Dandelion Root / TumCP Cancer Research Results

DRE, Dandelion Root: Click to Expand ⟱
Features:
Dandelion root (Taraxacum officinale)
-Various phytochemicals, including flavonoids and phenolic compounds, which have antioxidant properties.
-Root extract can induce apoptosis
-Anti-inflammatory properties
-Immune System Support
Dosage: dried root 2-8g/d. Extract 250-500mg/d Tea 1-2g, 1-3x/d
aqueous Dandelion flower extracts (DFE), dandelion leaf extract (DLE), and dandelion root extract (DRE) may have different effects.
Common Names: Blowball, Puffball, Lion's tooth, Pu gong ying, Swine snout, Wild endive
Taraxacum officinale is rich in flavonoids (e.g., luteolin, quercetin glycosides), phenolic acids (chicoric, chlorogenic, and caffeic acids), terpenoids (taraxasterol, taraxerol), sesquiterpene lactones (taraxinic acid β-D-glucopyranosyl ester), and phytosterols (β-sitosterol, cycloartenol)

Dandelion Root — Dandelion root is the root material or root extract of Taraxacum officinale, a polychemical botanical preparation containing phenolic acids, flavonoids, sesquiterpene lactones, triterpenes, inulin-type carbohydrates, and other phytochemicals. It is formally classified as a botanical dietary supplement or herbal extract rather than a defined single-molecule oncology drug. Standard abbreviations include DRE for dandelion root extract and T. officinale for the plant species. Current oncology relevance is mainly preclinical, with repeated in-vitro and xenograft signals but no completed convincing human cancer efficacy trial.

Primary mechanisms (ranked):

  1. Selective programmed cell death induction in cancer cells, especially extrinsic caspase-8 signaling with downstream mitochondrial destabilization and caspase execution.
  2. Mitochondrial stress and pro-death autophagy, including loss of mitochondrial integrity and context-dependent mitochondrial ROS involvement.
  3. Multi-pathway growth suppression through cell-cycle disruption, PI3K-Akt/JAK-STAT/PPAR pathway modulation, and reduced survival signaling.
  4. Anti-invasive and anti-metastatic signaling, including reduced migration/invasion phenotypes and reduced MMP-9/IL-1β expression in some models.
  5. Chemosensitization or adjunctive enhancement in preclinical models, especially with taxol and mitoxantrone in prostate cancer models.
  6. Anti-inflammatory and antioxidant effects in non-cancer contexts; these are biologically relevant but not the central cancer-killing mechanism.

Bioavailability / PK relevance: Dandelion root extract is not a standardized single active agent, so formal human PK is not well established. Oral use is plausible as a botanical preparation, but systemic exposure to the same complex extract composition used in cell culture is unknown. Inulin-rich root material may also act partly through gastrointestinal or microbiome-facing exposure rather than direct plasma-equivalent exposure.

In-vitro vs systemic exposure relevance: Many anticancer experiments use crude extract concentrations in the mg/mL range and exposure windows of 24–96 hours. These concentrations should not be assumed to be systemically achievable after oral use. Colorectal and gastrointestinal tumor models may have relatively better luminal-exposure plausibility than distant solid-tumor systemic exposure, but clinical translation remains unproven.

Clinical evidence status: Preclinical. Evidence includes cell-line studies, some xenograft studies, and case-report-level human observations. A phase I cancer trial effort was reported as Health Canada-approved/recruiting, but there is no clear completed trial demonstrating cancer efficacy. It should not be treated as an established anticancer therapy.

Safety / deployment status: Dandelion is widely marketed as a food/herbal dietary supplement and is generally considered likely safe at food-level intake, but concentrated medicinal doses have less safety evidence. Important constraints include possible allergy in Asteraceae-sensitive individuals, theoretical interactions with antidiabetic, anticoagulant/antiplatelet, lithium, diuretic, and other medications, and uncertainty in pregnancy or breastfeeding. Hormone-sensitive cancer caution is reasonable because some preclinical evidence suggests estrogenic activity and possible stimulation of hormone-sensitive breast cancer models.

Dandelion Root Cancer Mechanism Table

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Extrinsic apoptosis and caspase activation ↑ caspase-8, ↑ Annexin V positivity, ↑ programmed cell death ↔ or lower toxicity in tested PBMCs, fibroblasts, colon mucosa, and mammary epithelial cells G Selective cancer-cell apoptosis Most central recurring anticancer signal across melanoma, leukemia, colorectal, pancreatic, prostate, and breast models; strongest evidence remains in vitro.
2 Mitochondrial destabilization ↓ mitochondrial integrity, ↓ mitochondrial membrane potential, ↑ downstream death signaling ↔ or relatively spared in several comparator normal-cell models G Amplifies intrinsic death execution Mitochondrial injury appears downstream of extrinsic death signaling in some leukemia models and more direct in melanoma/pancreatic models.
3 Pro-death autophagy ↑ autophagy with apoptosis linkage ↔ uncertain G Contributes to programmed cell death Reported in CMML and pancreatic cancer studies; autophagy direction should be interpreted as pro-death in those models, not automatically cytoprotective.
4 Cell cycle arrest ↑ S phase and G2/M accumulation, ↓ proliferation ↔ or less affected in tested normal mammary epithelial cells G Restricts proliferation Best supported in newer breast cancer fractionation/proteomics work; extract-specific and concentration-dependent.
5 PI3K-Akt and JAK-STAT survival signaling ↓ PI3K/Akt-related survival proteins, ↓ JAK/STAT-associated signaling markers (model-dependent) ↔ uncertain G Reduces survival signaling Mechanistic support is strongest in MDA-MB-231 fraction studies; requires caution because crude extracts and fractions differ substantially.
6 Mitochondrial ROS increase secondary ↑ ROS (context-dependent), ↑ oxidative mitochondrial stress ↔ uncertain; antioxidant effects may occur in normal inflammatory injury models R/G Stress-mediated death amplification ROS is not uniformly the primary DRE mechanism; in prostate work, DRE apoptosis was described as caspase-dependent while lemongrass was more ROS-dependent.
7 Migration invasion and metastasis markers ↓ migration, ↓ invasion, ↓ MMP-9, ↓ IL-1β, ↑ KAI1 (model-dependent) ↔ uncertain G Anti-invasive phenotype Observed in breast and pediatric/neuroblastoma models; translational strength is lower than the apoptosis signal.
8 Chemosensitization ↑ taxol-induced apoptosis, ↑ mitoxantrone-induced apoptosis, ↓ xenograft tumor burden with oral extract in prostate models ↔ or reduced toxicity signal in selected comparator normal-cell assays G Adjunctive enhancement Preclinical adjunct signal only; drug interaction risk means this should not be assumed safe with chemotherapy without oncology supervision.
9 Inflammation and NF-κB linked signaling ↓ inflammatory signaling markers (context-dependent) ↓ inflammatory injury markers in non-cancer models G Anti-inflammatory modulation Relevant to tumor microenvironment hypotheses but less directly established as a dominant cancer-cell killing mechanism for root extract.
10 NRF2 antioxidant axis ↔ insufficient direct cancer-specific evidence for root extract ↑ antioxidant defense may occur in injury/metabolic models (context-dependent) G Not a core cancer axis Do not tag NRF2 as a primary DRE anticancer mechanism unless a specific study directly supports it in the target cancer model.
11 Clinical Translation Constraint High in-vitro extract concentrations; variable extract chemistry; no validated human anticancer exposure target Food-level safety generally favorable but concentrated-dose interaction and allergy concerns remain G Limits clinical inference Evidence is promising but mostly preclinical; oral dosing cannot be translated directly from mg/mL cell-culture exposure.

TSF legend: P: 0–30 min; R: 30 min–3 hr; G: >3 hr
TumCP, Tumor Cell proliferation: Click to Expand ⟱
Source:
Type:
Tumor cell proliferation is a key characteristic of cancer. It refers to the rapid and uncontrolled growth of cells that can lead to the formation of tumors.
Scientific Papers found: Click to Expand⟱
6360- DRE,    Dandelion Seed Extract Affects Tumor Progression and Enhances the Sensitivity of Cisplatin in Esophageal Squamous Cell Carcinoma
- in-vitro, ESCC, KYSE450 - in-vitro, ESCC, Eca109
TumCG↓, TumCP↓, TumCMig↓, TumCI↓, angioG↓, Apoptosis↑, PI3K↓, Akt↓, p‑Akt↓, survivin↓, Bax:Bcl2↑, Casp3↑, Casp9↑, MMP2↓, MMP9↓, VEGF↓, EMT↓, eff↑, DNAdam↑, p‑STAT3↑, ChemoSen↑,
6364- DRE,    Dandelion Root Extract Sensitizes Leukemia Cells to VP-16 Induced Cell Death
- in-vitro, CLL, NA
TumCP↓, MMP↓, ROS↑, TumCD↑, ChemoSen↑, chemoP↑, QoL↑,
6321- DRE,    Dandelion root extract suppressed gastric cancer cells proliferation and migration through targeting lncRNA-CCAT1
- in-vitro, GC, NA
CCAT1↓, TumCP↓, TumCMig↓,
6328- DRE,    Hydroalcoholic extract of Taraxacum officinale induces apoptosis and autophagy in 4T1 breast cancer cells
- in-vitro, BC, 4T1
TumCG↓, TumCP↓, Apoptosis↑, TumAuto↑, DNAdam↑, BAX↑, Bax:Bcl2↑, P53↑, Beclin-1↑, ATG7↑, Bcl-2↓, NO↓,
6317- DRE,    The efficacy of dandelion root extract in inducing apoptosis in drug-resistant human melanoma cells
- in-vitro, Melanoma, A375
Apoptosis↑, selectivity↑, Casp8↑, mt-ROS↑, eff↑, *toxicity↓, Diff↑, TumCP↓, chemoPv↑, *ROS↓, *NO↓, *COX2↓, *RNS↓, TumCI↓, MMP2↓, MMP9↓, p‑Src↓, p‑FAK↓,
6342- DRE,    Mechanistic Study on the Inhibitory Effect of Dandelion Extract on Breast Cancer Cell Proliferation and Its Induction of Apoptosis
- in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
eff↑, selectivity↑, Apoptosis↑, TumCCA↑, PI3K↓, Akt↓, JAK1↓, STAT↓, PPARγ↑, TumCP↓, SIRT6↓, SCD1↓, STAT3↓, Casp8↓, STAT6↓, PAK1↓, FABP4↓,
6343- DRE,    Dandelion root extract affects ESCC progression via regulating multiple signal pathways
- vitro+vivo, ESCC, NA
*Inflam↓, TumCG↓, TumCP↓, TumCMig↓, TumCI↓, Apoptosis↓, TumCG↓, PI3K↓, p‑Akt↓, RAS↓, Raf↓, p‑ERK↓, Bcl-2↓, BAX↑,
6348- DRE,    New prospects in oncotherapy: bioactive compounds from Taraxacum officinale
- Review, Var, NA
Dose↝, TumCP↓, toxicity↓, *AntiDiabetic↑, *antiOx↑, *hepatoP↑, *diuretic↑, *Inflam↓, *neuroP↑, *Imm↑, eff↑, Apoptosis↑, tumCV↓, selectivity↑, TumCMig↓, EMT↓, MMP2↓, MMP9↓, Wnt↓, β-catenin/ZEB1↓, PI3K↓, Akt↓, JNK↓, ERK↓,

Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

ATG7↑, 1,   FABP4↓, 1,   PPARγ↑, 1,   SCD1↓, 1,  

Cell Death ⓘ

Akt↓, 3,   p‑Akt↓, 2,   Apoptosis↓, 1,   Apoptosis↑, 5,   BAX↑, 2,   Bax:Bcl2↑, 2,   Bcl-2↓, 2,   Casp3↑, 1,   Casp8↓, 1,   Casp8↑, 1,   Casp9↑, 1,   JNK↓, 1,   survivin↓, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 1,   SIRT6↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,   EMT↓, 2,   ERK↓, 1,   p‑ERK↓, 1,   PI3K↓, 4,   RAS↓, 1,   p‑Src↓, 1,   STAT↓, 1,   STAT3↓, 1,   p‑STAT3↑, 1,   STAT6↓, 1,   TumCG↓, 4,   Wnt↓, 1,  

Migration ⓘ

CCAT1↓, 1,   p‑FAK↓, 1,   MMP2↓, 3,   MMP9↓, 3,   PAK1↓, 1,   TumCI↓, 3,   TumCMig↓, 4,   TumCP↓, 8,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   NO↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

JAK1↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,   Dose↝, 1,   eff↑, 4,   selectivity↑, 3,  

Functional Outcomes ⓘ

chemoP↑, 1,   chemoPv↑, 1,   QoL↑, 1,   toxicity↓, 1,  
Total Targets: 63

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

diuretic↑, 1,  

Redox & Oxidative Stress ⓘ

antiOx↑, 1,   RNS↓, 1,   ROS↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Imm↑, 1,   Inflam↓, 2,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   toxicity↓, 1,  
Total Targets: 12

Scientific Paper Hit Count for: TumCP, Tumor Cell proliferation
8 Dandelion Root
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#:222  Target#:327  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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