Phenethyl isothiocyanate / TumCCA 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)


TumCCA, Tumor cell cycle arrest: Click to Expand ⟱
Source:
Type:
Tumor cell cycle arrest refers to the process by which cancer cells stop progressing through the cell cycle, which is the series of phases that a cell goes through to divide and replicate. This arrest can occur at various checkpoints in the cell cycle, including the G1, S, G2, and M phases. S, G1, G2, and M are the four phases of mitosis.


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↓,
4947- PEITC,    Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G0/G1   Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death
- in-vitro, Oral, HSC3
AntiCan↑, chemoPv↑, TumCG↓, Apoptosis↑, TumCCA↑, P53↑, P21↑, BAX↑, BID↑, Bcl-2↓, MMP↓, Cyt‑c↑, AIF↑, ROS↑, Ca+2↑,
4948- PEITC,    Sensory acceptable equivalent doses of β-phenylethyl isothiocyanate (PEITC) induce cell cycle arrest and retard the growth of p53 mutated oral cancer in vitro and in vivo
- vitro+vivo, Oral, CAL27 - vitro+vivo, Oral, FaDu - vitro+vivo, Oral, SCC4 - vitro+vivo, Oral, SCC9
TumCD↑, TumCG↓, OS↑, ROS↑, P53↑, P21↑, TumCCA↑, Ki-67↓,
4955- PEITC,    Phenethyl isothiocyanate-induced cytoskeletal changes and cell death in lung cancer cells
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
TumCG↓, α-tubulin↓, TumCD↑, TumCCA↑, Apoptosis↑,
4963- PEITC,    Sensory Acceptable Equivalent Doses of β - Phenylethyl isothiocyanate (PEITC) Induce Cell Cycle Arrest and Retard Growth of p53 Mutated Oral Cancer In Vitro and In Vivo
- vitro+vivo, Oral, CAL27 - vitro+vivo, Oral, FaDu - vitro+vivo, Oral, SCC4 - vitro+vivo, Oral, SCC9
Dose↝, selectivity↑, TumCG↓, OS↑, ROS↑, P53↑, P21↑, TumCCA↑, Ki-67↓,
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↑,
4919- PEITC,    Natural compound PEITC inhibits gain of function of p53 mutants in cancer cells by switching YAP-binding partners between p53 and p73
- in-vitro, Var, NA
Apoptosis↑, TumCCA↑, P53↓,
4921- PEITC,    The Potential Use of Phenethyl Isothiocyanate for Cancer Prevention
- Review, Var, NA
antiOx↑, Inflam↓, AntiCan↑, TumCP↓, TumCCA↑, Apoptosis↑, TumAuto↑, HDAC↓, Risk↓,
4924- PEITC,    Nutri-PEITC Jelly Significantly Improves Progression-Free Survival and Quality of Life in Patients with Advanced Oral and Oropharyngeal Cancer: A Blinded Randomized Placebo-Controlled Trial
- Trial, Oral, NA
QoL↑, P53↑, OS↑, Cyt‑c↝, other↝, ROS↑, selectivity↑, P21↑, TumCCA↑, Dose↝, BioAv↑, Weight↑, chemoP↑,
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⇅,
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↑,
4945- PEITC,    Phenethyl isothiocyanate (PEITC) promotes G2/M phase arrest via p53 expression and induces apoptosis through caspase- and mitochondria-dependent signaling pathways in human prostate cancer DU 145 cells
- in-vitro, Pca, DU145
AntiCan↑, TumCG↓, Apoptosis↑, tumCV↓, TumCCA↑, DNAdam↑, P53↑, CDC25↓, Casp9↑, Casp8↑, mtDam↑, Cyt‑c↑,
4932- PEITC,    Pharmacokinetics and Pharmacodynamics of Phenethyl Isothiocyanate: Implications in Breast Cancer Prevention
- Review, BC, NA
TumCCA↑, ROS↑, GSH↓, ERα/ESR1↓, TumMeta↓, angioG↓,
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↓,
4940- PEITC,    Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G 0/G 1 Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death
- in-vitro, Oral, HSC3
TumCCA↑, Apoptosis↑, BAX↑, BID↑, Bcl-2↓, MMP↓, Cyt‑c↑, AIF↑, tumCV↓, ROS↑, Ca+2↑, CDC25↓, CDK6↓, cycD1/CCND1↓, CDK2↓, cycE/CCNE↓, P53↑, p27↑, P21↑, Casp9↑, Casp3↑, GRP78/BiP↑,
4942- PEITC,    Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G(0)/G(1) Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death
- in-vitro, Oral, HSC3
chemoPv↑, TumCG↓, TumCCA↑, Apoptosis↑, BAX↑, BID↑, Bcl-2↓, MMP↓, Cyt‑c↑, AIF↑, ROS↑, Ca+2↑,
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 17 of 17

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 17

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

antiOx↑, 1,   Ferroptosis↑, 1,   GSH↓, 5,   GSH/GSSG↓, 1,   GSSG↓, 1,   lipid-P↑, 1,   Nrf1↑, 1,   ROS↑, 12,  

Mitochondria & Bioenergetics

AIF↑, 4,   CDC25↓, 2,   MMP↓, 5,   mtDam↑, 1,  

Cell Death

Akt↓, 1,   Apoptosis↑, 12,   BAX↑, 5,   Bcl-2↓, 4,   BID↑, 3,   Casp3↑, 3,   Casp8↑, 1,   Casp9↑, 3,   Chk2↑, 1,   Cyt‑c↑, 5,   Cyt‑c↝, 1,   DR4↑, 1,   DR5↑, 1,   Ferroptosis↑, 1,   JNK↓, 1,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↓, 1,   p27↑, 1,   TumCD↑, 2,  

Transcription & Epigenetics

other↝, 1,   tumCV↓, 3,  

Protein Folding & ER Stress

GRP78/BiP↑, 1,  

Autophagy & Lysosomes

TumAuto↑, 2,  

DNA Damage & Repair

ATM↑, 1,   DNAdam↑, 2,   P53↓, 1,   P53↑, 7,   cl‑PARP↑, 1,  

Cell Cycle & Senescence

CDK1↓, 1,   CDK2↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21↑, 5,   TumCCA↑, 18,  

Proliferation, Differentiation & Cell State

HDAC↓, 1,   SAL↑, 1,   STAT3↓, 2,   TumCG↓, 9,  

Migration

Ca+2↑, 3,   Ki-67↓, 2,   MMP2↓, 1,   MMP9↓, 1,   PKCδ↓, 1,   TumCP↓, 4,   TumMeta↓, 2,   α-tubulin↓, 1,  

Angiogenesis & Vasculature

angioG↓, 2,   Hif1a↓, 1,   NO↑, 1,  

Immune & Inflammatory Signaling

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

Hormonal & Nuclear Receptors

AR↓, 1,   CDK6↓, 1,   ERα/ESR1↓, 1,  

Drug Metabolism & Resistance

BioAv↑, 1,   ChemoSen↑, 2,   Dose⇅, 1,   Dose↝, 2,   eff↓, 3,   eff↑, 1,   Half-Life↓, 1,   selectivity↑, 2,  

Clinical Biomarkers

AR↓, 1,   ERα/ESR1↓, 1,   Ki-67↓, 2,  

Functional Outcomes

AntiCan↑, 3,   chemoP↑, 1,   chemoPv↑, 3,   OS↑, 3,   QoL↑, 1,   Risk↓, 1,   Weight↑, 1,  
Total Targets: 88

Pathway results for Effect on Normal Cells:


Drug Metabolism & Resistance

BioAv↓, 2,  
Total Targets: 1

Scientific Paper Hit Count for: TumCCA, Tumor cell cycle arrest
17 Phenethyl isothiocyanate
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#:322  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

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