lagou V., Overbergh L., Vandenbussche J., Allemeersch J., Chabot-Roy G., Dahlstrom J.E., Laybutt D.R., Petrovsky N., Socha L., Gevaert K., Jetten A.M., Lambrechts D., Linterman M.A., Goodnow C.C., Nolan C.J., Lesage S., Schlenner S.M, & Liston A. (2016). Genetic Predisposition for Beta Cell Fragility Underlies Type 1 and Type 2 Diabetes. Nature genetics, 48(5), 519-527.

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MTT Assay for Cell Viability

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At day 7 and 21 post-transduction, HMCs were seeded onto a 96-well plate at a concentration of 500 cells/well. Non-transduced HMCs were seeded at the same concentration, as a control. 10 μl of MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide, Sigma) diluted in ddH₂O (5 mg/ml) was added to each well, and the plate was incubated at 37 °C for 4 hours. Following incubation, 100 μl of dimethyl sulphoxide (DMSO, Sigma) was added to each well. Optical Density (OD) was read at 570 nm and 650 nm with an ELISA reader (Molecular Devices). In one set of experiments cells were treated at the time of the seeding with 5 μM DZnep.
To trigger apoptosis, HMCs were incubated with 50 μM of etoposide (Merck) for 24 h as follow. At day 7 post transduction miR302, scramble and non-transduced cells were seeded at confluency of 50%. The day after the cells were gently washed with PBS (Sigma) and fresh media was added along with 50 μM of etoposide. The cells were lysed in RIPA buffer after 24 h.

De Chiara L., Andrews D., Watson A., Oliviero G., Cagney G, & Crean J. (2017). miR302 regulates SNAI1 expression to control mesangial cell plasticity. Scientific Reports, 7, 42407.

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Etoposide Toxicity Assessment in Mice

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For etoposide assessment, adult mice were injected intraperitoneally with a single dose of etoposide (80 mg/kg body weight; Sigma; Lee et al., 1995 (link); Marchetti et al., 2006 (link)). After injection, the mice were monitored daily before being killed at 3, 5, or 8 d after treatment.

Hwang G., Verver D.E., Handel M.A., Hamer G, & Jordan P.W. (2018). Depletion of SMC5/6 sensitizes male germ cells to DNA damage. Molecular Biology of the Cell, 29(25), 3003-3016.

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Etoposide-Induced Apoptosis Pathway

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Etoposide (Sigma-Aldrich), was used at different concentrations as indicated, and kept throughout the experiments. Caffeine (Sigma-Aldrich, 1 mM) was used as inhibitor of ATM-mediated DNA damage response (Caputo et al., 2012 (link)) and added together with Etoposide. Phorbol 12-myristate 13-acetate (PMA, 200 ng/mL) was used as degranulating agent (Parmley et al., 1983 (link)) or as stimulator of oxidative burst (Collins et al., 1979 (link)), and kept for 30 min before either measurement. Z-DEVD-fmk (50 uM) was used to inhibit caspase-3; Z-VDVAD-fmk (2 uM) as caspase-2 inhibitor; Z-VAD-fmk (10 uM) as pan caspase-inhibitor. Each inhibitor was added 1 h before the apoptotic inducer.

Bruni E., Reichle A., Scimeca M., Bonanno E, & Ghibelli L. (2018). Lowering Etoposide Doses Shifts Cell Demise From Caspase-Dependent to Differentiation and Caspase-3-Independent Apoptosis via DNA Damage Response, Inducing AML Culture Extinction. Frontiers in Pharmacology, 9, 1307.

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Etoposide Treatment of Cell Lines

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Etoposide (Sigma, St. Louis, MO) was dissolved in Me₂SO and added to growth medium at final concentration of 10 uM. Cells were plated in 6-well plates for 24 h and replaced by growth medium with Etoposide for 3 days. Growth medium add Me₂SO only was as control.

Qian H., Xu X, & Niklason L.E. (2015). PCH-2 regulates Caenorhabditis elegans lifespan. Aging (Albany NY), 7(1), 1-11.

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Ras and Etoposide Senescence Induction

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For Ras-induced senescence, IMR90T-Ras-ERT2 were treated with 200 nM tamoxifen (Sigma) continuously for 10 days. Fresh media and tamoxifen were added every 2–3 days. Cells were treated with an equal volume of ethanol as control. On day 8 of Ras induction, media was replaced with serum-free media and harvested after 48 h. For etoposide-induced senescence, cells were treated with 50 μM etoposide (Sigma) or an equal volume of DMSO as a control for 48 hours. etoposide-containing medium was then replaced by normal culture media for 5 days. 7 days after etoposide treatment, media was replaced with serum-free media and harvested after 48 h. Conditioned media was aliquoted and flash frozen in liquid nitrogen before storing at −80 C.

Morales-Valencia J., Lau L., Martí-Nin T., Ozerdem U, & David G. (2022). Therapy-induced senescence promotes breast cancer cells plasticity by inducing Lipocalin-2 expression. Oncogene.

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Cytotoxicity Assay for Doxorubicin and Etoposide

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Doxorubicin (Sigma, St. Louis, MO, USA) and Etoposide (Sigma) stock solution (10 mM) was prepared by dissolving it in DMSO, and solution was diluted as ten concentration gradients from 0 μM to 2 μM for Doxorubicin and 0 μM to 16 μM for Etoposide before experiment. SK-N-BE(2) cells were plated at a density of 1 × 10⁴ cells per well in 96-well plates. After 24 h, cells were divided two groups and infected with pGC-shANXA2-LV or pGC-vector-LV. 48 h later, cells of two groups were treated with Doxorubicin and Etoposide respectively in the above ten concentration gradients for 72 h. Cell viability was determined using a Cell Counting Kit-8 (CCK-8) reagent (Yeasen, China) according to the manufacturer’s instructions. The absorbance of the samples at a wavelength of 450 nm was measured using a microplate reader (BioTek, USA). Drug-response curve was draw according the result of CCK-8 assay.

Wang Y., Chen K., Cai Y., Cai Y., Yuan X., Wang L., Wu Z, & Wu Y. (2017). Annexin A2 could enhance multidrug resistance by regulating NF-κB signaling pathway in pediatric neuroblastoma. Journal of Experimental & Clinical Cancer Research : CR, 36, 111.

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Ionizing Radiation and Etoposide Protocols

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For X-ray irradiation, cultured cells at 80% confluency were subjected to the indicated dose of radiation and then re-cultured in fresh medium for the indicated time. X-ray irradiation was delivered using an RS2000pro Ras Source biological X-ray irradiator (Rad Source Techologies, GA, USA) with a radiation output of 160 KV, 25 mA at a dose rate of 4.125 Gy/min.
For etoposide treatment, cells were treated with 40 μM etoposide (E1383, Sigma-Aldrich) for the indicated time, washed with phosphate-buffered saline (PBS) four times, and re-cultured in fresh medium for the indicated time before being harvested.
For micro-irradiation, cells were grown on a thin glass-bottom dish (Corning Incorporated, New York, NY, USA) and then sensitized by BrdU and locally irradiated with a 365 nm pulsed nitrogen UV laser (16 Hz pulse, 41% laser output) generated from a MicroPoint system (Andor Technology, Belfast, Ireland). This system was directly coupled to the epifluorescence path of a Nikon A1 confocal imaging system (Nikon, Tokyo, Japan). The relative intensity represents the gray-scale changes (I_t-I₀) calculated from at least 10 cells per treatment. The data represent the means ± standard deviation (SD). All data were analyzed in Image J.

Lu X., Tang M., Zhu Q., Yang Q., Li Z., Bao Y., Liu G., Hou T., Lv Y., Zhao Y., Wang H., Yang Y., Cheng Z., Wen H., Liu B., Xu X., Gu L, & Zhu W.G. (2019). GLP-catalyzed H4K16me1 promotes 53BP1 recruitment to permit DNA damage repair and cell survival. Nucleic Acids Research, 47(21), 10977-10993.

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