Phenethyl isothiocyanate / eff 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)


eff, efficacy: Click to Expand ⟱
Source:
Type:
Power to enhance an anti cancer effect


Scientific Papers found: Click to Expand⟱
4959- PEITC,    Phenethyl isothiocyanate hampers growth and progression of HER2-positive breast and ovarian carcinoma by targeting their stem cell compartment
- in-vitro, Ovarian, NA
CSCs↓, ALDH↓, CSCsMark↓, eff↑,
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↓,
4953- PEITC,    effective-in-killing">PEITC: a natural compound effective in killing primary leukemia cells and overcoming drug resistance
- in-vitro, CLL, NA
ROS↑, GSH↓, TumCD↓, eff↓, Mcl-1↓, Casp3↑,
4954- PEITC,    Selective killing of oncogenically transformed cells through a ROS-mediated mechanism by β-phenylethyl isothiocyanate
- vitro+vivo, Ovarian, SKOV3
ROS↑, GSH↓, selectivity↑, mtDam↑, TumCD↑, OS↑, eff↑, *toxicity↓, H2O2↑, NO↑, eff↓, GPx↓, Dose↝, eff↑,
4946- PEITC,    Phenethyl Isothiocyanate Inhibits Oxidative Phosphorylation to Trigger Reactive Oxygen Species-mediated Death of Human Prostate Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
Apoptosis↑, TumAuto↑, ROS↑, OXPHOS↓, ATP↓, selectivity↑, ETC↓, eff↓, eff↓, BAX↑,
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↓,
5184- PEITC,    Phenethyl isothiocyanate exhibits antileukemic activity in vitro and in vivo by inactivation of Akt and activation of JNK pathways
- vitro+vivo, AML, U937
Casp3↑, Casp9↑, Casp8↑, cl‑PARP↑, Apoptosis↑, Mcl-1↓, Akt↓, JNK↑, 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↑,
4926- PEITC,    PEITC inhibits the invasion and migration of colorectal cancer cells by blocking TGF-β-induced EMT
- in-vitro, CRC, SW48
TumCI↓, TumCMig↓, EMT↓, Smad1↓, AntiCan↑, Snail↓, Slug↓, Zeb1↓, ZEB2↓, TGF-β1↓, eff↑, E-cadherin↑, N-cadherin↓, Vim↓,
4929- PEITC,  PacT,    Phenethyl isothiocyanate and paclitaxel synergistically enhanced apoptosis and alpha-tubulin hyperacetylation in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
ChemoSen↑, Apoptosis↑, TumCCA↑, eff↑, CDK1↓, Bcl-2↓, BAX↑, cl‑PARP↑, SAL↑,
4934- PEITC,    Differential induction of apoptosis in human breast cancer cell lines by phenethyl isothiocyanate, a glutathione depleting agent
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
GSH↓, ROS↑, chemoPv↑, Apoptosis↑, Casp9↑, Casp3↑, eff↓, TumCG↓, TumCCA↑, BAX↑, Nrf1↑, GSH↓, GSSG↓, GSH/GSSG↓,
4935- PEITC,    Phenethyl Isothiocyanate Suppresses Inhibitor of Apoptosis Family Protein Expression in Prostate Cancer Cells in Culture and In Vivo
- in-vivo, Pca, LNCaP - in-vivo, Pca, PC3
Apoptosis↑, XIAP↓, survivin↓, *BioAv↑, tumCV↓, eff↓,
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↓,
4944- PEITC,    Phenethyl isothiocyanate induces DNA damage-associated G2/M arrest and subsequent apoptosis in oral cancer cells with varying p53 mutations
- in-vitro, Oral, NA
TumCG↓, TumCCA↑, Apoptosis↑, ROS↑, NO↑, GSH↓, MMP↓, DNAdam↑, ATM↑, Chk2↑, P53↑, 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

GPx↓, 1,   GSH↓, 6,   GSH/GSSG↓, 1,   GSSG↓, 1,   H2O2↑, 1,   Nrf1↑, 1,   OXPHOS↓, 1,   ROS↑, 8,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics

ATP↓, 1,   ETC↓, 1,   MMP↓, 1,   mtDam↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis

cMyc↓, 1,  

Cell Death

Akt↓, 2,   Apoptosis↑, 9,   BAX↑, 4,   Bcl-2↓, 2,   Casp↑, 1,   Casp3↑, 5,   Casp8↑, 1,   Casp9↑, 3,   Chk2↑, 1,   JNK↑, 2,   Mcl-1↓, 2,   p38↑, 1,   survivin↓, 1,   TumCD↓, 1,   TumCD↑, 2,  

Transcription & Epigenetics

tumCV↓, 2,  

Protein Folding & ER Stress

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

Autophagy & Lysosomes

TumAuto↑, 1,  

DNA Damage & Repair

ATM↑, 1,   DNAdam↑, 2,   P53↑, 1,   cl‑PARP↑, 2,  

Cell Cycle & Senescence

CDK1↓, 1,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State

ALDH↓, 1,   CSCs↓, 1,   CSCsMark↓, 1,   EMT↓, 1,   ERK↓, 1,   SAL↑, 1,   STAT3↓, 1,   TumCG↓, 3,  

Migration

E-cadherin↑, 1,   N-cadherin↓, 1,   Slug↓, 1,   Smad1↓, 1,   Snail↓, 1,   TGF-β1↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 4,   Vim↓, 1,   Zeb1↓, 1,   ZEB2↓, 1,  

Angiogenesis & Vasculature

NO↑, 2,  

Immune & Inflammatory Signaling

p‑JAK2↓, 1,  

Hormonal & Nuclear Receptors

AR↓, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 2,   Dose↝, 1,   eff↓, 11,   eff↑, 6,   selectivity↑, 4,  

Clinical Biomarkers

AR↓, 1,  

Functional Outcomes

AntiCan↑, 1,   chemoPv↑, 1,   OS↑, 1,   toxicity↓, 1,  
Total Targets: 77

Pathway results for Effect on Normal Cells:


Drug Metabolism & Resistance

BioAv↑, 1,  

Functional Outcomes

toxicity↓, 1,  
Total Targets: 2

Scientific Paper Hit Count for: eff, efficacy
14 Phenethyl isothiocyanate
1 Cisplatin
1 Paclitaxel
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#:961  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

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