Phenethyl isothiocyanate / TumCP Cancer Research Results

PEITC, Phenethyl isothiocyanate: Click to Expand ⟱
Features:
Phenethyl isothiocyanate (PEITC) is a naturally occurring small-molecule phytochemical best known for its role in cancer chemoprevention research. It belongs to the isothiocyanate class of organosulfur compounds and has the chemical formula C₉H₉NS.
Source: Derived from glucosinolates in cruciferous vegetables
PEITC in plants exists mainly as the glucosinolate precursor (gluconasturtiin). Upon tissue disruption (chewing, chopping), myrosinase converts gluconasturtiin → PEITC.
-PEITC bioavailability from fresh, chopped microgreens is high
-Co-consumption with other isothiocyanates is additive/synergistic
-Peak plasma levels: ~1–3 hours post-consumption
-Half-life: ~4–6 hours
-Generally well tolerated up to 40 mg/day (mild GI irritation at higher dose)

PEITC is best characterized for its dual role in xenobiotic metabolism:
Inhibition of Phase I enzymes
-Suppresses cytochrome P450 enzymes (e.g., CYP1A1, CYP2E1)
-Reduces activation of pro-carcinogens

-Selectively depletes GSH in cancer cells
-Directly increases ROS beyond buffering capacity

Key pathways in cancer cells
-GSH depletion
-Mitochondrial ROS amplification
-ASK1/JNK apoptosis

Chemo relevance
-Frequently chemo-sensitizing
-Opposite of NAC/GSH

Induction of Phase II enzymes
-Activates NRF2–KEAP1 signaling
-Increases expression of detoxification and antioxidant enzymes such as:
 -Glutathione S-transferases (GSTs)
 -NAD(P)H quinone oxidoreductase 1 (NQO1)
 -Heme oxygenase-1 (HMOX1)

In preclinical systems, PEITC has been shown to:
-Deplete intracellular glutathione (GSH), increasing oxidative stress in cancer cells
-Induce mitochondrial dysfunction and apoptosis
-Inhibit histone deacetylases (HDACs) (context-dependent)
-Suppress pro-survival signaling pathways (e.g., STAT3, NF-κB)
-Target cancer stem–like cells in some models

Dietary origins

PEITC present in vegetables such as:
-Watercress (the richest source)
-Broccoli
-Cabbage
-Brussels sprouts
-Radish

Bioavailability depends on:
-Food preparation
-Gut microbiota (myrosinase activity if plant enzyme is inactive)

watercress microgreens generally have higher PEITC (and/or its precursor gluconasturtiin) per gram than mature watercress.
-The enrichment is most pronounced per unit fresh weight in the 7–14 day window.
-Absolute values vary substantially with cultivar, light intensity, sulfur/nitrogen nutrition, and post-harvest handling.
| Growth stage    |      Age | PEITC potential (mg / 100 g FW) |         Relative |
| --------------- | -------: | ------------------------------: | ---------------: |
| **Microgreens** |   7–10 d |                     **3.0–6.0** | **~2–4×** mature |
| **Microgreens** |  11–14 d |                     **2.5–5.0** |            ~2–3× |
| Baby leaf       |  21–28 d |                         1.5–3.0 |            ~1–2× |
| Mature leaf     | 35–45+ d |                         0.8–1.5 |         baseline |

Dry weight basis
| Growth stage          | PEITC potential (mg / g DW) |
| --------------------- | --------------------------: |
| Microgreens (7–10 d)  |                 **1.8–3.5** |
| Microgreens (11–14 d) |                     1.5–3.0 |
| Mature leaf           |                     0.6–1.2 |

Expect 2–5× variability depending on:
-Light spectrum (blue light ↑ glucosinolates)
-Sulfur availability

Practical optimization tips
Lighting
-12–16 h/day
-150–300 µmol/m²/s PAR (typical shop LEDs at 20–30 cm distance)
Soil
-Peat or peat-blend preferred
-Avoid over-watering (dilutes concentration)
Nutrition (optional but effective)
-One light watering with ¼-strength sulfate-containing fertilizer around day 4–5 can increase PEITC ~15–30%
Harvest & use
-Cut, rest 5–10 minutes, then consume (allows myrosinase to fully convert gluconasturtiin → PEITC)

Dose: (100 g fresh microgreens ≈ 2–4 mg bioavailable PEITC)
-ie below doses are not really acheivable from fresh microgreens
Minimum biologically active dose (humans): ~10–15 mg PEITC/day
Common efficacy range used in human trials: 20–40 mg/day
Upper short-term doses studied (generally tolerated): 60 mg/day
Diet-achievable with watercress microgreens: Yes, at realistic portions
These doses are chemopreventive / pathway-modulating, not cytotoxic chemotherapy.
| PEITC dose (mg/day) | Dominant biological effects                     |
| ------------------: | ----------------------------------------------- |
|         **5–10 mg** | Phase II enzymes, mild NRF2                     |
|        **10–20 mg** | HDAC inhibition, ROS signaling                  |
|        **20–40 mg** | Apoptosis, cell-cycle arrest, anti-inflammatory |
|        **40–60 mg** | Strong redox stress in cancer cells             |
|              >60 mg | Limited data; GI irritation risk                |



Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 GSH / thiol buffering (PEITC–GSH conjugation → GSH depletion) ↓ GSH Upstream redox collapse PEITC drives a GSH-iron-ROS axis; GSH depletion is upstream of multiple death programs (ref)
2 ROS accumulation ↑ ROS Oxidative stress trigger PEITC increases intracellular ROS, which then drives mitochondrial disruption and apoptosis (ref)
3 Ferroptosis (lipid peroxidation; anti-ferroptotic machinery overwhelmed) ↑ ferroptosis Iron-dependent oxidative death Direct evidence that PEITC induces ferroptosis (alongside other death programs) via GSH-iron-ROS mechanisms (ref)
4 Mitochondrial integrity (ΔΨm; cytochrome-c release) ↓ ΔΨm / ↑ cytochrome-c release Mitochondrial dysfunction PEITC promotes ROS, decreases ΔΨm, increases cytochrome-c release in cancer cells (ref)
5 Intrinsic apoptosis (caspase-9 → caspase-3) ↑ caspase activation / ↑ apoptosis Execution-phase cell death PEITC activates caspase-9 and caspase-3 and induces apoptosis downstream of mitochondrial dysfunction (ref)
6 Akt → JNK → Mcl-1 axis ↓ Akt / ↑ JNK / ↓ Mcl-1 Pro-survival signaling collapse Leukemia study: PEITC-initiated death is linked to Akt inactivation → JNK activation → Mcl-1 downregulation (ref)
7 NF-κB signaling ↓ NF-κB transcriptional activity / ↓ p65 nuclear translocation Reduced pro-survival / inflammatory transcription PEITC inhibits NF-κB activity and NF-κB–regulated genes (e.g., cyclin D1, VEGF, Bcl-xL) in prostate cancer cells (ref)
8 JAK–STAT3 signaling ↓ STAT3 activation Reduced survival / growth signaling PEITC inhibits IL-6–driven JAK–STAT3 activation in prostate cancer cells (STAT3 signaling direction shown) (ref)
9 Cell-cycle regulation ↑ G2/M arrest Proliferation blockade PEITC inhibits proliferation and induces G2/M cell-cycle arrest in prostate cancer cells (ref)
10 Autophagy program ↑ autophagy Stress response (can interact with death) PEITC induces autophagy along with ferroptosis and apoptosis in osteosarcoma cells (ref)
11 Migration / invasion (MMPs, FAK, RhoA) ↓ migration & invasion / ↓ MMPs Anti-metastatic phenotype PEITC suppresses migration/invasion and downregulates MMP-2/-7/-9 and motility regulators (FAK, RhoA) (ref)
12 In vivo anti-tumor effect ↓ tumor burden / ↑ survival (model-dependent) Demonstrated efficacy in animal model Leukemia study reports PEITC anti-leukemic activity including mechanistic signaling changes and in vivo efficacy evidence (ref)


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⟱
4918- PEITC,    Nutritional Sources and Anticancer Potential of Phenethyl Isothiocyanate: Molecular Mechanisms and Therapeutic Insights
- Review, Var, NA
Apoptosis↑, TumCP↓, angioG↓, TumMeta↓, NF-kB↓, Akt↓, MAPK↓, *BioAv↓, ROS↑, lipid-P↑, AIF↑, Cyt‑c↑, DR4↑, DR5↑, TumCCA↑, JAK↓, STAT3↓, MMP2↓, MMP9↓, PKCδ↓, Hif1a↓, JNK↓, Mcl-1↓, COX2↓, MMP↓, Casp3↑, ChemoSen↑, *BioAv↓, Half-Life↓,
4949- PEITC,    Phenethyl Isothiocyanate Exposure Promotes Oxidative Stress and Suppresses Sp1 Transcription Factor in Cancer Stem Cells
- in-vitro, Cerv, HeLa
ROS↑, selectivity↑, CSCs↓, Sp1/3/4↓, P-gp↓, ALDH↓, GSH↓, TumCP↓, Apoptosis↑,
4951- PEITC,    ROS accumulation by PEITC selectively kills ovarian cancer cells via UPR-mediated apoptosis
- in-vitro, Ovarian, PA1 - in-vitro, Ovarian, SKOV3
ROS↑, TumCP↓, GSH↓, selectivity↑, UPR↑, CHOP↑, ER Stress↑, GRP78/BiP↑, PERK↑, ATF6↑, eff↓, TumCG↓, Apoptosis↑, toxicity↓,
4960- PEITC,    Phenethyl isothiocyanate upregulates death receptors 4 and 5 and inhibits proliferation in human cancer stem-like cells
- in-vivo, Cerv, HeLa
CD44↓, CD24↓, CSCs↓, cl‑PARP↑, DR4↑, DR5↑, TumCP↓,
5014- PEITC,  Xan,    Combination of xanthohumol and phenethyl isothiocyanate inhibits NF-κB and activates Nrf2 in pancreatic cancer cells
- in-vitro, PC, NA
NF-kB↓, NRF2↑, GSTP1/GSTπ↑, NQO1↑, SOD↑, TumCP↓,
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↓,
5186- PEITC,    Phenethyl Isothiocyanate inhibits STAT3 activation in prostate cancer cells
- in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP
TumCP↓, TumCCA↑, STAT3↓, p‑JAK2↓, eff↓, TumCCA↑, AR↓, ROS↑,
5187- PEITC,    Phenethyl Isothiocyanate Inhibits Migration and Invasion of Human Gastric Cancer AGS Cells through Suppressing MAPK and NF-κB Signal Pathways
- in-vitro, GC, AGS
TumMeta↓, ERK↓, MKK7↓, PKCδ↓, Rho↓, uPA↓, MMP2↓, MMP9↓, RAS↓, VEGF↓, FAK↓, iNOS↓, COX2↓, TumCP↓,
4921- PEITC,    The Potential Use of Phenethyl Isothiocyanate for Cancer Prevention
- Review, Var, NA
antiOx↑, Inflam↓, AntiCan↑, TumCP↓, TumCCA↑, Apoptosis↑, TumAuto↑, HDAC↓, Risk↓,
4922- PEITC,    Phenethyl Isothiocyanate: A comprehensive review of anti-cancer mechanisms
- Review, Var, NA
Risk↓, AntiCan↑, TumCP↓, TumMeta↓, ChemoSen↑, *BioAv↑, *other↝, *Dose↝, Dose↓, *BioAv↑, *Dose↝, *Half-Life↝, *toxicity↝, GSH↓, ROS↑, CYP1A1↑, CYP1A2↑, P450↓, CYP2E1↑, CYP3A4↓, CYP2A3/CYP2A6↓, *ROS↓, *GPx1↑, *SOD1↑, *SOD2↑, Akt↓, EGFR↓, HER2/EBBR2↓, P53↑, Telomerase↓, selectivity↑, MMP↓, Cyt‑c↑, Apoptosis↑, DR4↑, Fas↑, XIAP↓, survivin↓, TumAuto↑, Hif1a↓, angioG↓, MMPs↓, ERK↓, NF-kB↓, EMT↓, TumCI↓, TumCMig↓, Glycolysis↓, ATP↓, selectivity↑, *antiOx↑, Dose↝, other↝, OCR↓, GSH↓, ITGB1↓, ITGB6↓, ChemoSen↑,
4925- PEITC,    PEITC triggers multiple forms of cell death by GSH-iron-ROS regulation in K7M2 murine osteosarcoma cells
- in-vitro, OS, NA
tumCV↓, TumCP↓, TumCCA↑, GSH↓, ROS↑, Ferroptosis↑, Apoptosis↑, TumAuto↑, MAPK↑, TumCG↓, Dose⇅,
4930- PEITC,    Targeted anti-cancer therapy: Co-delivery of VEGF siRNA and Phenethyl isothiocyanate (PEITC) via cRGD-modified lipid nanoparticles for enhanced anti-angiogenic efficacy
- vitro+vivo, Lung, A549
VEGF↓, Hif1a↓, TumCG↓, TumCP↓,
4933- PEITC,    Phenethyl isothiocyanate inhibits metastasis potential of non-small cell lung cancer cells through FTO mediated TLE1 m6A modification
- vitro+vivo, Lung, H1299 - vitro+vivo, SCC, H226
AntiCan↓, TumCP↓, TumMeta↓, ChemoSen↑, tumCV↓, TumCI↓, TumCMig↓, FTO↓, TLE1↓, Akt↓, NF-kB↓,
4943- PEITC,    Phenethyl isothiocyanate (PEITC) inhibits growth of ovarian cancer cells by inducing apoptosis: role of caspase and MAPK activation
- in-vitro, Ovarian, OVCAR-3
TumCD↑, TumCP↓, Apoptosis↑, Casp3↑, Casp9↑, Bcl-2↓, BAX↑, Akt↓, ERK↓, cMyc↓, p38↑, JNK↑, eff↓,

Showing Research Papers: 1 to 14 of 14

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

antiOx↑, 1,   CYP1A1↑, 1,   CYP2E1↑, 1,   Ferroptosis↑, 1,   GSH↓, 5,   GSTP1/GSTπ↑, 1,   lipid-P↑, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↑, 7,   mt-ROS↑, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics

AIF↑, 1,   ATP↓, 1,   MKK7↓, 1,   MMP↓, 2,   OCR↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis

cMyc↓, 1,   CYP3A4↓, 1,   Glycolysis↓, 1,  

Cell Death

Akt↓, 4,   Apoptosis↑, 8,   BAX↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   Casp3↑, 3,   Casp9↑, 1,   Cyt‑c↑, 2,   DR4↑, 3,   DR5↑, 2,   Fas↑, 1,   Ferroptosis↑, 1,   iNOS↓, 1,   JNK↓, 1,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↓, 1,   p38↑, 1,   survivin↓, 1,   Telomerase↓, 1,   TumCD↑, 1,  

Kinase & Signal Transduction

HER2/EBBR2↓, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics

other↝, 1,   TLE1↓, 1,   tumCV↓, 3,  

Protein Folding & ER Stress

ATF6↑, 1,   CHOP↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes

TumAuto↑, 3,  

DNA Damage & Repair

DNAdam↑, 1,   P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence

TumCCA↑, 5,  

Proliferation, Differentiation & Cell State

ALDH↓, 1,   CD24↓, 1,   CD44↓, 1,   CSCs↓, 2,   EMT↓, 1,   ERK↓, 3,   HDAC↓, 1,   RAS↓, 1,   STAT3↓, 2,   TumCG↓, 3,  

Migration

FAK↓, 1,   FTO↓, 1,   ITGB1↓, 1,   ITGB6↓, 1,   MMP2↓, 2,   MMP9↓, 2,   MMPs↓, 1,   PKCδ↓, 2,   Rho↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 14,   TumMeta↓, 4,   uPA↓, 1,  

Angiogenesis & Vasculature

angioG↓, 2,   EGFR↓, 1,   Hif1a↓, 3,   VEGF↓, 2,  

Barriers & Transport

P-gp↓, 1,  

Immune & Inflammatory Signaling

COX2↓, 2,   Inflam↓, 1,   JAK↓, 1,   p‑JAK2↓, 1,   NF-kB↓, 4,  

Hormonal & Nuclear Receptors

AR↓, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 5,   CYP1A2↑, 1,   CYP2A3/CYP2A6↓, 1,   Dose↓, 1,   Dose⇅, 1,   Dose↝, 1,   eff↓, 4,   Half-Life↓, 1,   P450↓, 1,   selectivity↑, 5,  

Clinical Biomarkers

AR↓, 1,   EGFR↓, 1,   HER2/EBBR2↓, 1,  

Functional Outcomes

AntiCan↓, 1,   AntiCan↑, 2,   Risk↓, 2,   toxicity↓, 1,  
Total Targets: 111

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 1,   GPx1↑, 1,   ROS↓, 1,   SOD1↑, 1,   SOD2↑, 1,  

Transcription & Epigenetics

other↝, 1,  

Drug Metabolism & Resistance

BioAv↓, 2,   BioAv↑, 2,   Dose↝, 2,   Half-Life↝, 1,  

Functional Outcomes

toxicity↝, 1,  
Total Targets: 11

Scientific Paper Hit Count for: TumCP, Tumor Cell proliferation
14 Phenethyl isothiocyanate
1 xanthohumol
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#:388  Target#:327  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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