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Cisplatin

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Cisplatin is a platinum-based inorganic compound used in various laboratory applications. It is a colorless crystalline solid that is soluble in water and polar organic solvents. Cisplatin is commonly utilized as a reference standard or reagent in scientific research and analysis.

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Lab products found in correlation

Facs lyse, by BD (6 mentions) Facs perm 2, by BD (6 mentions) Gentlemacs dissociator, by Miltenyi Biotec (4 mentions) Paraformaldehyde (pfa), by Electron Microscopy Sciences (4 mentions) Permeabilization buffer, by Thermo Fisher Scientific (4 mentions) Paclitaxel, by Merck Group (3 mentions) 5 fluorouracil, by US Biological (3 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (3 mentions) Macs tissue storage solution, by Miltenyi Biotec (3 mentions) Dimethyl sulfoxide (dmso), by Merck Group (3 mentions) Helios mass cytometer, by Standard BioTools (3 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (3 mentions) Vincristine, by Merck Group (2 mentions) Verapamil, by Merck Group (2 mentions) 96 well deep well plates, by Merck Group (2 mentions) Cell id intercalator ir, by Standard BioTools (2 mentions) Mkn45, by American Type Culture Collection (2 mentions) Gefitinib, by Selleck Chemicals (2 mentions) Pd0325901, by Selleck Chemicals (2 mentions) Mycoalert mycoplasma detection kit, by Lonza (2 mentions)

59 protocols using cisplatin

1

Mass Cytometry Signaling in Human Bone Marrow

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Conditions were derived from prior mass cytometry signaling studies of healthy human bone marrow.4 (link) Briefly, cryopreserved cells were thawed into RPMI containing 10% fetal bovine serum, heparin (20 U/mL, Sigma, St. Louis, MO), and benzonase (25 mU/mL, Sigma), and labeled with cisplatin (2.5 μM, Enzo Life Sciences, Farmingdale, NY) in serum free RPMI.34 (link) cisplatin-treated cells were incubated in serum-containing RPMI for 30 minutes, followed by 1 hour incubation in the presence or absence of inhibitor (5 μM ruxolitinib or 2 μM IKK inhibitor VII), followed by 15 minute stimulation with cytokine and subsequent fixation and staining. Stimulation conditions in the screening experiment (Figure 1) were: basal (unstimulated), ruxolitinib, thrombopoietin (TPO, 50 ng/mL), TPO plus ruxolitinib, granulocyte colony stimulating factor (G-CSF, 20 ng/mL), and sodium pervanadate (125 μM). Subsequent experiments also included 2 μM IKKiVII, TNFα (20 ng/mL), and IKKiVII plus TNFα. Cytokines were obtained from Peprotech (Rocky Hill, NJ), ruxolitinib from Chemie-Tek (Indianapolis, IN), and IKKiVII from EMD Millipore (Billerica, MA). Intracellular TNFα profiling (Figure 6) included secretion inhibitor (brefeldin A/monensin, Ebioscience, San Diego, CA), and stimulation with phorbol-N-myristyl-acetate (PMA, Invivogen, San Diego, CA) and ionomycin (EMD Millipore).
Fisher D.A., Malkova O., Engle E.K., Miner C., Fulbright M.C., Behbehani G.K., Collins T.B., Bandyopadhyay S., Zhou A., Nolan G.P, & Oh S.T. (2016). Mass Cytometry Analysis Reveals Hyperactive NF Kappa B Signaling in Myelofibrosis and Secondary Acute Myeloid Leukemia. Leukemia, 31(9), 1962-1974.
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2

Mass Cytometry Signaling in Human Bone Marrow

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Conditions were derived from prior mass cytometry signaling studies of healthy human bone marrow.4 (link) Briefly, cryopreserved cells were thawed into RPMI containing 10% fetal bovine serum, heparin (20 U/mL, Sigma, St. Louis, MO), and benzonase (25 mU/mL, Sigma), and labeled with cisplatin (2.5 μM, Enzo Life Sciences, Farmingdale, NY) in serum free RPMI.34 (link) cisplatin-treated cells were incubated in serum-containing RPMI for 30 minutes, followed by 1 hour incubation in the presence or absence of inhibitor (5 μM ruxolitinib or 2 μM IKK inhibitor VII), followed by 15 minute stimulation with cytokine and subsequent fixation and staining. Stimulation conditions in the screening experiment (Figure 1) were: basal (unstimulated), ruxolitinib, thrombopoietin (TPO, 50 ng/mL), TPO plus ruxolitinib, granulocyte colony stimulating factor (G-CSF, 20 ng/mL), and sodium pervanadate (125 μM). Subsequent experiments also included 2 μM IKKiVII, TNFα (20 ng/mL), and IKKiVII plus TNFα. Cytokines were obtained from Peprotech (Rocky Hill, NJ), ruxolitinib from Chemie-Tek (Indianapolis, IN), and IKKiVII from EMD Millipore (Billerica, MA). Intracellular TNFα profiling (Figure 6) included secretion inhibitor (brefeldin A/monensin, Ebioscience, San Diego, CA), and stimulation with phorbol-N-myristyl-acetate (PMA, Invivogen, San Diego, CA) and ionomycin (EMD Millipore).
Fisher D.A., Malkova O., Engle E.K., Miner C., Fulbright M.C., Behbehani G.K., Collins T.B., Bandyopadhyay S., Zhou A., Nolan G.P, & Oh S.T. (2016). Mass Cytometry Analysis Reveals Hyperactive NF Kappa B Signaling in Myelofibrosis and Secondary Acute Myeloid Leukemia. Leukemia, 31(9), 1962-1974.
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3

Gastric Cancer Cell Culture Protocol

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AGS, NCI-N87, and MKN-45 cells were obtained from the America Type Culture Collection (ATCC). SNU-668 cells were obtained from the Korean Cell Line Bank (KCLB). AGS, MKN-45 and SNU-668 cells were maintained in RPMI 1640. NCI-N87 gastric cancer cell line was maintained in DMEM/F12. All media were supplemented with 10% FBS, 100 U/mL penicillin and 100 mg/mL streptomycin, and L-glutamine 2 mmol/L (“regular media”). Cancer cell lines were actively passaged for less than 6 months from the time that they were received from ATCC and United Kingdom Coordinating Committee on Cancer Research (UKCCCR) guidelines were followed (41 (link)). 5-fluorouracil was purchased from US Biological, and cisplatin was purchased from Enzo Life Sciences. PI3K inhibitor (LY294002), JNK inhibitor (SP600125), ERK inhibitor (U0126) and p38 MAP kinase inhibitor SB203580 were purchased from Calbiochem. Rac1 inhibitor (NSC23766) was purchased from Santa Cruz Biotechnology. 5-fluorouracil was purchased from US Biological, and cisplatin was purchased from Enzo Life Sciences. Gastric cancer cell lines were grown as spheroids and spheroids were counted as previously described (14 ).
Yoon C., Cho S.J., Chang K.K., Park D.J., Ryeom S.W, & Yoon S.S. (2017). Role of Rac1 pathway in epithelial-to-mesenchymal transition and cancer stem-like cell phenotypes in gastric adenocarcinoma. Molecular cancer research : MCR, 15(8), 1106-1116.
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4

Cytotoxicity Evaluation of Chemotherapeutics

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A modified MTT colorimetric assay was performed to determine the cytotoxicity of chemotherapeutic agents with or without an inhibitor as described previously [34]. In short, each cell line was evenly seeded into 96‐well plates at 5,000 cells/well one day before treatment. The cells were pretreated with or without TKIs (sitravatinib was purchased from ChemieTek [Indianapolis, IN, USA], and other TKIs were kindly provided as free sample from Selleckchem (Houston, TX, USA)] at indicated concentrations or with a reference inhibitor to ABCB1 or ABCC10 (verapamil [Sigma‐Aldrich, St. Louis, MO, USA] or cepharanthine [Apexbio Technology, Houston, TX, USA] at 3 µmol/L, respectively). Following 2 h pretreatment, cells were treated with serial‐diluted chemotherapeutic agents (paclitaxel [Sigma‐Aldrich], vincristine [Sigma‐Aldrich], doxorubicin [Enzo Life Sciences], and cisplatin [Enzo Life Sciences]). After 68 h treatment, MTT (Fisher Sci., NJ, USA) was added at a final concentration of 4 mg/mL, and cells were incubated at 37°C for another 4 h protected from light. The formazan crystals were dissolved using dimethyl sulfoxide (DMSO; Sigma‐Aldrich) after the supernatant was discarded. The light absorbance at 570 nm was determined using accuSkan™ microplate spectrophotometer (Fisher Sci.). All experiments were performed independently at least 3 times.
Yang Y., Ji N., Cai C., Wang J., Lei Z., Teng Q., Wu Z., Cui Q., Pan Y, & Chen Z. (2020). Modulating the function of ABCB1: in vitro and in vivo characterization of sitravatinib, a tyrosine kinase inhibitor. Cancer Communications, 40(7), 285-300.
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5

Mass Cytometry Staining Protocol

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Detailed staining protocols have been described (42 (link), 43 (link)). Briefly, cells were transferred to 96-well deep-well plates (Sigma), resuspended in 25 μM cisplatin (Enzo Life Sciences) for 1 min (44 (link)), and quenched with 100% serum. Cells were stained for 30 min on ice, fixed (BD FACS Lyse), permeabilized (BD FACS Perm II), and stained with intracellular antibodies for 45 min on ice. Staining panels are described in table S1. All antibodies were conjugated using MaxPar X8 labeling kits (DVS Sciences). Cells were suspended overnight in iridium interchelator (DVS Sciences) in 2% paraformaldehyde in phosphate-buffered saline (PBS) and washed 1× in PBS and 2× in H2O immediately before acquisition. Stained cells were analyzed on a mass cytometer (Fluidigm).
Strauss-Albee D.M., Fukuyama J., Liang E.C., Yao Y., Jarrell J.A., Drake A.L., Kinuthia J., Montgomery R.R., John-Stewart G., Holmes S, & Blish C.A. (2015). Human NK cell repertoire diversity reflects immune experience and correlates with viral susceptibility. Science translational medicine, 7(297), 297ra115.
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6

Phenotypic Profiling of Activated T Cells

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Human frozen PBMCs were thawed and rested for 12–15h. The samples were washed with Ca- and Mg-free PBS (Sigma; D8537) and stained with 50µM Cisplatin (Enzo Life Sciences; ALX-400–040-M250) in PBS for 1 minute to exclude dead cells. The cells were washed and resuspended with Human TruStain FcX (Biolegend; 422302) for five minutes before adding the primary surface staining cocktail for 20m, washing and staining with the secondary surface cocktail for 20m. Intracellular staining was performed following fixation and permeabilization using the Maxpar Nuclear Antigen Staining Buffer Set (Fluidigm; 201063) for 60 minutes, after which cells were incubated overnight at 4°C with Maxpar Fix and Perm Solution containing 125nM Cell-ID Intercalator-Ir (Fluidigm; 201192A) for DNA staining. Cells were washed with MilliQ H2O and resuspended in MilliQ H2O spiked with 1/20th Maxpar EQ Four Element Calibration Beads (Fluidigm; 201078) to a density of <5×105 cells/mL. Data was acquired on a CyTOF 1.5 (Fluidigm) instrument. For analysis, FCS files on gated CD3+CLA+ cells were generated using FlowJo software (Tree Star, Inc.). t-distributed Stochastic Neighbor Embedding (t-SNE) analysis was performed in R using the cytofkit R package, and clustering was performed with FlowSOM.
Klicznik M.M., Morawski P.A., Höllbacher B., Varkhande S.R., Motley S., Kuri-Cervantes L., Goodwin E., Rosenblum M.D., Long S.A., Brachtl G., Duhen T., Betts M.R., Campbell D.J, & Gratz I.K. (2019). Human CD4+CD103+ cutaneous resident memory T cells are found in the circulation of healthy subjects. Science immunology, 4(37), eaav8995.
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7

Gastric Cancer Cell Line Characterization

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SNU-638, SNU-719, AGS, and NCI-N87 (subsequently referred to as N87) are Lauren intestinal-type gastric adenocarcinoma cell lines, and KATOIII, SNU-668, SNU-601, and MKN-45 are Lauren diffuse-type gastric adenocarcinoma cell lines. AGS, N87, SNU-601, and MKN-45 cells were obtained from the America Type Culture Collection (ATCC). SNU-638, SNU-719, KATOIII, and SNU-601 are from the Korean Cell Line Bank (KCLB). KATOIII cells were maintained in Dulbecco’s modified Eagle’s medium (DMEM). All other gastric cancer cell lines were maintained in RPMI 1640. All media were supplemented with 10% FBS, 100 U/mL penicillin and 100 mg/mL streptomycin, and L-glutamine 2 mmol/L (“regular media”). Cancer cell lines were actively passaged for less than 6 months from the time that they were received from ATCC, and UKCCCR guidelines were followed (13 (link)). 5-fluorouracil was purchased from US Biological, and cisplatin was purchased from Enzo Life Sciences. RhoA inhibitor (Rhosin), PI3K inhibitor (LY294002), JNK inhibitor (SP600125), MEK I and II inhibitor (U0126) and p38 MAP kinase inhibitor (SB202190) were purchased from Calbiochem. ROCK inhibitor (Fasudil) was purchased from Abcam.
Yoon C., Cho S.J., Aksoy B.A., Park D.J., Schultz N., Ryeom S.W, & Yoon S.S. (2015). Chemotherapy resistance in diffuse type gastric adenocarcinoma is mediated by RhoA activation in cancer stem-like cells. Clinical cancer research : an official journal of the American Association for Cancer Research, 22(4), 971-983.
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8

Molecular Profiling of Nuclear Receptors

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Thiazolyl Blue Tetrazolium Bromide (MTT), 3, 3′, 5 Triiodothyronine and puromycin were obtained from Sigma (St. Louis, MO). MEM, RPMI 1640, DMEM, L-glutamine, penicillin/streptomycin, SeaPlaque™ Agarose was from Lonza (Walkersville, MD). Fetal bovine serum was from Gemini Bio Products, (West Sacramento, CA). Lipofectamine LTX, SuperScript® III Reverse Transcriptase and qPCR probes (ESR1, THRB, COUP-TF1 and GAPDH) were provided by Life Technologies (Grand Island, NY). The renilla luciferase assay kit was from Promega (Madison, WI). TRβ and GAPDH antibodies were from Santa Cruz Biotechnology (Dallas, TX). Total ERα antibody was from Vector Laboratories (Burlingame, CA). AR, c-PARP, PARP, c-Caspase 3, Caspase 3, pPKA and PKA antibodies were from Cell Signaling Technology (Beverly, MA). ChemiGlow Chemiluminescent Substrate kit was from Protein Simple (Santa Clara, CA). Docetaxel and doxorubicin were from LC Laboratories (Woburn, MA). Cisplatin was from ENZO (Plymouth Meeting, PA). c-AMP inhibitor bupivacaine and H89 were obtained from Selleck Chemicals (Houston, TX)..
Gu G., Gelsomino L., Covington K.R., Beyer A.R., Wang J., Rechoum Y., Huffman K., Carstens R., Ando S, & Fuqua S.A. (2015). Targeting Thyroid Hormone Receptor Beta in Triple Negative Breast Cancer. Breast cancer research and treatment, 150(3), 535-545.
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9

Establishing Cisplatin-Resistant Breast Cancer Cell Lines

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All cell lines (MDA-MB-157, MDA-MB-468, MDA-MB-231, HCC38, HCC1937, HS578T) were obtained from the Massachusetts General Hospital Center for Molecular Therapeutics bank and subjected to high-density SNP genotyping to confirm their identity. Cells were grown in RPMI medium (Lonza) supplemented with 10% FBS (Sigma) as well as 1% penicillin/streptomycin (Gibco), and were used up to a maximum of 20 passages following thawing. Cell lines were tested negative for Mycoplasma using MycoAlert Mycoplasma Detection Kit (Lonza). Cisplatin resistance state cells were generated using a previously reported protocol (13 (link)). Cisplatin (Enzo Life Sciences) was dissolved in 0.9% sodium chloride; PD0325901 (Selleck Chemicals) and gefitinib (Selleck Chemicals) were dissolved in DMSO.
Koh S.B., Ross K., Isakoff S.J., Melkonjan N., He L., Matissek K.J., Schultz A., Mayer E.L., Traina T.A., Carey L.A., Rugo H.S., Liu M.C., Stearns V., Langenbucher A., Saladi S.V., Ramaswamy S., Lawrence M.S, & Ellisen L.W. (2021). RASAL2 Confers Collateral MEK/EGFR Dependency in Chemoresistant Triple-Negative Breast Cancer. Clinical Cancer Research, 27(17), 4883-4897.
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10

Cisplatin-induced Bone Marrow Protection

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Cisplatin (Enzo; 10 mg per kg of body weight, once per week) was used for chemotherapy, and the mice received i.p. injections of Cisplatin for 7 weeks. To investigate the protective effect of NPY against Cisplatin-induced BM dysfunction, the mice received i.p. injections of NPY (Bachem; 50 μg per kg body weight, H-6375) daily during the 7-week Cisplatin-treatment period. After 1 h from the last injection, the BM and blood were collected and analyzed.
Park M.H., Jung I.K., Min W.K., Choi J.H., Kim G.M., Jin H.K, & Bae J.S. (2017). Neuropeptide Y improves cisplatin-induced bone marrow dysfunction without blocking chemotherapeutic efficacy in a cancer mouse model. BMB Reports, 50(8), 417-422.
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