Cisplatin / Apoptosis 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)

Apoptosis, Apoptosis: Click to Expand ⟱

Source:

Type: type of cell death

Situation in which a cell actively pursues a course toward death upon receiving certain stimuli.
Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not die.

Scientific Papers found: Click to Expand⟱

1295-

AG,

Cisplatin,

Chemosensitizing Effect of Astragalus Polysaccharides on Nasopharyngeal Carcinoma Cells by Inducing Apoptosis and Modulating Expression of Bax/Bcl-2 Ratio and Caspases

in-vivo,

Laryn,

mice

AntiTum↑, Apoptosis↑, Bcl-2↓, BAX↑, Casp3↑, Casp9↑, Bax:Bcl2↑,

5651-

BNL,

Cisplatin,

Natural borneol sensitizes human glioma cells to cisplatin-induced apoptosis by triggering ROS-mediated oxidative damage and regulation of MAPKs and PI3K/AKT pathway

in-vitro,

GBM,

U251

in-vitro,

GBM,

U87MG

ChemoSen↑, tumCV↓, TumCCA↑, Apoptosis↑, ROS↑, DNAdam↑, ATR↑, ATM↑, P53↑, Histones↑, eff↓, Casp3↑, Casp7↑, Casp9↑,

1450-

Bos,

Cisplatin,

3-Acetyl-11-keto-β-boswellic acid (AKBA) induced antiproliferative effect by suppressing Notch signaling pathway and synergistic interaction with cisplatin against prostate cancer cells

in-vitro,

Pca,

DU145

16.50 µM at 48 h

ROS↑, MMP↓, Casp↑, Apoptosis↑, Bax:Bcl2↑, TumCCA?, cycD1/CCND1↓, CDK4↓, P21↑, p27↑, NOTCH↓, ChemoSen↑,

5919-

Cats,

Cisplatin,

Uncaria tomentosa Leaves Decoction Modulates Differently ROS Production in Cancer and Normal Cells, and Effects Cisplatin Cytotoxicity

in-vitro,

Liver,

HepG2

580 µg/mL

ROS↑, GSH↓, Apoptosis↑, Casp3↑, Casp7↑, NF-kB↓, selectivity↑, ChemoSen↑, chemoP↑,

5965-

CEL,

Cisplatin,

Celecoxib enhances anticancer effect of cisplatin and induces anoikis in osteosarcoma via PI3K/Akt pathway

in-vitro,

OS,

MG63

COX2↓, ChemoSen↑, MDR1↓, MRP1↓, E-cadherin↓, β-catenin/ZEB1↓, Apoptosis↑, TumCCA↑, TumCG↓, P-gp↓, PI3K↓, Akt↓,

444-

CUR,

Cisplatin,

LncRNA KCNQ1OT1 is a key factor in the reversal effect of curcumin on cisplatin resistance in the colorectal cancer cells

vitro+vivo,

CRC,

HCT8

10 μM, 48 h; 1 g/kg/week, 42 days

TumVol↓, Apoptosis↑, Bcl-2↓, Cyt‑c↑, BAX↑, cl‑Casp3↑, cl‑PARP1↑, miR-497↑, KCNQ1OT1↓,

801-

GAR,

Cisplatin,

Garcinol sensitizes human head and neck carcinoma to cisplatin in a xenograft mouse model despite downregulation of proliferative biomarkers

in-vivo,

HNSCC,

0.5 mg/kg

mouse

Apoptosis↑, cycD1/CCND1↓, Bcl-2↓, survivin↓, VEGF↓, TumCG↓, Ki-67↓, CD31↓,

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↓,

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

2 µM, 4 µM, 6 µM, and 8 µM

5.739 µM

in-vitro,

Lung,

PC9

6.302 µM

in-vivo,

NA,

mice

tumCV↓, TumCP↓, TumCI↓, TumCMig↓, Apoptosis↑, PKM2↓, Glycolysis↓, GlucoseCon↓, lactateProd↓, ChemoSen↑, TumVol↓, TumW↓, GLUT1↓,

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,

mice

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: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: Apoptosis, Apoptosis

11 Cisplatin
1 Astragalus
1 borneol
1 Boswellia (frankincense)
1 Cat’s Claw
1 Celecoxib
1 Curcumin
1 Garcinol
1 Phenethyl isothiocyanate
1 Shikonin
1 Thymoquinone
1 Zerumbone
1 Radiotherapy/Radiation

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#:14  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

Cisplatin / Apoptosis Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

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