Sulforaphane (mainly Broccoli) / NRF2 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">NRF2↓(contrary, actually most raises NRF2), TrxR↓**, GSH↓, Catalase↓(contrary), HO1↓(contrary), GPx↓
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑">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


NRF2, nuclear factor erythroid 2-related factor 2: Click to Expand ⟱
Source: TCGA
Type: Antiapoptotic
Nrf2 is responsible for regulating an extensive panel of antioxidant enzymes involved in the detoxification and elimination of oxidative stress. Thought of as "Master Regulator" of antioxidant response.
-One way to estimate Nrf2 induction is through the expression of NQO1.
NQO1, the most potent inducer:
SFN 0.2 μM,
quercetin (2.5 μM),
curcumin (2.7 μM),
Silymarin (3.6 μM),
tamoxifen (5.9 μM),
genistein (6.2 μM ),
beta-carotene (7.2μM),
lutein (17 μM),
resveratrol (21 μM),
indol-3-carbinol (50 μM),
chlorophyll (250 μM),
alpha-cryptoxanthin (1.8 mM),
and zeaxanthin (2.2 mM)

1. Raising Nrf2 enhances the cell's antioxidant defenses and ↓ROS. This strategy is used to decrease chemo-radio side effects.
2. Downregulating Nrf2 lowers antioxidant defenses and ↑ROS. In cancer cells this leads to DNA damage, and cell death.
3. However there are some cases where increasing Nrf2 paradoxically causes an increase in ROS (cancer cells). Such as cases of Mitochondial overload, signal crosstalk, reductive stress

-In some cases, Nrf2 is overexpressed in cancer cells, which can lead to the activation of genes involved in cell proliferation, angiogenesis, and metastasis. This can contribute to the development of resistance to chemotherapy and targeted therapies.
-Increased Nrf2 expression: Lung, Breast, Colorectal, Prostrate.
Decreased Nrf2 expression: Skine, Liver, Pancreatic.
-Nrf2 is a cytoprotective transcription factor which demonstrated both a negative effect as well as a positive effect on cancer
- "promotes Nrf2 translocation from the cytoplasm to the nucleus," means facilitates the movement of Nrf2 into the nucleus, thereby enhancing the cell's antioxidant and cytoprotective responses. -Major regulator of Nrf2 activity in cells is the cytosolic inhibitor Keap1.

Nrf2 Inhibitors and Activators
Nrf2 Inhibitors: Brusatol, Luteolin, Trigonelline, VitC, Retinoic acid, Chrysin
Nrf2 Activators: SFN, OPZ EGCG, Resveratrol, DATS, CUR, CDDO, Api
- potent Nrf2 inducers from plants include sulforaphane, curcumin, EGCG, resveratrol, caffeic acid phenethyl ester, wasabi, cafestol and kahweol (coffee), cinnamon, ginger, garlic, lycopene, rosemany

Nrf2 plays dual roles in that it can protect normal tissues against oxidative damage and can act as an oncogenic protein in tumor tissue.
– In healthy tissues, NRF2 activation helps protect cells from oxidative damage and maintains cellular homeostasis.
– In many cancers, constitutive activation of NRF2 (often through mutations in NRF2 itself or loss-of-function mutations in KEAP1) leads to an enhanced antioxidant capacity.
– This upregulation can promote tumor cell survival by enabling cancer cells to thrive under oxidative stress, resist chemotherapeutic agents, and sustain metabolic reprogramming.
– Elevated NRF2 levels have been implicated in promoting tumor growth, metastasis, and resistance to therapy in various malignancies.
– High or sustained NRF2 activity is frequently associated with aggressive tumor phenotypes, poorer prognosis, and decreased overall survival in several cancer types.
– While its activation is essential for protecting normal cells from oxidative stress, aberrant or sustained NRF2 activation in tumor cells can lead to enhanced survival, therapeutic resistance, and tumor progression.

NRF2 inhibitors: (to decrease antioxidant defenses and increase cell death from ROS).
-Brusatol: most cited natural inhibitors of Nrf2.
-Luteolin: luteolin can reduce Nrf2 activity in specific cancer models and may enhance cell sensitivity to chemotherapy. However, luteolin is also known as an antioxidant, and its influence on Nrf2 can sometimes be context dependent.
-Apigenin: certain studies to down‑regulate Nrf2 in cancer cells: Dose and context dependent .
-Oridonin:
-Wogonin: although its effects might be cell‑ and dose‑specific.
- Withaferin A

Scientific Papers found: Click to Expand⟱
4881- CUR,  SFN,  RES,  EGCG,  Lyco  An update of Nrf2 activators and inhibitors in cancer prevention/promotion
- Review, Var, NA
*NRF2↑, *antiOx↑,
4736- Se,  SFN,    Synergy between sulforaphane and selenium in protection against oxidative damage in colonic CCD841 cells
- in-vitro, Nor, CCD841
*TrxR1↑, *H2O2↓, *NRF2↑,
2448- SFN,    Sulforaphane and bladder cancer: a potential novel antitumor compound
- Review, Bladder, NA
Apoptosis↑, TumCG↓, TumCI↓, TumMeta↓, glucoNG↓, ChemoSen↑, TumCCA↑, Casp3↑, Casp7↑, cl‑PARP↑, survivin↓, EGFR↓, HER2/EBBR2↓, ATP↓, Glycolysis↓, mt-OXPHOS↓, AKT1↓, HK2↓, Hif1a↓, ROS↑, NRF2↑, EMT↓, COX2↓, MMP2↓, MMP9↓, Zeb1↓, Snail↓, HDAC↓, HATs↓, MMP↓, Cyt‑c↓, Shh↓, Smo↓, Gli1↓, BioAv↝, BioAv↝, Dose↝,
2552- SFN,  Chemo,    Chemopreventive activity of sulforaphane
- Review, Var, NA
chemoPv↑, TumCG↓, *ROS↓, *Inflam↓, *Dose↝, *NRF2↑, *HO-1↑, *NQO1↑, NF-kB↓, ROS↑,
2553- SFN,    Mechanistic review of sulforaphane as a chemoprotective agent in bladder cancer
- Review, Bladder, NA
antiOx↓, Inflam↓, ChemoSen↑, ROS⇅, *NRF2↑, *GSH↑, Catalase↑, HO-1↑, NAD↑, chemoP↑,
2555- SFN,    Chemopreventive functions of sulforaphane: A potent inducer of antioxidant enzymes and apoptosis
- Review, Var, NA
chemoPv↑, HDAC↓, TumCCA↑, Apoptosis↑, Mets↑, *NRF2↑, ROS⇅,
3180- SFN,    Exploring the therapeutic effects of sulforaphane: an in-depth review on endoplasmic reticulum stress modulation across different disease contexts
- Review, Var, NA
*cardioP↑, *ER Stress↓, GRP78/BiP↑, XBP-1↑, Apoptosis↑, *NRF2↑, UPR↑,
2444- SFN,    Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage
- in-vitro, Nor, MRC-5
*GlucoseCon↓, *ROS↓, *Trx↓, *HK2↓, *NRF2↑, *Catalase↑, *TXNIP↑, *PFKFB2↓, *G6PD↑,
2168- SFN,    Amelioration of Alzheimer's disease by neuroprotective effect of sulforaphane in animal model
- in-vivo, AD, NA
*NRF2↑, *cognitive↑, other↓,
4202- SFN,    Regulation of BDNF transcription by Nrf2 and MeCP2 ameliorates MPTP-induced neurotoxicity
- Review, Park, NA
*NRF2↑, *BDNF↑,
4201- SFN,    Activation of BDNF by transcription factor Nrf2 contributes to antidepressant-like actions in rodents
- in-vivo, NA, NA
*NRF2↑, *BDNF↑, *HDAC2↓, *Mood↑,
4200- SFN,    Sulforaphane activates anti-inflammatory microglia, modulating stress resilience associated with BDNF transcription
- in-vitro, NA, NA
*NRF2↑, *BDNF↑, *Inflam↓,
4199- SFN,    Sulforaphane and Brain Health: From Pathways of Action to Effects on Specific Disorders
- Review, AD, NA - Review, Park, NA
*BBB↑, *BDNF↑, *neuroG↑, *NRF2↑, *HO-1↑, *Catalase↑, *SOD↑, *HSPs↑, *GSTs↑, *Trx↑, *GPx↑, *GSR↑, *GSH↑, *NQO1↑, *GutMicro↑, *Inflam↓, *neuroP↑,
3663- SFN,    Efficacy of Sulforaphane in Neurodegenerative Diseases
- Review, AD, NA - Review, Park, NA
*antiOx↑, *Inflam↓, *Half-Life↝, *NRF2↑, *NQO1↑, *HO-1↑, *TrxR↑, *ROS↓, *TNF-α↓, *IL1β↓, *IL6↓, *iNOS↓, *COX2↓, *Aβ↓, *GSH↑, *cognitive↑, *BACE↓, *HSP70/HSPA5↑, *neuroP↑, *ROS↓, *BBB↑, *MMP9↓,
3660- SFN,    Sulforaphane - role in aging and neurodegeneration
- Review, AD, NA
*antiOx↑, *Inflam↓, *NRF2↑, *NF-kB↓, *HDAC↓, *DNMTs↓, *neuroP↑, *AntiAge↑, *DNMT1↓, *DNMT3A↓, *memory↑, *HO-1↑, *ROS↓, *NO↓, *GSH↑, *NF-kB↓, *TNF-α↓, *IL10↑,
3659- SFN,    Epigenetic modification of Nrf2 by sulforaphane increases the antioxidative and anti-inflammatory capacity in a cellular model of Alzheimer's disease
- in-vitro, AD, NA
*NRF2↑, *ROS↓, *MDA↓, *SOD↑, *IL1β↓, *IL6↓, *NF-kB↓, *COX2↓, *iNOS↓, *Inflam↓,
3658- SFN,    Pre-Clinical Neuroprotective Evidences and Plausible Mechanisms of Sulforaphane in Alzheimer’s Disease
- Review, AD, NA
*NRF2↑, *antiOx↑, *neuroP↑, *Aβ↓, *BACE↓, *NQO1↑, *IL1β↓, *TNF-α↓, *IL6↓, *COX2↓, *iNOS↓, *NF-kB↓, *NLRP3↓, *Ca+2↓, *GSH↑, *MDA↓, *ROS↓, *SOD↑, *HO-1↑, *TrxR↑, *cognitive↑, *tau↓, *HSP70/HSPA5↑,
3657- SFN,    Sulforaphane exerts its anti-inflammatory effect against amyloid-β peptide via STAT-1 dephosphorylation and activation of Nrf2/HO-1 cascade in human THP-1 macrophages
- NA, AD, THP1
*NLRP3↓, *Inflam↓, *IL1β↓, *NRF2↑, *HO-1↑,
3656- SFN,    Chronic diseases, inflammation, and spices: how are they linked?
- Review, AD, NA
*AntiCan↑, *cardioP↑, *NRF2↑, *Inflam↓, *NF-kB↓, *STAT3↓, *ERK↓, *MAPK↓, AP-1↑, Bcl-2↓, Casp3↑, Casp9↑,
3184- SFN,    The Integrative Role of Sulforaphane in Preventing Inflammation, Oxidative Stress and Fatigue: A Review of a Potential Protective Phytochemical
- Review, Nor, NA
*NRF2↑, *Inflam↓, *NF-kB↓, *ROS↓, *BioAv↝, *BioAv↝, *BioAv↝, *BioAv↝, *cardioP↑, *GPx↑, *SOD↑, *Catalase↑, *GPx↑, *HO-1↑, *NADPH↑, *NQO1↑, *LDH↓, *hepatoP↑, *ALAT↓, *AST↓, *IL6↓,
3193- SFN,    Epigenetic Therapeutics Targeting NRF2/KEAP1 Signaling in Cancer Oxidative Stress
- Review, Var, NA
DNMTs↓, HDAC↑, NRF2↑, DNMT1↓, DNMT3A↓, NQO1↑, COMT↑, TumCG↓, *toxicity↓,
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↓,
1458- SFN,    Sulforaphane Impact on Reactive Oxygen Species (ROS) in Bladder Carcinoma
- Review, Bladder, NA
HDAC↓, eff↓, TumW↓, TumW↓, angioG↓, *toxicity↓, GutMicro↝, AntiCan↑, ROS↑, MMP↓, Cyt‑c↑, Bax:Bcl2↑, Casp3↑, Casp9↑, Casp8∅, cl‑PARP↑, TRAIL↑, DR5↑, eff↓, NRF2↑, ER Stress↑, COX2↓, EGFR↓, HER2/EBBR2↓, ChemoSen↑, NF-kB↓, TumCCA?, p‑Akt↓, p‑mTOR↓, p70S6↓, p19↑, P21↑, CD44↓, CSCs↓,
1465- SFN,    TRAIL attenuates sulforaphane-mediated Nrf2 and sustains ROS generation, leading to apoptosis of TRAIL-resistant human bladder cancer cells
- NA, Bladder, NA
eff↑, Apoptosis↑, Casp↑, MMP↓, BID↑, DR5↑, ROS↑, NRF2↑, eff↑, eff↓,
1428- SFN,    Broccoli or Sulforaphane: Is It the Source or Dose That Matters?
- Review, NA, NA
HDAC↓, NRF2↑,
1437- SFN,    Dietary Sulforaphane in Cancer Chemoprevention: The Role of Epigenetic Regulation and HDAC Inhibition
- Review, NA, NA
HDAC↓, HDAC1↓, HDAC2↓, HDAC3↓, HDAC8↓, eff↑, ac‑HSP90↑, DNMT1↓, DNMT3A↓, hTERT/TERT↓, NRF2↑, HO-1↑, NQO1↑, miR-155↓, miR-200c↑, SOX9↓, *toxicity↓,
1723- SFN,    Sulforaphane as a potential remedy against cancer: Comprehensive mechanistic review
- Review, Var, NA
*NRF2↑, ROS↑, MMP↓, Cyt‑c↑, cl‑PARP↑, Apoptosis↑, AMPK↑, GSH↓,
1501- SFN,    The Inhibitory Effect of Sulforaphane on Bladder Cancer Cell Depends on GSH Depletion-Induced by Nrf2 Translocation
- in-vitro, CRC, T24/HTB-9
Dose↝, NRF2↑, GSH↓, eff↑,
1508- SFN,    Nrf2 targeting by sulforaphane: A potential therapy for cancer treatment
- Review, Var, NA
*BioAv↑, HDAC↓, TumCCA↓, eff↓, Wnt↓, β-catenin/ZEB1↓, Casp12?, Bcl-2↓, cl‑PARP↑, Bax:Bcl2↑, IAP1↓, Casp3↑, Casp9↑, Telomerase↓, hTERT/TERT↓, ROS?, DNMTs↓, angioG↓, VEGF↓, Hif1a↓, cMYB↓, MMP1↓, MMP2↓, MMP9↓, ERK↑, E-cadherin↑, CD44↓, MMP2↓, eff↑, IL2↑, IFN-γ↑, IL1β↓, IL6↓, TNF-α↓, NF-kB↓, ERK↓, NRF2↑, RadioS↑, ChemoSideEff↓,
1509- SFN,    Combination therapy in combating cancer
- Review, NA, NA
NRF2↑, ChemoSideEff↓, eff↑, TumCP↓, Apoptosis↑, TumCCA↑, eff↑, PSA↓, P53↑, Hif1a↓, CAIX↓, chemoR↓, 5HT↓,
1513- SFN,  acetaz,    Next-generation multimodality of nutrigenomic cancer therapy: sulforaphane in combination with acetazolamide actively target bronchial carcinoid cancer in disabling the PI3K/Akt/mTOR survival pathway and inducing apoptosis
- in-vitro, BrCC, H720 - in-vivo, BrCC, NA - in-vitro, BrCC, H727
eff↑, tumCV↓, Apoptosis↑, P21↑, PI3K↓, Akt↓, mTOR↓, 5HT↓, NRF2↑,
1724- SFN,    Sulforaphane: A review of its therapeutic potentials, advances in its nanodelivery, recent patents, and clinical trials
- Review, Var, NA
antiOx↑, NRF2↑, HDAC↓, neuroP↑,
1725- SFN,    Anticancer Activity of Sulforaphane: The Epigenetic Mechanisms and the Nrf2 Signaling Pathway
- Review, Var, NA
*toxicity∅, AntiCan↑, antiOx↑, NRF2↑, DNMTs↓, HDAC↓, Hif1a↓, VEGF↓, P21↑, TumCCA↑, ac‑H3↑, ac‑H4↑, DNAdam↑, Dose↝,
1730- SFN,    Sulforaphane: An emergent anti-cancer stem cell agent
- Review, Var, NA
BioAv↓, BioAv↑, GSTA1↑, P450↓, TumCCA↑, HDAC↓, P21↑, p27↑, DNMT1↓, DNMT3A↓, cycD1/CCND1↑, DNAdam↑, BAX↑, Cyt‑c↑, Apoptosis↑, ROS↑, AIF↑, CDK1↑, Casp3↑, Casp8↑, Casp9↑, NRF2↑, NF-kB↓, TNF-α↓, IL1β↓, CSCs↓, CD133↓, CD44↓, ALDH↓, Nanog↓, OCT4↓, hTERT/TERT↓, MMP2↓, EMT↓, ALDH1A1↓, Wnt↓, NOTCH↓, ChemoSen↑, *Ki-67↓, *HDAC3↓, *HDAC↓,
1482- SFN,    Sulforaphane induces apoptosis in T24 human urinary bladder cancer cells through a reactive oxygen species-mediated mitochondrial pathway: the involvement of endoplasmic reticulum stress and the Nrf2 signaling pathway
- in-vitro, Bladder, T24/HTB-9
tumCV↓, Apoptosis↑, Cyt‑c↑, Bax:Bcl2↑, Casp9↑, Casp3↑, Casp8∅, cl‑PARP↑, ROS↑, MMP↓, eff↓, ER Stress↑, p‑NRF2↑, HO-1↑,
1484- SFN,    Sulforaphane’s Multifaceted Potential: From Neuroprotection to Anticancer Action
- Review, Var, NA - Review, AD, NA
neuroP↑, AntiCan↑, NRF2↑, HDAC↓, eff↑, *ROS↓, neuroP↑, HDAC↓, *toxicity∅, BioAv↑, eff↓, cycD1/CCND1↓, CDK4↓, p‑RB1↓, Glycolysis↓, miR-30a-5p↑, TumCCA↑, TumCG↓, TumMeta↓, eff↑, ChemoSen↑, RadioS↑, CardioT↓, angioG↓, Hif1a↓, VEGF↓, *BioAv?, *Half-Life∅,
1494- SFN,  doxoR,    Sulforaphane potentiates anticancer effects of doxorubicin and attenuates its cardiotoxicity in a breast cancer model
- in-vivo, BC, NA - in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
CardioT↓, *GSH↑, *ROS↓, *NRF2↑, NRF2∅, HDAC↓, DNMTs↓, Casp3↑, ER-α36↓, Remission↑, eff↑, ROS↑, selectivity?,
1495- SFN,  doxoR,    Sulforaphane protection against the development of doxorubicin-induced chronic heart failure is associated with Nrf2 Upregulation
- in-vivo, Nor, NA
*CardioT↓, *NRF2↑, *eff↓, *ROS↓,

Showing Research Papers: 1 to 38 of 38

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 38

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 2,   Catalase↑, 1,   GSH↓, 2,   GSTA1↑, 1,   HO-1↑, 4,   Mets↑, 1,   NQO1↑, 3,   NRF2↑, 15,   NRF2∅, 1,   p‑NRF2↑, 1,   mt-OXPHOS↓, 1,   ROS?, 1,   ROS↑, 8,   ROS⇅, 2,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 1,   MMP↓, 5,  

Core Metabolism/Glycolysis ⓘ

AKT1↓, 1,   AMPK↑, 1,   CAIX↓, 1,   glucoNG↓, 1,   Glycolysis↓, 2,   HK2↓, 1,   NAD↑, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 9,   BAX↑, 1,   Bax:Bcl2↑, 3,   Bcl-2↓, 2,   BID↑, 2,   Casp↑, 1,   Casp12?, 1,   Casp3↑, 7,   Casp7↑, 1,   Casp8↑, 1,   Casp8∅, 2,   Casp9↑, 5,   Cyt‑c↓, 1,   Cyt‑c↑, 5,   Diablo↑, 1,   DR5↑, 2,   hTERT/TERT↓, 3,   IAP1↓, 1,   IAP1↑, 1,   ICAD↑, 1,   p27↑, 1,   survivin↓, 2,   Telomerase↓, 1,   TRAIL↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 2,   p70S6↓, 1,   SOX9↓, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   ac‑H4↑, 1,   HATs↓, 1,   miR-30a-5p↑, 1,   other↓, 1,   tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 2,   GRP78/BiP↑, 1,   HSP27↑, 1,   ac‑HSP90↑, 1,   UPR↑, 1,   XBP-1↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   DNMT1↓, 3,   DNMT3A↓, 3,   DNMTs↓, 5,   P53↑, 1,   cl‑PARP↑, 5,  

Cell Cycle & Senescence ⓘ

CDK1↑, 1,   CDK2↓, 1,   CDK4↓, 2,   cycD1/CCND1↓, 1,   cycD1/CCND1↑, 1,   p19↑, 1,   P21↑, 4,   p‑RB1↓, 1,   TumCCA?, 1,   TumCCA↓, 1,   TumCCA↑, 7,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   ALDH1A1↓, 1,   CD133↓, 1,   CD44↓, 3,   cMYB↓, 1,   CSCs↓, 2,   EMT↓, 2,   ERK↓, 1,   ERK↑, 1,   Gli1↓, 1,   HDAC↓, 13,   HDAC↑, 1,   HDAC1↓, 1,   HDAC2↓, 1,   HDAC3↓, 1,   HDAC8↓, 1,   mTOR↓, 1,   p‑mTOR↓, 1,   Nanog↓, 1,   NOTCH↓, 1,   OCT4↓, 1,   PI3K↓, 1,   Shh↓, 1,   Smo↓, 1,   TumCG↓, 4,   Wnt↓, 2,  

Migration ⓘ

AP-1↑, 1,   E-cadherin↑, 1,   ER-α36↓, 1,   miR-155↓, 1,   miR-200c↑, 1,   MMP1↓, 1,   MMP2↓, 4,   MMP9↓, 2,   Smad1↑, 1,   Snail↓, 1,   TumCI↓, 1,   TumCP↓, 2,   TumMeta↓, 2,   Zeb1↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   EGFR↓, 2,   Hif1a↓, 5,   VEGF↓, 4,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IFN-γ↑, 1,   IL1β↓, 2,   IL2↑, 1,   IL6↓, 1,   Inflam↓, 1,   NF-kB↓, 4,   PSA↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

5HT↓, 2,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   COMT↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   BioAv↝, 2,   chemoR↓, 1,   ChemoSen↑, 5,   Dose↝, 3,   eff↓, 6,   eff↑, 11,   P450↓, 1,   RadioS↑, 2,   selectivity?, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 2,   GutMicro↝, 1,   HER2/EBBR2↓, 2,   hTERT/TERT↓, 3,   IL6↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 3,   CardioT↓, 2,   chemoP↑, 1,   chemoPv↑, 2,   ChemoSideEff↓, 2,   neuroP↑, 3,   Remission↑, 1,   TumW↓, 2,  
Total Targets: 168

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 4,   Catalase↑, 3,   GPx↑, 3,   GSH↑, 6,   GSR↑, 1,   GSTs↑, 1,   H2O2↓, 1,   HO-1↑, 7,   MDA↓, 2,   NQO1↑, 5,   NRF2↑, 22,   ROS↓, 11,   SOD↑, 4,   Trx↓, 1,   Trx↑, 1,   TrxR↑, 2,   TrxR1↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   G6PD↑, 1,   GlucoseCon↓, 1,   HK2↓, 1,   LDH↓, 1,   NADPH↑, 1,   PFKFB2↓, 1,  

Cell Death ⓘ

Cyt‑c↓, 1,   IAP1↓, 1,   iNOS↓, 3,   MAPK↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,   HSP27↓, 1,   HSP70/HSPA5↑, 2,   HSPs↑, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,   DNMT3A↓, 1,   DNMTs↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   HDAC↓, 2,   HDAC2↓, 1,   HDAC3↓, 1,   neuroG↑, 1,   STAT3↓, 1,  

Migration ⓘ

Ca+2↓, 1,   Ki-67↓, 1,   MMP9↓, 1,   TXNIP↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Barriers & Transport ⓘ

BBB↑, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   IL10↑, 1,   IL1β↓, 4,   IL6↓, 4,   Inflam↓, 9,   NF-kB↓, 6,   TNF-α↓, 3,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 4,   tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 2,   BACE↓, 2,   NLRP3↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv?, 1,   BioAv↑, 1,   BioAv↝, 4,   Dose↝, 1,   eff↓, 1,   Half-Life↝, 1,   Half-Life∅, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   GutMicro↑, 1,   IL6↓, 4,   Ki-67↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   AntiCan↑, 1,   cardioP↑, 3,   CardioT↓, 1,   cognitive↑, 3,   hepatoP↑, 1,   memory↑, 1,   Mood↑, 1,   neuroP↑, 4,   toxicity↓, 3,   toxicity∅, 2,  
Total Targets: 83

Scientific Paper Hit Count for: NRF2, nuclear factor erythroid 2-related factor 2
38 Sulforaphane (mainly Broccoli)
2 doxorubicin
1 Curcumin
1 Resveratrol
1 EGCG (Epigallocatechin Gallate)
1 Lycopene
1 Selenium
1 Chemotherapy
1 acetazolamide
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#:226  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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