Sulforaphane (mainly Broccoli) / TumCP Cancer Research Results

SFN, Sulforaphane (mainly Broccoli): Click to Expand ⟱
Features:
Sulforaphane is an isothiocyanate derived from glucoraphanin, a compound found predominantly in cruciferous vegetables such as broccoli, Brussels sprouts, and cabbage. It is well known for its potent antioxidant and detoxification properties and has gained significant attention for its potential chemopreventive and anticancer effects.

Summary
1.primarily attenuates both DNMTs and HDACs, individually suppressing DNA hypermethylation and histones deacetylation, ultimately upregulating NRF2 (best known for NRF2↑)
2.Antioxidant Activity:
• Nrf2 activation leads to the upregulation of a host of antioxidant and detoxification enzymes (e.g., glutathione S-transferase, NAD(P)H:quinone oxidoreductase 1, heme oxygenase-1), which in turn decrease oxidative stress and lower ROS levels.
3.Pro-oxidant Effects in Cancer Cells and Under High-Dose Conditions (>=10uM?)
• In certain cancer cell types or at higher concentrations, sulforaphane can paradoxically lead to an increase in ROS levels.
• The elevated ROS may overwhelm the cancer cells’ antioxidant defenses, leading to oxidative stress–mediated cell death (apoptosis).
• This context-dependent pro-oxidant effect has been explored for its potential in selectively targeting cancer cells while leaving normal cells less affected.

- Might not be a good candidate for pro-oxidant strategy depending on concentration >10uM?.
- Strong Activation of Nrf2 (best known for) at low to moderate concentrations, hence reduces oxidative stress in both cancer and normal cells.
- AMPK signaling activated by SFN, high concentrations of ROS are produced
- ROS generation also results in depletion of GSH levels
- HIF-1α and VEGF inhibitor
- Might be effective against cancer stem cells
- But I would not combine that with radiation, as Sulforaphane activates the anti-oxidant master regulator of cells.
- “I very much agree: Sulforaphane is a very good addition, even more when the choice is an anti-oxidant therapy”
- well known as HDAC inhibitor (typically 5-10um concentrations)
-A transient decrease in HDAC activity has also been observed in healthy humans 3 h after providing a daily 200 µM SFN dose, resulting in a plasma concentration of SFN metabolites of 0.1–0.2 µM.


Dose/Bioavailabilty information:
SFN at a daily dose of 2.2 µM/kg body weight, with a mean plasma level of 0.13 µM Sprout 127.6 grams = 205uM±19.9 content yields SFN 0.5 to 2uM in plasma.
However, it is important to consider that at lower doses, specifically 2.5 μM, SFN resulted in a slight increase in cell proliferation by 5.18–11.84% within a 6 to 48 h treatment window.
-A therapeutic dose starts at approx 60 grams of the sprouts.
-100 g of Broccoli sprouts contain about 15–20 mg of sulforaphane
–Organic Broccoli Sprout Powder (Health Ranger) – Avmacol® – NanoPSA (a blend of NanoStilbene™ and Broccoli Sprout Extract).
- -750 mg Sulforaphane Glucosinolate in Daily One Serving (2 capsules) (30mg Sulforaphane)

Total sulforaphane metabolite concentration in plasma was the highest (>2 μM) at 3 h in human subjects who consumed fresh broccoli sprouts (40g)
-human studies with broccoli sprouts or extracts report plasma sulforaphane levels in the low micromolar range (typically 1–2 µM) after ingesting realistic, food-based quantities of sprouts (often in the range of 30–50 g of sprouts or a concentrated extract).

BroccoSprouts are young broccoli sprouts that have garnered attention because they contain high amounts of glucoraphanin—a precursor molecule to sulforaphane. Studies have shown that broccoli sprouts can have sulforaphane precursor levels (i.e., glucoraphanin levels) that are 10 to 100 times higher than those found in mature broccoli heads. Glucoraphanin content in broccoli sprouts can range anywhere from about 30 to over 100 mg per 100 grams of fresh sprouts. Once activated (e.g., during consumption when myrosinase acts on glucoraphanin), these levels translate into a significant sulforaphane yield, meaning that even a small amount of broccoli sprouts can deliver a potent dose of this bioactive compound.

Importantly, glucoraphanin itself is not bioactive. Rather, enzymatic hydrolysis by myrosinase, present in the plant tissue or in the mammalian microbiome, is necessary to form the active component, SFN.
- GFN (glucoraphanin) is hydrolyzed in vivo to SFN via the myrosinase, which is present in gut bacteria as well as the plant itself (also in Radish)
- Do not cook the vegetables, or if you do add myrosinase back in by adding radish.
- mild heat of broccoli (60–70 °C) inactivated ESP and preserved myrosinase and increased SF yield 3–7-fold
- chewing of fresh broccoli sprouts increases the interaction of glucosinolates with myrosinase and consequently, increases the bioavailability of SFN in the body

-Note half-life 2-3 hrs.
BioAv is good (15-80%) but requires myrosinase
Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓(contrary, actually most raises NRF2), TrxR↓**, GSH↓, Catalase↓(contrary), HO1↓(contrary), GPx↓
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, CXCR4↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, Hh↓, GLi↓, GLi1↓, CD133↓, β-catenin↓, sox2↓, notch2↓, nestin↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, 5↓, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 NRF2 / KEAP1 antioxidant response ↑ NRF2 (often insufficient for rescue) ↑ NRF2 (protective) Driver Electrophile-driven stress response Sulforaphane covalently modifies KEAP1, activating NRF2 signaling
2 Histone deacetylases (HDACs) ↓ HDAC activity ↔ mild modulation Driver Epigenetic reprogramming HDAC inhibition alters transcription of cell-cycle and apoptosis genes
3 Reactive oxygen species (ROS) ↑ ROS (transient / stress-inducing) ↓ ROS Secondary Redox signaling perturbation ROS rise reflects electrophilic stress rather than classic redox cycling
4 Cell cycle regulation ↑ G2/M or G1 arrest ↔ largely spared Secondary Cytostatic growth control Cell-cycle arrest is a prominent phenotype in cancer cells
5 Intrinsic apoptosis ↑ apoptosis (context-dependent) ↔ protected Phenotypic Threshold-dependent cell death Apoptosis occurs when stress exceeds adaptive capacity
6 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Secondary Suppression of inflammatory survival programs NF-κB inhibition supports anti-proliferative and anti-inflammatory effects


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⟱
2446- SFN,  CAP,    The Molecular Effects of Sulforaphane and Capsaicin on Metabolism upon Androgen and Tip60 Activation of Androgen Receptor
- in-vitro, Pca, LNCaP
AR↓, Bcl-xL↓, TumCP↓, Glycolysis↓, HK2↓, PKA↓, Hif1a↓, PSA↓, ECAR↓, BioAv↑, BioAv↓, *toxicity↓,
2405- SFN,    Sulforaphane Targets the TBX15/KIF2C Pathway to Repress Glycolysis and Cell Proliferation in Gastric Carcinoma Cells
- in-vitro, GC, SGC-7901 - in-vitro, GC, BGC-823
TumCP↓, Glycolysis↓, TBX15↑, GlucoseCon↓, lactateProd↓, tumCV↓, PKM2↓, KIF2C↓,
2164- SFN,  dietP,    Broccoli Sprouts Delay Prostate Cancer Formation and Decrease Prostate Cancer Severity with a Concurrent Decrease in HDAC3 Protein Expression in Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) Mice
- in-vitro, Pca, NA
HDAC↓, Dose↝, Risk↓, TumCP↓, H3↓,
1734- SFN,    Sulforaphane Inhibits Nonmuscle Invasive Bladder Cancer Cells Proliferation through Suppression of HIF-1α-Mediated Glycolysis in Hypoxia
- in-vitro, Bladder, RT112
selectivity↑, TumCP↓, Glycolysis↓, Hif1a↓,
3197- SFN,    Sulforaphane Inhibits Self-renewal of Lung Cancer Stem Cells Through the Modulation of Polyhomeotic Homolog 3 and Sonic Hedgehog Signaling Pathways
- in-vitro, Lung, A549 - in-vitro, Lung, H460
TumCP↓, CSCs↓, Shh↓, Smo↓, Gli1↓,
3192- SFN,    Transcriptome analysis reveals a dynamic and differential transcriptional response to sulforaphane in normal and prostate cancer cells and suggests a role for Sp1 in chemoprevention
- in-vitro, Pca, PC3
Sp1/3/4↓, selectivity↑, NRF2↑, HDAC↓, DNMTs↓, TumCCA↑, selectivity↑, HO-1↑, NQO1↑, CDK2↓, TumCP↓, BID↑, Smad1↑, Diablo↑, ICAD↑, Cyt‑c↑, IAP1↑, HSP27↑, *Cyt‑c↓, *IAP1↓, *HSP27↓, survivin↓, CDK4↓, VEGF↓, AR↓,
1456- SFN,    Sulforaphane regulates cell proliferation and induces apoptotic cell death mediated by ROS-cell cycle arrest in pancreatic cancer cells
- in-vitro, PC, MIA PaCa-2 - in-vitro, PC, PANC1
tumCV↓, TumCP↓, cl‑PARP↑, cl‑Casp3↑, TumCCA↑, ROS↑, MMP↓, γH2AX↑, eff↓, *toxicity↓,
1457- SFN,    Sulforaphane Inhibits IL-1β-Induced IL-6 by Suppressing ROS Production, AP-1, and STAT3 in Colorectal Cancer HT-29 Cells
- in-vitro, CRC, HT-29
IL6↓, ROS↓, TumCP↓, TumCI↓, p38↓, AP-1↓,
1461- SFN,    Targets and mechanisms of sulforaphane derivatives obtained from cruciferous plants with special focus on breast cancer - contradictory effects and future perspectives
- Review, BC, NA
TumCP↓, Apoptosis↑, TumCCA↑, antiOx↑,
1466- SFN,    Sulforaphane inhibits thyroid cancer cell growth and invasiveness through the reactive oxygen species-dependent pathway
- vitro+vivo, Thyroid, FTC-133
TumCP↓, TumCCA↑, Apoptosis↑, TumCMig↓, TumCI↓, EMT↓, Slug↓, Twist↓, MMP2↓, MMP9↓, TumCG↓, p‑Akt↓, P21↑, ERK↑, p38↑, ROS↑, *toxicity∅, MMP↓, eff↓,
1469- SFN,    Sulforaphane enhances the therapeutic potential of TRAIL in prostate cancer orthotopic model through regulation of apoptosis, metastasis, and angiogenesis
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vivo, Pca, NA
eff↑, ROS↑, MMP↓, Casp3↑, Casp9↑, DR4↑, DR5↑, BAX↑, Bak↑, BIM↑, NOXA↑, Bcl-2↓, Bcl-xL↓, Mcl-1↓, eff↓, TumCG↓, TumCP↓, eff↑, NF-kB↓, PI3K↓, Akt↓, MEK↓, ERK↓, angioG↓, FOXO3↑,
1471- SFN,    ROS-mediated activation of AMPK plays a critical role in sulforaphane-induced apoptosis and mitotic arrest in AGS human gastric cancer cells
- in-vitro, GC, AGS
TumCP↓, Apoptosis↑, TumCCA↑, CycB/CCNB1↑, P21↑, p‑H3↑, p‑AMPK↑, eff↓, MMP↓, Cyt‑c↑, ROS↑, eff↓,
1315- SFN,    Sulforaphane Induces Apoptosis of Acute Human Leukemia Cells Through Modulation of Bax, Bcl-2 and Caspase-3
- in-vitro, AML, K562
TumCP↓, BAX↑, Casp3↑, Bcl-2↓,
1472- SFN,    Sulforaphane Inhibits Autophagy and Induces Exosome-Mediated Paracrine Senescence via Regulating mTOR/TFE3
- in-vitro, ESCC, NA
TumCP↓, ROS↑, DNAdam↑,
1434- SFN,  GEM,    Sulforaphane Potentiates Gemcitabine-Mediated Anti-Cancer Effects against Intrahepatic Cholangiocarcinoma by Inhibiting HDAC Activity
- in-vitro, CCA, HuCCT1 - in-vitro, CCA, HuH28 - in-vivo, NA, NA
HDAC↓, ac‑H3↑, ChemoSen↑, tumCV↓, TumCP↓, TumCCA↑, Apoptosis↑, cl‑Casp3↑, TumCI↓, VEGF↓, VEGFR2↓, Hif1a↓, eNOS↓, EMT?, TumCG↓, Ki-67↓, TUNEL↑, P21↑, p‑Chk2↑, CDC25↓, BAX↑, *ROS↓, NQO1?,
1453- SFN,    Sulforaphane Reduces Prostate Cancer Cell Growth and Proliferation In Vitro by Modulating the Cdk-Cyclin Axis and Expression of the CD44 Variants 4, 5, and 7
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
TumCG↓, TumCP↓, TumCCA↑, H3↑, H4↑, HDAC↓, CDK1↑, CDK2↑, p19↑, *BioAv↑,
1509- SFN,    Combination therapy in combating cancer
- Review, NA, NA
NRF2↑, ChemoSideEff↓, eff↑, TumCP↓, Apoptosis↑, TumCCA↑, eff↑, PSA↓, P53↑, Hif1a↓, CAIX↓, chemoR↓, 5HT↓,
1475- SFN,  Form,    Combination of Formononetin and Sulforaphane Natural Drug Repress the Proliferation of Cervical Cancer Cells via Impeding PI3K/AKT/mTOR Pathway
- in-vitro, Cerv, HeLa
TumCP↓, PI3K↓, Akt↓, mTOR↓, eff↑, ROS↑,

Showing Research Papers: 1 to 18 of 18

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 18

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   HO-1↑, 1,   NQO1?, 1,   NQO1↑, 1,   NRF2↑, 2,   ROS↓, 1,   ROS↑, 6,  

Mitochondria & Bioenergetics ⓘ

CDC25↓, 1,   KIF2C↓, 1,   MEK↓, 1,   MMP↓, 4,  

Core Metabolism/Glycolysis ⓘ

p‑AMPK↑, 1,   CAIX↓, 1,   ECAR↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 3,   HK2↓, 1,   lactateProd↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 1,   Apoptosis↑, 5,   Bak↑, 1,   BAX↑, 3,   Bcl-2↓, 2,   Bcl-xL↓, 2,   BID↑, 1,   BIM↑, 1,   Casp3↑, 2,   cl‑Casp3↑, 2,   Casp9↑, 1,   p‑Chk2↑, 1,   Cyt‑c↑, 2,   Diablo↑, 1,   DR4↑, 1,   DR5↑, 1,   IAP1↑, 1,   ICAD↑, 1,   Mcl-1↓, 1,   NOXA↑, 1,   p38↓, 1,   p38↑, 1,   survivin↓, 1,   TUNEL↑, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

H3↓, 1,   H3↑, 1,   p‑H3↑, 1,   ac‑H3↑, 1,   H4↑, 1,   tumCV↓, 3,  

Protein Folding & ER Stress ⓘ

HSP27↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMTs↓, 1,   P53↑, 1,   cl‑PARP↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↑, 1,   CDK2↓, 1,   CDK2↑, 1,   CDK4↓, 1,   CycB/CCNB1↑, 1,   p19↑, 1,   P21↑, 3,   TumCCA↑, 8,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT?, 1,   EMT↓, 1,   ERK↓, 1,   ERK↑, 1,   FOXO3↑, 1,   Gli1↓, 1,   HDAC↓, 4,   mTOR↓, 1,   PI3K↓, 2,   Shh↓, 1,   Smo↓, 1,   TBX15↑, 1,   TumCG↓, 4,  

Migration ⓘ

AP-1↓, 1,   Ki-67↓, 1,   MMP2↓, 1,   MMP9↓, 1,   PKA↓, 1,   Slug↓, 1,   Smad1↑, 1,   TumCI↓, 3,   TumCMig↓, 1,   TumCP↓, 18,   Twist↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   eNOS↓, 1,   Hif1a↓, 4,   VEGF↓, 2,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL6↓, 1,   NF-kB↓, 1,   PSA↓, 2,  

Synaptic & Neurotransmission ⓘ

5HT↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   chemoR↓, 1,   ChemoSen↑, 1,   Dose↝, 1,   eff↓, 5,   eff↑, 5,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

AR↓, 2,   IL6↓, 1,   Ki-67↓, 1,   PSA↓, 2,  

Functional Outcomes ⓘ

ChemoSideEff↓, 1,   Risk↓, 1,  
Total Targets: 114

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS↓, 1,  

Cell Death ⓘ

Cyt‑c↓, 1,   IAP1↓, 1,  

Protein Folding & ER Stress ⓘ

HSP27↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,  

Functional Outcomes ⓘ

toxicity↓, 2,   toxicity∅, 1,  
Total Targets: 7

Scientific Paper Hit Count for: TumCP, Tumor Cell proliferation
18 Sulforaphane (mainly Broccoli)
1 Capsaicin
1 diet Plant based
1 Gemcitabine (Gemzar)
1 Formononetin
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#:156  Target#:327  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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