condition found tbRes List
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


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⟱
1435- GEN,  SFN,    The Effects of Combinatorial Genistein and Sulforaphane in Breast Tumor Inhibition: Role in Epigenetic Regulation
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7
DNMTs↓, GEN extensively studied for its role as DNA methyltransferase (DNMT) inhibitor
HDAC↓, SFN), is known as a histone deacetylase (HDAC) inhibitor
eff↑, Our results indicate that the combination of GEN and SFN is much more effective than their single doses in increasing the rate of apoptosis
TumCCA↑, G2 phase in MDA-MB-231 and G1 phase in MCF-7
HMTs↓, histone methyltransferase (HMT) inhibitor
HDAC2↓, combination downregulates the levels of HDAC2 and HDAC3 both at the mRNA and protein levels
HDAC3↓,
KLF4↓, potential to downregulate KLF4 levels, which plays an important role in stem cell formation.
hTERT↓,

2445- SFN,    Sulforaphane-Induced Cell Cycle Arrest and Senescence are accompanied by DNA Hypomethylation and Changes in microRNA Profile in Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, SkBr3
TumCCA↑, SFN (5-10 µM) promoted cell cycle arrest, elevation in the levels of p21 and p27 and cellular senescence
P21↑,
p27↑,
NO↑, effects were accompanied by nitro-oxidative stress, genotoxicity and diminished AKT signaling
Akt↓,
ATP↓, decreased pools of ATP and AMPK activation, and autophagy induction
AMPK↑,
TumAuto↑,
DNMT1↓, decreased levels of DNA methyltransferases (DNMT1, DNMT3B)
HK2↓, A decrease in HK2 levels was observed in SFN-treated MDA-MB-231 cells
PKM2↓, and a decrease in PKM2 levels was noticed in SFN-treated MDA-MB-231 and SK-BR-3 cells
HDAC3↓, . In contrast, HDAC3 , HDAC4 , HDAC6 , HDAC7 , HDAC8 ), HDAC9 and HDAC10 (histone deacetylase 10) mRNA levels were decreased in SFN-treated MDA-MB-231 cells
HDAC4↓,
HDAC8↓,

1730- SFN,    Sulforaphane: An emergent anti-cancer stem cell agent
- Review, Var, NA
BioAv↓, When exposed to high temperatures during meal preparation, myrosinase can be degraded, lose its function, and subsequently compromise the synthesis of SFN.
BioAv↑, eating raw cruciferous vegetables, instead of heating them can significantly improve the biodisponibility of SFN and its subsequent beneficial effects.
GSTA1↑, induction of Phase II enzymes [glutathione S-transferase (GST)
P450↓, (cytochrome P450, CYP) inhibition
TumCCA↑, herb-derived agent can also promote cell cycle arrest and apoptosis by regulating different signaling pathways including Nuclear Factor erythroid Related Factor 2 (Nrf2)-Keap1 and NF-κB.
HDAC↓, modulate the activity of some epigenetic factors, such as histone deacetylases (HDAC),
P21↑, upregulation of p21 and p27,
p27↑,
DNMT1↓, SFN was able to decrease the expression of DNMT1 and DNMT3 in LnCap prostate cancer cells
DNMT3A↓,
cycD1↑, reduce methylation in Cyclin D2 promoter, thus inducing Cyclin D2 gene expression in those cells
DNAdam↑, SFN induced DNA damage, enhanced Bax expression and the release of cytochrome C followed by apoptosis
BAX↑,
Cyt‑c↑,
Apoptosis↑,
ROS↑, SFN increased reactive oxygen species (ROS), apoptosis-inducing factor (AIF)
AIF↑,
CDK1↑,
Casp3↑, activation of caspase-3, -8, and -9
Casp8↑,
Casp9↑,
NRF2↑, SFN significantly activated the major antioxidant marker Nrf2 and decreased NFκB, TNF-α, IL-1β
NF-kB↓,
TNF-α↓,
IL1β↓,
CSCs↓, SFN, have attracted attention due to their anti-CSC effect
CD133↓,
CD44↓,
ALDH↓,
Nanog↓,
OCT4↓,
hTERT↓,
MMP2↓,
EMT↓, SFN was reported to inhibit EMT and metastasis in the NSCLC, the cell lines H1299
ALDH1A1↓, ALDH1A1), Wnt3, and Notch4, other CSC-related genes inhibited by SFN treatment
Wnt↓,
NOTCH↓, SFN can inhibit aberrantly activated embryonic pathways in CSCs, including Sonic Hedgehog (SHH), Wnt/β-catenin, Cripto-1 (CR-1), and Notch.
ChemoSen↑, These results suggest that the antioxidant properties of SFN do not impact the cytotoxicity of antineoplastic drugs, but on the contrary, seems to improve it.
*Ki-67↓, Ki-67 and HDAC3 levels significantly decreased in benign breast tissues, and there was also a reduction in HDAC activity in blood cells
*HDAC3↓,
*HDAC↓,

1725- SFN,    Anticancer Activity of Sulforaphane: The Epigenetic Mechanisms and the Nrf2 Signaling Pathway
- Review, Var, NA
*toxicity∅, Sulforaphane (SFN), a compound derived from cruciferous vegetables that has been shown to be safe and nontoxic, with minimal/no side effects
AntiCan↑, such as anticancer and antioxidant activities.
antiOx↑,
NRF2↑, FN also upregulates a series of cytoprotective genes by activating nuclear factor erythroid-2- (NF-E2-) related factor 2 (Nrf2), a critical transcription factor activated in response to oxidative stress;
DNMTs↓, SFN can reverse such epigenetic alterations in cancers by targeting DNA methyltransferases (DNMTs), histone deacetyltransferases (HDACs)
HDAC↓,
Hif1a↓, By suppressing the expression and activity of hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF), SFN inhibited the angiogenesis and metastasis of ovarian and colon cancers
VEGF↓,
P21↑, 15 μM SFN treatment caused reexpression of p21WAF1/CIP1 due to reduced expression of class I and II HDACs
TumCCA↑, resulted in cell cycle arrest
ac‑H3↑, upregulation of acetylated histone H3 and H4
ac‑H4↑,
DNAdam↑, SFN induced DNA damage
Dose↝, To achieve the effective inhibition of HDAC activity, it was reported that the concentration of SFN used in vitro experiments was from 3 to 15 μM, a single oral dose of 10 μmol in mice, and 68 g broccoli sprouts in human

1722- SFN,    Sulforaphane as an anticancer molecule: mechanisms of action, synergistic effects, enhancement of drug safety, and delivery systems
- Review, Var, NA
TumCCA↑, arresting cell cycle in the G2/M and G1 phase
CYP1A1↓, Sulforaphane inhibits CYP1A1 and CYP3A4 and decease the activity of CYP3A4
CYP3A4↓,
Cyt‑c↑, release of cytochrome C from the mitochondria
Casp9↑,
Apoptosis↑,
ROS↑, generation of reactive oxygen species (ROS), and mitogen-activated protein kinases (MAPK)
MAPK↑,
P53↑, sulforaphane treatment increased p53 protein expression with associated increase in the protein levels of Bax
BAX↑,
ChemoSen↑, Combination therapies target multiple cell survival pathways, which results in synergism
HDAC↓, HDACi Histone deacetylase inhibition
GSH↓, fig 3
HO-1↑, They found that the protective effect of sulforaphane is mediated by the activation of the Keap1/Nrf2/ARE pathway, which consequently induce HO-1

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↓, Sp1 protein was significantly decreased by SFN treatment in prostate cancer cells . Because SFN decreased the expression of Sp1, and to a lesser extent Sp3
selectivity↑, SFN alters gene expression differentially in normal and cancer cells with key targets in chemopreventive processes, making it a promising dietary anti-cancer agent.
NRF2↑, through the induction of phase 2 enzymes via Keap1-Nrf2 signaling
HDAC↓, SFN also inhibits the activity and/or expression of genes that regulate epigenetic mechanisms including histone deactylases (HDACs) and DNA methyltransferases (DNMTs) in cancer cells
DNMTs↓,
TumCCA↑, 15 μM SFN treatment induces cell cycle arrest at the G1 phase and only modestly increases apoptosis
selectivity↑, Normal prostate epithelial cells (PREC) do not undergo cell cycle arrest or apoptosis in response to this SFN treatment
HO-1↑, In all cell lines and time points, HO1 and NQO1 were identified as significantly upregulated by SFN
NQO1↑,
CDK2↓, MX non-receptor tyrosine kinase (BMX), cyclin-dependent kinase 2 (CDK2), and polo-like kinase 1 (PLK1) had decreased expression with SFN treatment
TumCP↓, suppression of Sp1 expression decreased prostate cancer cells proliferation.
BID↑, SFN treatment produced a significant increase in the expression of the apoptosis related genes Bid, Smac/Diablo, and ICAD only in PC-3 cells (
Smad1↑,
Diablo↑,
ICAD↑,
Cyt‑c↑, It also increased the expression of cytochrome c, c-IAP1, and HSP27 in PC-3 cells while it decreased expression in PREC cells.
IAP1↑,
HSP27↑,
*Cyt‑c↓,
*IAP1↓,
*HSP27↓,
survivin↓, In these studies, inhibition of Sp1 is associated with inhibition of the cancer promoting genes survivin, CDK4, VEGF and the androgen receptor.
CDK4↓,
VEGF↓,
AR↓,

2555- SFN,    Chemopreventive functions of sulforaphane: A potent inducer of antioxidant enzymes and apoptosis
- Review, Var, NA
chemoP↑, induction of Metallothioneins MT by sulforaphane as a strategy for achieving chemoprevention and chemoprotection.
HDAC↓, sulforaphane supplementation resulted in slower tumor growth and significant histone deacetylase (HDAC) inhibition in the xenografts,
TumCCA↑, HDAC inhibition represents a novel chemoprevention mechanism by which sulforaphane can promote cell cycle arrest and apoptosis.
Apoptosis↑,
Mets↑, induction of Metallothioneins MT by sulforaphane
*NRF2↑, We have shown that sulforaphane can activate Nrf2 ...suggesting that increased expression of Nrf2 protein may play a key role in sulforaphane-induced MT gene activation.
ROS⇅, exposure to high concentrations of sulforaphane might generate an oxidant signal to stimulate caspase 3 pathway activation and DNA fragmentation, leading to cell death.

2448- SFN,    Sulforaphane and bladder cancer: a potential novel antitumor compound
- Review, Bladder, NA
Apoptosis↑, Recent studies have demonstrated that Sulforaphane not only induces apoptosis and cell cycle arrest in BC cells, but also inhibits the growth, invasion, and metastasis of BC cells
TumCG↓,
TumCI↓,
TumMeta↓,
glucoNG↓, Additionally, it can inhibit BC gluconeogenesis
ChemoSen↑, demonstrate definite effects when combined with chemotherapeutic drugs/carcinogens.
TumCCA↑, SFN can block the cell cycle in G2/M phase, upregulate the expression of Caspase3/7 and PARP cleavage, and downregulate the expression of Survivin, EGFR and HER2/neu
Casp3↑,
Casp7↑,
cl‑PARP↑,
survivin↓,
EGFR↓,
HER2/EBBR2↓,
ATP↓, SFN inhibits the production of ATP by inhibiting glycolysis and mitochondrial oxidative phosphorylation in BC cells in a dose-dependent manner
Glycolysis↓,
mt-OXPHOS↓,
AKT1↓, dysregulation of glucose metabolism by inhibiting the AKT1-HK2 axis
HK2↓,
Hif1a↓, Sulforaphane inhibits glycolysis by down-regulating hypoxia-induced HIF-1α
ROS↑, SFN can upregulate ROS production and Nrf2 activity
NRF2↑,
EMT↓, inhibiting EMT process through Cox-2/MMP-2, 9/ ZEB1 and Snail and miR-200c/ZEB1 pathways
COX2↓,
MMP2↓,
MMP9↓,
Zeb1↓,
Snail↓,
HDAC↓, FN modulates the histone status in BC cells by regulating specific HDAC and HATs,
HATs↓,
MMP↓, SFN upregulates ROS production, induces mitochondrial oxidative damage, mitochondrial membrane potential depolarization, cytochrome c release
Cyt‑c↓,
Shh↓, SFN significantly lowers the expression of key components of the SHH pathway (Shh, Smo, and Gli1) and inhibits tumor sphere formation, thereby suppressing the stemness of cancer cells
Smo↓,
Gli1↓,
BioAv↝, SFN is unstable in aqueous solutions and at high temperatures, sensitive to oxygen, heat and alkaline conditions, with a decrease in quantity of 20% after cooking, 36% after frying, and 88% after boiling
BioAv↝, It has been reported that the ability of individuals to use gut myrosinase to convert glucoraphanin into SFN varies widely
Dose↝, Excitingly, it has been reported that daily oral administration of 200 μM SFN in melanoma patients can achieve plasma levels of 655 ng/mL with good tolerance

1466- SFN,    Sulforaphane inhibits thyroid cancer cell growth and invasiveness through the reactive oxygen species-dependent pathway
- vitro+vivo, Thyroid, FTC-133
TumCP↓,
TumCCA↑, G2/M phase
Apoptosis↑,
TumCMig↓,
TumCI↓,
EMT↓,
Slug↓,
Twist↓,
MMP2↓,
MMP9↓,
TumCG↓,
p‑Akt↓,
P21↑,
ERK↑,
p38↑,
ROS↑, ROS was significantly induced in both FTC133 and K1 cells when cells were treated with 40 μM SFN for 4 h Several previous studies have shown that SFN induces ROS
*toxicity∅, we did not find significant effect of SFN on body weight and liver function of mice.
MMP↓,
eff↓, Like NAC, ASC treatment significantly attenuated anti-proliferative effect of SFN in these two cell lines

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↑,
NA↑,

1460- SFN,    High levels of EGFR prevent sulforaphane-induced reactive oxygen species-mediated apoptosis in non-small-cell lung cancer cells
- in-vitro, Lung, NA
ROS↑, Sulforaphane (SFN) has been shown to induce the production of reactive oxygen species (ROS) and inhibit epidermal growth factor receptor (EGFR)
EGFR↓,
eff↓, We present evidence that cells with high-level EGFR expression (CL1-5) are more resistant to SFN treatment than those with low-level expression (CL1-0)
TumCCA↑, S-phase
γH2AX↑,
DNAdam↑,
eff↓, Pretreatment with the antioxidant N-acetyl-L-cysteine prevented SFN-induced apoptosis in CL1-0 cells and production of γH2AX in both CL1-0 and CL1-5 cells.

1459- SFN,  Aur,    Auranofin Enhances Sulforaphane-Mediated Apoptosis in Hepatocellular Carcinoma Hep3B Cells through Inactivation of the PI3K/Akt Signaling Pathway
- in-vitro, Liver, Hep3B - in-vitro, Liver, HepG2
eff↑, sulforaphane significantly enhanced auranofin-induced apoptosis by inhibiting TrxR activity and cell proliferation compared to either single treatment
TumCCA↑, Sub-G1 cells
Apoptosis↑,
MMP↓,
BAX↑,
cl‑PARP↑,
Casp3↑,
Casp8↑,
Casp9↑,
ROS↑, combined treatment induced excessive generation of reactive oxygen species (ROS)
eff↓, treatment with N-acetyl-L-cysteine, a ROS scavenger, reduced combined treatment-induced ROS production and apoptosis.
PI3K↓,
Akt↓,
TrxR↓, treatment with either sulforaphane or auranofin alone at low concentrations weakly inhibit TrxR activity Combined treatment significantly reduced TrxR activity and cell viability
BAX↑,
Bcl-2∅,

1458- SFN,    Sulforaphane Impact on Reactive Oxygen Species (ROS) in Bladder Carcinoma
- Review, Bladder, NA
HDAC↓, SFN’s role as a natural HDAC-inhibitor is highly relevant
eff↓, SFN exerts stronger anti-proliferative effects on bladder cancer cell lines under hypoxia, compared to normoxic conditions
TumW↓, mice, SFN (52 mg/kg body weight) for 2 weeks reduced tumor weight by 42%
TumW↓, In another study a 63% inhibition was noted when tumor bearing mice were treated with SFN (12 mg/kg body weight) for 5 weeks
angioG↓,
*toxicity↓, In both investigations, the administration of SFN did not evoke apparent toxicity
GutMicro↝, SFN may protect against chemical-induced bladder cancer by normalizing the composition of gut microbiota and repairing pathophysiological destruction of the gut barrier,
AntiCan↑, A prospective study involving nearly 50,000 men indicated that high cruciferous vegetable consumption may reduce bladder cancer risk
ROS↑, Evidence shows that SFN upregulates the ROS level in T24 bladder cancer cells to induce apoptosis
MMP↓,
Cyt‑c↑,
Bax:Bcl2↑,
Casp3↑,
Casp9↑,
Casp8∅,
cl‑PARP↑,
TRAIL↑, ROS generation promotes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) sensitivity
DR5↑,
eff↓, Blockade of ROS generation inhibited apoptotic activity and prevented Nrf2 activation in cells treated with SFN, pointing to a direct effect of ROS on apoptosis
NRF2↑, SFN potently inhibits carcinogenesis via activation of the Nrf2 pathway
ER Stress↑, endoplasmic reticulum stress evoked by SFN
COX2↓, downregulates COX-2 in T24 cells
EGFR↓, downregulation of both the epidermal growth factor receptor (EGFR) and the human epidermal growth factor receptor 2 (HER2/neu
HER2/EBBR2↓,
ChemoSen↑, gemcitabine/cisplatin and SFN triggered pathway alterations in bladder cancer may open new therapeutic strategies, including a combined treatment regimen to cause additive effects.
NF-kB↓,
TumCCA?, cell cycle at the G2/M phase
p‑Akt↓,
p‑mTOR↓,
p70S6↓,
p19↑, p19 and p21, are elevated under SFN
P21↑,
CD44↓, CD44s expression correlates with induced intracellular levels of ROS in bladder cancer cells variants v3–v7 on bladder cancer cells following SFN exposure

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↑, accumulation in the sub G1 phase
ROS↑, SFN caused a considerable increase in ROS in MIA PaCa-2 and PANC-1 cells as compared to the control group
MMP↓, SFN increased ROS level and γH2A.X expression while decreasing mitochondrial membrane potential (ΔΨm).
γH2AX↑,
eff↓, (NAC) was shown to reverse SFN-induced cytotoxicity and ROS level.
*toxicity↓, HUVECs, used as normal control cells, did not show significant inhibitory effects at SFN concentrations below 20 μM

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↑, cell cycle arrest at the S- and G2/M-phase
H3↑,
H4↑,
HDAC↓, SFN acts as a histone deacetylase (HDAC) inhibitor.
CDK1↑, With 10 µM SFN, CDK1 and CDK2 increased in both cell lines,
CDK2↑,
p19↑,
*BioAv↑, 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

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↑, SFN synergistically augmented the GEM-mediated attenuation of cell viability and proliferation
tumCV↓,
TumCP↓,
TumCCA↑, G2/M cell cycle arrest
Apoptosis↑,
cl‑Casp3↑,
TumCI↓,
VEGF↓, VEGFA
VEGFR2↓,
Hif1a↓,
eNOS↓,
EMT?, SFN effectively inhibited the GEM-mediated induction of epithelial–mesenchymal transition (EMT)
TumCG↓,
Ki-67↓,
TUNEL↑, increased TUNEL+ apoptotic cells
P21↑,
p‑Chk2↑,
CDC25↓, decreased p-Cdc25C
BAX↑,
*ROS↓, SFN is also known to exert anti-oxidative effects via Nrf2 activation. in vivo study, optimization is performed by evaluating the anti-oxidative property of SFN in the liver.
NQO1?, identified 50 mg/kg/day as the minimal dose that significantly induced these anti-oxidative genes

1509- SFN,    Combination therapy in combating cancer
- Review, NA, NA
NRF2↑, chemopreventive properties that are thought to be due to potent upregulation of Nrf2
ChemoSideEff↓, chemopreventive properties
eff↑, combined SFN with taxol in treatment of prostate cancer cell line DU145, and observed that SFN potentiated the effects of low doses of taxol
TumCP↓,
Apoptosis↑,
TumCCA↑, induce G2/M cell cycle arrest in vitro and in vivo
eff↑, SFN positively enhanced bortezomib, lenalidomide, and conventional drugs, such as dexamethasone, doxorubicin, and melphalan in a synergistic manner
PSA↓, SFN has shown to significantly reduce levels of prostate-specific antigen (PSA) (44.4% SFN group vs. 71.8% in placebo)
P53↑, SFN activates various anti-cancer responses such as p53, ARE, IRF-1, Pax-6 and XRE while suppressing proteins involved in tumorigenesis and progression, such as HIF1α, AP-1 and CA IX
Hif1a↓, while suppressing proteins involved in tumorigenesis and progression, such as HIF1α, AP-1 and CA IX
CAIX↓,
chemoR↓, SFN has thus shown to reduce chemoresistance and may be a potential agent to be used in conjunction with chemotherapeutics
5HT↓, SFN downregulates 5-HT receptor expression in Caco-2 cells

1508- SFN,    Nrf2 targeting by sulforaphane: A potential therapy for cancer treatment
- Review, Var, NA
*BioAv↑, RAW: higher amounts were detected when broccoli were eaten raw (bioavailability equal to 37%), compared to the cooked broccoli (bioavailability 3.4%)
HDAC↓, Sulforaphane is able to down-regulate HDAC activity and induce histone hyper-acetylation in tumor cell
TumCCA↓, Sulforaphane induces cell cycle arrest in G1, S and G2/M phases,
eff↓, in leukemia stem cells, sulforaphane potentiates imatinib effect through inhibition of the Wnt/β-catenin functions
Wnt↓,
β-catenin/ZEB1↓,
Casp12?, inducing caspases activation
Bcl-2↓,
cl‑PARP↑,
Bax:Bcl2↑, unbalancing the ratio Bax/Bcl-2
IAP1↓, down-regulating IAP family proteins
Casp3↑,
Casp9↑,
Telomerase↓, In Hep3B cells, sulforaphane reduces telomerase activity
hTERT↓, inhibition of hTERT expression;
ROS?, increment of ROS, induced by this compound, is essential for the downregulation of transcription and of post-translational modification of hTERT in suppression of telomerase activity
DNMTs↓, (2.5 - 10 μM) represses hTERT by impacting epigenetic pathways, in particular through decreased DNA methyltransferases activity (DNMTs)
angioG↓, inhibit tumor development through regulation of angiogenesis
VEGF↓,
Hif1a↓,
cMYB↓,
MMP1↓, inhibition of migration and invasion activities induced by sulforaphane in oral carcinoma cell lines has been associated to the inhibition of MMP-1 and MMP-2
MMP2↓,
MMP9↓,
ERK↑, inhibits invasion by activating ERK1/2, with consequent upregulation of E-cadherin (an invasion inhibitor)
E-cadherin↑,
CD44↓, downregulation of CD44v6 and MMP-2 (invasion promoters)
MMP2↓,
eff↑, ombination of sulforaphane and quercetin synergistically reduces the proliferation and migration of melanoma (B16F10) cells
IL2↑, induces upregulation of IL-2 and IFN-γ
IFN-γ↑,
IL1β↓, downregulation of IL-1beta, IL-6, TNF-α, and GM-CSF
IL6↓,
TNF-α↓,
NF-kB↓, sulforaphane inhibits the phorbol ester induction of NF-κB, inhibiting two pathways, ERK1/2 and NF-κB
ERK↓,
NRF2↑, At molecular level, sulforaphane modulates cellular homeostasis via the activation of the transcription factor Nrf2.
RadioS↑, sulforaphane could be used as a radio-sensitizing agent in prostate cancer if clinical trials will confirm the pre-clinical results.
ChemoSideEff↓, chemopreventive effects of sulforaphane

1498- SFN,    Prolonged sulforaphane treatment activates survival signaling in nontumorigenic NCM460 colon cells but apoptotic signaling in tumorigenic HCT116 colon cells
- in-vitro, CRC, HCT116 - in-vitro, Nor, NCM460
selectivity↑, we demonstrated that SFN (15 μmol/L) exposure (72 h) inhibited cell proliferation by up to 95% in colon cancer cells (HCT116) and by 52% in normal colon mucosa-derived (NCM460) cells
TumCCA↑, reduction of G1 phase cell distribution
Apoptosis↑, apoptosis in HCT116 cells, but to a much lesser extent in NCM460 cells
*p‑ERK↑, in NCM460 cells but not in HCT116 cells
cMYB↓, decreased c-Myc expression in HCT116 cells but not NCM460 cells.
selectivity↑, decreased c-Myc expression in HCT116 cells but not NCM460 cells.
selectivity↑, upregulated p-ERK1/2 in NCM460 cells but not in HCT116 cells

1497- SFN,    Differential effects of sulforaphane on histone deacetylases, cell cycle arrest and apoptosis in normal prostate cells versus hyperplastic and cancerous prostate cells
- in-vitro, Nor, PrEC - in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
HDAC↓, ability of SFN to inhibit histone deacetylase enzymes
selectivity↑, 15 µM SFN selectively induced cell cycle arrest and apoptosis in BPH1, LnCap and PC3 cells but not PrEC cells
TumCCA↑,
Apoptosis↑,
selectivity↑, selectively decreased HDAC activity
H3↑,
P21↑, in prostate cancer cells
selectivity↑, we conclude that SFN exerts differential effects on cell proliferation, HDAC activity and downstream targets in normal and cancer cells.

1484- SFN,    Sulforaphane’s Multifaceted Potential: From Neuroprotection to Anticancer Action
- Review, Var, NA - Review, AD, NA
neuroP↑, current evidence supporting the neuroprotective and anticancer effects of SFN
AntiCan↑,
NRF2↑, neuroprotective effects through the activation of the Nrf2 pathway
HDAC↓, histone deacetylase was inhibited after human subjects ingested 68 g of broccoli sprouts
eff↑, sensitize cancer cells to chemotherapy
*ROS↓, protecting neurons [14] and microglia [15] against oxidative stress
neuroP↑, neuroprotective effects in Alzheimer’s disease (AD)
HDAC↓, capacity as a histone deacetylase (HDAC) inhibitor
*toxicity∅, normal cells are relatively resistant to SFN-induced cell death
BioAv↑, SFN has good bioavailability; it can reach high intracellular and plasma concentrations
eff↓, 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
cycD1↓, in breast cancer
CDK4↓, in breast cancer
p‑RB1↓, in breast cancer
Glycolysis↓, in prostate cancer
miR-30a-5p↑, ovarian cancer
TumCCA↑, gastric cancer
TumCG↓,
TumMeta↓,
eff↑, SFN emerged as a critical enhancer of ST’s efficacy by suppressing resistance in RCC cells, offering a potent approach to overcome ST monotherapy limitations.
ChemoSen↑, SFN may improve the effectiveness of chemotherapy by increasing cancer cell sensitivity to the drugs used to treat them
RadioS↑, SFN may help protect healthy cells and tissues from the harmful effects of radiation
CardioT↓, Several studies have demonstrated the protective role of SFN in cardiotoxicity
angioG↓, In colon cancers, SFN blocks cells’ progression and angiogenesis by inhibiting HIF-1α and VEGF expression
Hif1a↓,
VEGF↓,
*BioAv?, SFN is well absorbed in the intestine, with an absolute bioavailability of approximately 82%.
*Half-Life∅, In rats, after an oral dose of 50 μmol of SFN, the plasma concentration of SFN can peak at 20 μM at 4 h and decline with a half-life of about 2.2 h

1480- SFN,    Sulforaphane Induces Cell Death Through G2/M Phase Arrest and Triggers Apoptosis in HCT 116 Human Colon Cancer Cells
- in-vitro, CRC, HCT116
tumCV↓,
TumCCA↑, G2/M phase arrest
Apoptosis↑,
cycA1↑,
CycB↑,
CDC25↓, Cdc 25C
CDK1↓,
ROS↑, SFN induced the generation of reactive oxygen species (ROS)
eff↓, Ca[Formula: see text] and decreased mitochondria membrane potential and increased caspase-8, -9 and -3 activities in HCT 116 cell
Cyt‑c↑,
AIF↑,
ER Stress↑,

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↑, G2/M phase
CycB↑,
P21↑,
p‑H3↑,
p‑AMPK↑,
eff↓, compound C, an AMPK inhibitor, significantly blocked sulforaphane-induced apoptosis
MMP↓,
Cyt‑c↑,
ROS↑, sulforaphane provoked the generation of intracellular ROS
eff↓, sulforaphane provoked the generation of intracellular ROS; especially when ROS production was blocked by antioxidant N-acetylcysteine, both AMPK activation and growth inhibition by sulforaphane were completely abolished

1468- SFN,    Cellular responses to dietary cancer chemopreventive agent D,L-sulforaphane in human prostate cancer cells are initiated by mitochondrial reactive oxygen species
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
ROS↑,
DNAdam↑,
MMP↓,
Cyt‑c↑,
TumCCA↑, G2/M phase cell cycle arrest


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 24

Results for Effect on Cancer/Diseased Cells:
5HT↓,1,   AIF↑,2,   Akt↓,2,   p‑Akt↓,2,   AKT1↓,1,   ALDH↓,1,   ALDH1A1↓,1,   AMPK↑,1,   p‑AMPK↑,1,   angioG↓,3,   AntiCan↑,3,   antiOx↑,2,   Apoptosis↑,13,   AR↓,1,   ATP↓,2,   BAX↑,5,   Bax:Bcl2↑,2,   Bcl-2↓,1,   Bcl-2∅,1,   BID↑,1,   BioAv↓,1,   BioAv↑,2,   BioAv↝,2,   CAIX↓,1,   CardioT↓,1,   Casp12?,1,   Casp3↑,5,   cl‑Casp3↑,2,   Casp7↑,1,   Casp8↑,2,   Casp8∅,1,   Casp9↑,5,   CD133↓,1,   CD44↓,3,   CDC25↓,2,   CDK1↓,1,   CDK1↑,2,   CDK2↓,1,   CDK2↑,1,   CDK4↓,2,   chemoP↑,1,   chemoR↓,1,   ChemoSen↑,6,   ChemoSideEff↓,2,   p‑Chk2↑,1,   cMYB↓,2,   COX2↓,2,   CSCs↓,1,   cycA1↑,1,   CycB↑,2,   cycD1↓,1,   cycD1↑,1,   CYP1A1↓,1,   CYP3A4↓,1,   Cyt‑c↓,1,   Cyt‑c↑,7,   Diablo↑,1,   DNAdam↑,4,   DNMT1↓,2,   DNMT3A↓,1,   DNMTs↓,4,   Dose↝,2,   DR5↑,1,   E-cadherin↑,1,   eff↓,12,   eff↑,7,   EGFR↓,3,   EMT?,1,   EMT↓,3,   eNOS↓,1,   ER Stress↑,2,   ERK↓,1,   ERK↑,2,   Gli1↓,1,   glucoNG↓,1,   Glycolysis↓,2,   GSH↓,1,   GSTA1↑,1,   GutMicro↝,1,   H3↑,2,   p‑H3↑,1,   ac‑H3↑,2,   H4↑,1,   ac‑H4↑,1,   HATs↓,1,   HDAC↓,14,   HDAC2↓,1,   HDAC3↓,2,   HDAC4↓,1,   HDAC8↓,1,   HER2/EBBR2↓,2,   Hif1a↓,6,   HK2↓,2,   HMTs↓,1,   HO-1↑,2,   HSP27↑,1,   hTERT↓,3,   IAP1↓,1,   IAP1↑,1,   ICAD↑,1,   IFN-γ↑,1,   IL1β↓,2,   IL2↑,1,   IL6↓,1,   Ki-67↓,1,   KLF4↓,1,   MAPK↑,1,   Mets↑,1,   miR-30a-5p↑,1,   MMP↓,7,   MMP1↓,1,   MMP2↓,5,   MMP9↓,3,   p‑mTOR↓,1,   NA↑,1,   Nanog↓,1,   neuroP↑,2,   NF-kB↓,3,   NO↑,1,   NOTCH↓,1,   NQO1?,1,   NQO1↑,1,   NRF2↑,8,   OCT4↓,1,   mt-OXPHOS↓,1,   p19↑,2,   P21↑,8,   p27↑,2,   p38↑,1,   P450↓,1,   P53↑,2,   p70S6↓,1,   cl‑PARP↑,5,   PI3K↓,1,   PKM2↓,1,   PSA↓,1,   RadioS↑,2,   p‑RB1↓,1,   ROS?,1,   ROS↑,11,   ROS⇅,1,   selectivity↑,8,   Shh↓,1,   Slug↓,1,   Smad1↑,1,   Smo↓,1,   Snail↓,1,   Sp1/3/4↓,1,   survivin↓,2,   Telomerase↓,1,   TNF-α↓,2,   TRAIL↑,1,   TrxR↓,1,   TumAuto↑,1,   TumCCA?,1,   TumCCA↓,1,   TumCCA↑,22,   TumCG↓,5,   TumCI↓,3,   TumCMig↓,1,   TumCP↓,8,   tumCV↓,3,   TumMeta↓,2,   TumW↓,2,   TUNEL↑,1,   Twist↓,1,   VEGF↓,5,   VEGFR2↓,1,   Wnt↓,2,   Zeb1↓,1,   β-catenin/ZEB1↓,1,   γH2AX↑,2,  
Total Targets: 172

Results for Effect on Normal Cells:
BioAv?,1,   BioAv↑,2,   Cyt‑c↓,1,   p‑ERK↑,1,   Half-Life∅,1,   HDAC↓,1,   HDAC3↓,1,   HSP27↓,1,   IAP1↓,1,   Ki-67↓,1,   NRF2↑,1,   ROS↓,2,   toxicity↓,2,   toxicity∅,3,  
Total Targets: 14

Scientific Paper Hit Count for: TumCCA, Tumor cell cycle arrest
24 Sulforaphane (mainly Broccoli)
1 Genistein
1 Auranofin
1 Gemcitabine (Gemzar)
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:156  Target#:322  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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