Dandelion Root / Cyt‑c 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
Cyt‑c, cyt-c Release into Cytosol: Click to Expand ⟱
Source:
Type:
Cytochrome c
** The term "release of cytochrome c" ** an increase in level for the cytosol.
Small hemeprotein found loosely associated with the inner membrane of the mitochondrion where it plays a critical role in cellular respiration. Cytochrome c is highly water-soluble, unlike other cytochromes. It is capable of undergoing oxidation and reduction as its iron atom converts between the ferrous and ferric forms, but does not bind oxygen. It also plays a major role in cell apoptosis.

The term "release of cytochrome c" refers to a critical step in the process of programmed cell death, also known as apoptosis.
In its new location—the cytosol—cytochrome c participates in the apoptotic signaling pathway by helping to form the apoptosome, which activates caspases that execute cell death.
Cytochrome c is a small protein normally located in the mitochondrial intermembrane space. Its primary role in healthy cells is to participate in the electron transport chain, a process that helps produce energy (ATP) through oxidative phosphorylation.
Mitochondrial outer membrane permeability leads to the release of cytochrome c from the mitochondria into the cytosol.
The release of cytochrome c is a pivotal event in apoptosis where cytochrome c moves from the mitochondria to the cytosol, initiating a chain reaction that leads to programmed cell death.

On the one hand, cytochrome c can promote cancer cell survival and proliferation by regulating the activity of various signaling pathways, such as the PI3K/AKT pathway. This can lead to increased cell growth and resistance to apoptosis, which are hallmarks of cancer.
On the other hand, cytochrome c can also induce apoptosis in cancer cells by interacting with other proteins, such as Apaf-1 and caspase-9. This can lead to the activation of the intrinsic apoptotic pathway, which can result in the death of cancer cells.
Overexpressed in Breast, Lung, Colon, and Prostrate.
Underexpressed in Ovarian, and Pancreatic.
Scientific Papers found: Click to Expand⟱
6350- DRE,    Tracking Evidences of Dandelion for the Treatment of Cancer: From Chemical Composition, Bioactivity, Signaling Pathways in Cancer Cells to Perspective Study
- Review, Var, NA
AntiCan↑, *Bacteria↓, *Inflam↓, *antiOx↑, TumCCA↑, Apoptosis↑, MOMP↑, Cyt‑c↑, APAF1↑, Casp9↑, Casp3↑, MMP↓, Bcl-2↓, TumCMig↓, TumCI↓, Wnt↓, β-catenin/ZEB1↓, MMP2↓, MMP9↓, TumAuto↑, mTOR↓, 4E-BP1↓, Glycolysis↓, angioG↓,
6353- DRE,  Cisplatin,    Insights Into Protective Mechanisms of Dandelion Leaf Extract Against Cisplatin-Induced Nephrotoxicity in Rats: Role of Inhibitory Effect on Inflammatory and Apoptotic Pathways
- in-vivo, Nor, NA
*antiOx↑, *Inflam↓, *Apoptosis↓, *NF-kB↓, *Cyt‑c↓, *DNAdam↓, *GSH↑, *SOD↑, *Albumin↝, *creat↓, *BUN↓, *RenoP↑, *lipid-P↓, *TNF-α↓, *Casp3↓, *Casp9↓, *chemoP↑,
6363- DRE,    Therapeutic Potential of Dandelion (Taraxacum officinale) Root Extract in Colon Cancer: A Comprehensive Review
- in-vitro, CRC, NA
Apoptosis↑, *Inflam↓, TLR4↓, NF-kB↓, *GutMicro↑, mtDam↑, *ROS↓, Casp1↑, TNF-α↑, Bcl-2↓, PARP↓, MMP↓, Cyt‑c↓, Casp3↑, TumVol↓, COX2↓, iNOS↓, ROS↑, selectivity↑, TumCMig↓, TumCI↓, ER Stress↑, PERK↑, eIF2α↑, ATF4↑, CHOP↑, TumCCA↑, cycD1/CCND1↓, P21↓, P53↑, BioAv↝, Half-Life↝,

Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,  

Cell Death ⓘ

APAF1↑, 1,   Apoptosis↑, 2,   Bcl-2↓, 2,   Casp1↑, 1,   Casp3↑, 2,   Casp9↑, 1,   Cyt‑c↓, 1,   Cyt‑c↑, 1,   iNOS↓, 1,   MOMP↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   eIF2α↑, 1,   ER Stress↑, 1,   PERK↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,   PARP↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

4E-BP1↓, 1,   mTOR↓, 1,   Wnt↓, 1,  

Migration ⓘ

MMP2↓, 1,   MMP9↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   ATF4↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,   TLR4↓, 1,   TNF-α↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   Half-Life↝, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   TumVol↓, 1,  
Total Targets: 43

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   GSH↑, 1,   lipid-P↓, 1,   ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

BUN↓, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   Casp3↓, 1,   Casp9↓, 1,   Cyt‑c↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 3,   NF-kB↓, 1,   TNF-α↓, 1,  

Clinical Biomarkers ⓘ

Albumin↝, 1,   creat↓, 1,   GutMicro↑, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   RenoP↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 20

Scientific Paper Hit Count for: Cyt‑c, cyt-c Release into Cytosol
3 Dandelion Root
1 Cisplatin
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#:77  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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