Cisplatin Cancer Research Results

Cisplatin, Cisplatin: Click to Expand ⟱
Features:
Cisplatin is a chemotherapy medication used to treat various types of cancer. It is a platinum-based drug that works by interfering with the DNA of cancer cells, preventing them from reproducing and ultimately leading to cell death.
Cisplatin (cis-diamminedichloroplatinum II; CDDP) is a platinum-based chemotherapeutic agent that forms covalent DNA crosslinks, primarily intrastrand adducts at adjacent guanine bases. These distort DNA structure, block replication and transcription, and activate DNA damage response pathways (ATM/ATR → p53), leading to cell-cycle arrest and apoptosis. Secondary mechanisms include ROS generation, stress MAPK activation, and modulation of NF-κB. Clinical resistance frequently involves enhanced DNA repair (ERCC1/NER), altered drug transport (CTR1, ATP7A/B), and increased antioxidant defenses. Major toxicities include nephrotoxicity, ototoxicity, and peripheral neuropathy.

Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 DNA crosslink formation (intrastrand adducts) DNA adducts ↑; replication block ↑ Normal dividing cells also affected P, R, G Direct DNA cytotoxicity Cisplatin forms covalent intrastrand crosslinks (primarily at adjacent guanines), distorting DNA and blocking replication and transcription.
2 DNA damage response (ATM / ATR → p53) Checkpoint activation ↑; p53 signaling ↑ ↔ (toxicity in proliferating tissues) R, G Damage signaling cascade DNA distortion activates ATM/ATR pathways leading to p53-mediated cell-cycle arrest and apoptosis.
3 Intrinsic apoptosis (mitochondrial pathway) Bax ↑; Bcl-2 ↓; caspase-9/3 ↑ Nephrotoxicity & ototoxicity risk G Execution of cell death Persistent DNA damage triggers mitochondrial outer membrane permeabilization and caspase activation.
4 Cell-cycle arrest (G2/M emphasis) G2/M arrest ↑ ↔ G Cytostasis → apoptosis Cells accumulate in G2/M phase due to unrepaired DNA lesions.
5 ROS generation / oxidative stress ROS ↑ (secondary mechanism) Oxidative injury ↑ (kidney, cochlea) R, G Stress amplification Cisplatin increases mitochondrial ROS and oxidative stress, contributing to cytotoxicity and organ toxicity.
6 MAPK signaling (JNK / p38 activation) Stress MAPK activation ↑ ↔ R, G Stress-response signaling JNK and p38 activation contribute to apoptosis and stress signaling.
7 NF-κB activation (resistance axis) NF-κB ↑ may promote survival ↔ R, G Resistance modulation NF-κB activation can reduce sensitivity; inhibition enhances cytotoxicity in some models.
8 DNA repair pathways (NER / ERCC1) NER ↑ → resistance — G Resistance determinant Nucleotide excision repair (ERCC1) removes platinum adducts; high ERCC1 correlates with resistance.
9 Drug transport (CTR1 uptake; ATP7A/B efflux) CTR1 ↓ or ATP7A/B ↑ → resistance — G Exposure constraint Copper transporters influence intracellular cisplatin accumulation and resistance.
10 Clinical toxicity profile — Nephrotoxicity, ototoxicity, neurotoxicity — Translation constraint Major dose-limiting toxicities arise from DNA damage and oxidative stress in normal tissues.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (DNA aquation and initial adduct formation)
  • R: 30 min–3 hr (checkpoint activation / stress signaling)
  • G: >3 hr (apoptosis, phenotype outcomes, resistance development)
Scientific Papers found: Click to Expand⟱
1064- LT,  Cisplatin,    Inhibition of cell survival, invasion, tumor growth and histone deacetylase activity by the dietary flavonoid luteolin in human epithelioid cancer cells
- vitro+vivo, Lung, LNM35 - in-vitro, CRC, HT-29 - in-vitro, Liver, HepG2 - in-vitro, BC, MCF7 - in-vitro, BC, MDA-MB-231
Casp3↑, Casp7↑, HDAC↓,
4781- Lyco,  5-FU,  Chemo,  Cisplatin,    Antioxidant and anti-inflammatory activities of lycopene against 5-fluorouracil-induced cytotoxicity in Caco2 cells
- in-vitro, Colon, Caco-2
chemoP↑, Inflam↓, COX2/PTGS2↓, IL1β↓, IL6↓, TNF-α↓, ROS↑, ChemoSen↑, SOD↓,
4518- MAG,  Cisplatin,    Evaluating the Magnolol Anticancer Potential in MKN-45 Gastric Cancer Cells
- in-vitro, GC, MKN45
ChemoSen↑, tumCV↓, BAX↑, Bcl-2↓, P21↑, P53↑, MMP9↓,
4532- MAG,  Cisplatin,    Magnolol Attenuates Cisplatin-Induced Muscle Wasting by M2c Macrophage Activation
- in-vivo, Var, NA
cachexia↓, *IGF-1↑, chemoP↑, *M2 MC↑,
2043- PB,  Cisplatin,    Phenylbutyrate interferes with the Fanconi anemia and BRCA pathway and sensitizes head and neck cancer cells to cisplatin
- in-vitro, HNSCC, UM-SCC-1
ChemoSen↑, eff↑, HDAC↓, BRCA1↓, RadioS↑,
4920- PEITC,  Cisplatin,    PEITC restores chemosensitivity in cisplatin-resistant non-small cell lung cancer by targeting c-Myc/miR-424-5p
- vitro+vivo, NSCLC, A549
TumCG↓, ChemoSen↑, cMyc↓, PI3K↓, Akt↓, mTOR↓, BioAv↝, tumCV↓, ChemoSen↑,
5183- PEITC,  Cisplatin,    Phenethyl Isothiocyanate Induces Apoptosis Through ROS Generation and Caspase-3 Activation in Cervical Cancer Cells
- in-vitro, Cerv, HeLa - in-vitro, Nor, HaCaT
DNAdam↑, Apoptosis↑, ChemoSen↑, ROS↑, mt-ROS↑, Casp↑, Casp3↑, selectivity↑, TumCP↓, tumCV↓, eff↓,
4965- PSO,  Cisplatin,    The synergistic antitumor effects of psoralidin and cisplatin in gastric cancer by inducing ACSL4-mediated ferroptosis
- vitro+vivo, GC, HGC27 - vitro+vivo, GC, MKN45
TumCP↓, TumCMig↓, TumCI↓, TumCG↓, *toxicity↓, eff↑, Ferroptosis↑, ACSL4↑, GPx4↓, ChemoSen↑, chemoP↑, AntiTum↑, Sepsis↓,
4704- PTS,  Cisplatin,    Pterostilbene Sensitizes Cisplatin-Resistant Human Bladder Cancer Cells with Oncogenic HRAS
- in-vitro, Bladder, NA
PI3K↓, mTOR↓, P70S6K↓, MEK↑, ERK↑, ChemoSen↑, TumAuto↑,
5041- SAS,  Cisplatin,    Xc− inhibitor sulfasalazine sensitizes colorectal cancer to cisplatin by a GSH-dependent mechanism
- in-vitro, CRC, NA
xCT/SLC7A11↓, Inflam↓, Apoptosis↓, GSH↓, ROS↑, TumCG↓, selectivity↑, eff↑, eff↓,
2184- SK,  Cisplatin,    PKM2 Inhibitor Shikonin Overcomes the Cisplatin Resistance in Bladder Cancer by Inducing Necroptosis
- in-vitro, CRC, T24/HTB-9
PKM2↓, ChemoSen↑, Necroptosis↑,
2182- SK,  Cisplatin,    Shikonin inhibited glycolysis and sensitized cisplatin treatment in non-small cell lung cancer cells via the exosomal pyruvate kinase M2 pathway
- in-vitro, Lung, A549 - in-vitro, Lung, PC9 - in-vivo, NA, NA
tumCV↓, TumCP↓, TumCI↓, TumCMig↓, Apoptosis↑, PKM2↓, Glycolysis↓, GlucoseCon↓, lactateProd↓, ChemoSen↑, TumVol↓, TumW↓, GLUT1↓,
2008- SK,  Cisplatin,    Enhancement of cisplatin-induced colon cancer cells apoptosis by shikonin, a natural inducer of ROS in vitro and in vivo
- in-vitro, CRC, HCT116 - in-vivo, NA, NA
ChemoSen↑, selectivity↑, i-ROS↑, DNAdam↑, MMP↓, TumCCA↑, eff↓, *toxicity↓,
5330- TFdiG,  Cisplatin,    Theaflavin-3,3′-Digallate Enhances the Inhibitory Effect of Cisplatin by Regulating the Copper Transporter 1 and Glutathione in Human Ovarian Cancer Cells
- in-vitro, Ovarian, A2780S - in-vitro, Ovarian, OVCAR-3
selectivity↑, ChemoSen↑, DNAdam↑, GSH↓, CTR1↑,
2133- TQ,  CUR,  Cisplatin,    Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity by attenuating NFκB, KIM-1 and ameliorating Nrf2/HO-1 signalling
- in-vitro, Nor, HEK293 - in-vivo, NA, NA
*creat↓, *TNF-α↓, *IL6↓, *MRP↓, *GFR↑, *mt-ATPase↑, *p‑Akt↑, *NRF2↑, *HO-1↑, *Casp3↓, *NF-kB↓, *RenoP↑,
2116- TQ,  Cisplatin,    Oral administration of Nigella sativa oil ameliorates the effect of cisplatin on membrane enzymes, carbohydrate metabolism and oxidative damage in rat liver
- in-vivo, Nor, NA
*hepatoP↑, *antiOx↑, *ROS↓, ALAT↓, AST↓,
2099- TQ,  Cisplatin,    Thymoquinone and cisplatin as a therapeutic combination in lung cancer: In vitro and in vivo
- in-vitro, Lung, H460 - in-vitro, Lung, H146 - in-vivo, NA, NA
ChemoSen↑, TumCP↓, tumCV↓, Apoptosis↑, NF-kB↓,
4887- ZER,  Rad,  Cisplatin,    Zerumbone acts as a radiosensitizer in head and neck squamous cell carcinoma
- in-vitro, HNSCC, CAL27
Apoptosis↑, ChemoSen↑, RadioS↑, tumCV↓,

Showing Research Papers: 51 to 68 of 68
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 68

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 2,   ROS↑, 3,   i-ROS↑, 1,   mt-ROS↑, 1,   SOD↓, 1,   xCT/SLC7A11↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MEK↑, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACSL4↑, 1,   ALAT↓, 1,   cMyc↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   lactateProd↓, 1,   PKM2↓, 2,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↓, 1,   Apoptosis↑, 4,   BAX↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   Casp3↑, 2,   Casp7↑, 1,   Ferroptosis↑, 1,   Necroptosis↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 6,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

BRCA1↓, 1,   DNAdam↑, 3,   P53↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↑, 1,   HDAC↓, 2,   mTOR↓, 2,   P70S6K↓, 1,   PI3K↓, 2,   TumCG↓, 3,  

Migration(tgid=13) ⓘ

MMP9↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 4,  

Barriers & Transport(tgid=15) ⓘ

CTR1↑, 1,   GLUT1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 2,   NF-kB↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,   ChemoSen↑, 14,   eff↓, 3,   eff↑, 3,   RadioS↑, 2,   selectivity↑, 4,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   BRCA1↓, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiTum↑, 1,   cachexia↓, 1,   chemoP↑, 3,   TumVol↓, 1,   TumW↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

Sepsis↓, 1,  
Total Targets: 68

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   HO-1↑, 1,   NRF2↑, 1,   ROS↓, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↑, 1,   Casp3↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

IGF-1↑, 1,  

Migration(tgid=13) ⓘ

mt-ATPase↑, 1,  

Barriers & Transport(tgid=15) ⓘ

MRP↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL6↓, 1,   M2 MC↑, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

creat↓, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

GFR↑, 1,   hepatoP↑, 1,   RenoP↑, 1,   toxicity↓, 2,  
Total Targets: 19

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:197  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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