Cisplatin

Catalog No.S1166

Cisplatin Chemical Structure

Molecular Weight(MW): 300.05

Cisplatin is an inorganic platinum complex, which is able to inhibit DNA synthesis by conforming DNA adducts in tumor cells. DMF is recommended for dissolution.

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Cited by 85 Publications

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Biological Activity

Description Cisplatin is an inorganic platinum complex, which is able to inhibit DNA synthesis by conforming DNA adducts in tumor cells. DMF is recommended for dissolution.
Features One of the most widely used and most potent chemotherapeutic agents.
Targets
DNA synthesis [1]
(Tumor cells)
In vitro

Cisplatin induces cytotoxic by interaction with DNA to form DNA adducts which activate several signal transduction pathways, including Erk, p53, p73, and MAPK, which culminates in the activation of apoptosis. [1] Cisplatin (30 μM) treated for 6 h induces an apparent activation of Erk in HeLa cells, which is sustained over the following 14 h period. Cisplatin also shows an effective antineoplastic activity by inducing tumor cells death[2]. Cisplatin displays ability to cause renal proximal tubular cell (RPTC) apoptosis, causing cell shrinkage, a 50-fold increase in caspase 3 activity, a 4-fold increase in phosphatidylserine externalization, and 5- and 15-fold increases in chromatin condensation and DNA hypoploidy, respectively. [4] Cisplatin (800 μM) causes typical features of necrosis of RPTC after treatment for 4 hr. [5]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
Human osteosarcoma cells (HOS, 143B, U2OS and MG‑63) NVeyfow2S2WubDDjfYNt\SCjbnHsfZNqew>? MX2yJO69VQ>? NY[3[5NSPDhiaB?= NEj1UnVEcXOybHH0bY4hfHKnYYTt[Y51KG2jcnvl[Ix6KGmwY4LlZZNm\CC2aHWgS|IwVSCyb4D1cIF1cW:wIHnuJIFtdCClZXzsJIxqdmW|Lh?= MlmyN|ExPTlyOEO=
OVC cells (A2780, TOV-112D, and cis-A2780) M2XDbGNmdGxiQ4n0c5RwgGmlaYT5JGF{e2G7 NUTlUokyOC53LDCxMEAzNjVuIEWsJFExNCB{MDygZY5lKDVyIN88US=> NV[2c2k2PDhiaB?= M1HpT2NwdWKrbnH0bY9vKG:oIHPpd5Bt[XSrbjDhcoQhVUWNIHnubIljcXSxcjDjc4JqdWW2aX7pZkApOTBibl2pJIVvcGGwY3XzJINmdGxiZHXheIghcW5idHjy[YUhd3[jcnnhckBk[W6lZYKgZ4VtdCCuaX7ld{ApSTJ5OECsJHRQXi1zMULEMEBidmRiY3nzMWEzPzhyKT6= NYj1UYtkOzFyNUe2NVE>
HCC cell lines HepG2 and Huh7 MkPxR4VtdCC4aXHibYxqfHliYYPzZZk> NEjYeVgxNTNyIN88US=> M1vEPVQ5KGh? MVnDSFE{OytiSFPDJINmdGy|IHX4bIljcXRicnXzbZN1[W6lZTD0c{BkcXOybHH0bY4v NHTFOJA{OTB3NkWzNi=>

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
ATF3; 

PubMed: 20651982     


ATF3 protein expression levels after treatment with low and cytotoxic doses of cisplatin (1 and 10 µg/ml) and carboplatin (27 and 270 µg/ml) in SKOV-3, MCF-7, PC3, A2780-cp, and A549 cell lines.

FEN1; 

PubMed: 29541412     


MCF-7, BT-474, and MDA-MB-231 cells were treated with increasing concentrations of cisplatin for 24 h, and FEN1 protein expression was analyzed by western blotting.

PD-L1 / p-MEK / MEK / p-STAT3 / STAT3; 

PubMed: 29228662     


Expression of PD-L1, phosphor-MEK (p-MEK), total MEK, phosphor-STAT3 (p-STAT3), and total STAT3 in HNSCC cells was measured by western blotting. Cisplatin treatment increased PD-L1 and p-MEK expression.

LC3B-I / LC3B-II / Beclin-1; 

PubMed: 26715839     


Cells seeded and treated with 2 μg/mL cisplatin for 0 hours (h) (control), 24, 48, and 72 hours, then subjected to Western blot analysis of LC3B and Beclin-1 expression. β-Actin used as loading control. Data showed LC3B-II accumulation and Beclin-1 upregulation in a time-dependent manner.

p-AMPK / AMPK / p-mTOR / mTOR; 

PubMed: 26715839     


A549 cells treated with 2 μg/mL cisplatin for 0 hours (h) (control), 24, 48, and 72 hours; protein extracts were subjected to Western blot analysis of p-AMPK, AMPK, p-mTOR, mTOR, and β-actin. 

20651982 29541412 29228662 26715839
Immunofluorescence
H2A.X / RPA; 

PubMed: 28993682     


Representative immunofluorescence of RPA and γH2A.X foci in cisplatin and/or olaparib treated cell CC cell lines along with PARP1 silenced cell treated with cisplatin.

γ-H2A.X / 53BP1; 

PubMed: 28993682     


Representative immunofluorescence of 53BP1 foci and γH2A.X foci in indicated treatment or siRNA transfection in CC cells. Cisplatin and olaparib both induce 53BP1 foci in CC cell line but combination of both drug or cisplatin treatment in PARP1 depleted cells produces higher number of 53BP1 foci and display more number of γH2A.X foci which co-localizes with each other.

N-cadherin / E-cadherin / Vimentin ; 

PubMed: 28105207     


Cell shape was observed by phase contrast microscopy and immunocytofluorescence. Staining of E-cadherin, N-cadherin and vimentin for the two groups of cells was observed by fluorescence microscope (magnification, ×400; Scale, 25 µm). Cells treated with cisplatin had higher N-cadherin expression.

LC3B; 

PubMed: 26715839     


A549 cells were treated with 4 μg/mL cisplatin for 24 hours and stained by indirect immunofluorescence for LC3B. Distribution of endogenous LC3B was reviewed and scored under fluorescent microscope.

28993682 28105207 26715839
Growth inhibition assay
Cell viability; 

PubMed: 26062553     


Quercetin enhanced cisplatin sensitivity of 143B. 143B cells were treated with cisplatin at 0, 2, 4, 6, 8, 10, and 12 μM for 24 h. Quercetin was dissolved in water with 0.5 % (v/v) ethanol. Water with 0.5 % ethanol was used for the control. 143B cells co-treated with 5 μM quercetin and 5 μM cisplatin showed a cisplatin IC50 of 4.21 μM, while an IC50 of 6.12 μM was observed in cisplatin treatment. In “Cisplatin + quercetin” group, cells were treated with 5 μM quercetin for 12 h before cisplatin treatment. 

26062553
In vivo Cisplatin has been demonstrated to be efficient in regression tumor growth in a wide variety of animal tumors models, including head and neck cancer xenografts, cervical squamous carcinoma xenografts, testicular carcinoma xenografts, ovarian cancer xenografts, breast carcinoma xenografts, colonic carcinoma, heterotransplanted hepatoblastoma, and so on. Cisplatin (5 mg/kg) given weekly i.v. at the day 1 and 7 induces a tumor growth inhibition (GI) of 77.5% and 85.1% of the serous xenografts Ov.Ri(C) and OVCAR-3, respectively. [6]

Protocol

Cell Research:

[3]

+ Expand
  • Cell lines: Leukemia L1210/0 cells
  • Concentrations: 7 μg/mL
  • Incubation Time: 2 hours
  • Method:

    L1210/0 cells are maintained in an exponential suspension culture at 37 ℃ in a humidified atmosphere of 5% CO2 in McCoy's medium 5a (modified), supplemented with 15% calfserum, and Fungizone. L1210/0 cells are incubated in Cisplatin (7 μg/mL) for 2 hr at 37 ℃. To measure growth inhibition, the cells are centrifuged, washed once, resuspended in fresh medium at 30 × 103 to 50 × 103 cells/mL, and incubated for 3 days. Cell numbers are determined on a Coulter Counter. An aliquot of cells is diluted with an equal volume of 0.4% trypan blue. Viability is recorded as the percentage of cells that has excluded trypan blue. Cells incubated with Cisplatin as above are also diluted into 0.1% agar and allowed to grow for 2 weeks when colonies are counted.


    (Only for Reference)

Solubility (25°C)

Chemical Information

Molecular Weight 300.05
Formula

Cl2H6N2Pt

CAS No. 15663-27-1
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03875144 Not yet recruiting Peritoneal Mesothelioma|Peritoneal Carcinomatosis Institut du Cancer de Montpellier - Val d''Aurelle November 2019 Phase 2
NCT03875144 Not yet recruiting Peritoneal Mesothelioma|Peritoneal Carcinomatosis Institut du Cancer de Montpellier - Val d''Aurelle November 2019 Phase 2
NCT03811002 Not yet recruiting Limited Stage Lung Small Cell Carcinoma|Stage IIB Lung Cancer AJCC v8|Stage III Lung Cancer AJCC v8|Stage IIIA Lung Cancer AJCC v8|Stage IIIB Lung Cancer AJCC v8|Stage IIIC Lung Cancer AJCC v8 National Cancer Institute (NCI) September 6 2019 Phase 2|Phase 3
NCT03811002 Not yet recruiting Limited Stage Lung Small Cell Carcinoma|Stage IIB Lung Cancer AJCC v8|Stage III Lung Cancer AJCC v8|Stage IIIA Lung Cancer AJCC v8|Stage IIIB Lung Cancer AJCC v8|Stage IIIC Lung Cancer AJCC v8 National Cancer Institute (NCI) September 6 2019 Phase 2|Phase 3
NCT03811015 Not yet recruiting Clinical Stage II HPV-Mediated (p16-Positive) Oropharyngeal Carcinoma AJCC v8|Clinical Stage III HPV-Mediated (p16-Positive) Oropharyngeal Carcinoma AJCC v8|Human Papillomavirus-16 Positive|Pathologic Stage II HPV-Mediated (p16-Positive) Oropharyngeal Carcinoma AJCC v8|Pathologic Stage III HPV-Mediated (p16-Positive) Oropharyngeal Carcinoma AJCC v8|Smoker National Cancer Institute (NCI) July 10 2019 Phase 2|Phase 3
NCT03811015 Not yet recruiting Clinical Stage II HPV-Mediated (p16-Positive) Oropharyngeal Carcinoma AJCC v8|Clinical Stage III HPV-Mediated (p16-Positive) Oropharyngeal Carcinoma AJCC v8|Human Papillomavirus-16 Positive|Pathologic Stage II HPV-Mediated (p16-Positive) Oropharyngeal Carcinoma AJCC v8|Pathologic Stage III HPV-Mediated (p16-Positive) Oropharyngeal Carcinoma AJCC v8|Smoker National Cancer Institute (NCI) July 10 2019 Phase 2|Phase 3

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Frequently Asked Questions

  • Question 1:

    What is the appropriate concentration of DMF for cell culture and animal study?

  • Answer:

    It depends on the cell type. The final concentration of DMF should be better limited to less than 0.1% if possible, or below 1%. Using saline as a vehicle for cisplatin at up to 3mg/ml is recommended. it's a suspension and can be administrated via oral gavage.

DNA/RNA Synthesis Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID