Sulforaphane (mainly Broccoli) 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

Scientific Papers found: Click to Expand⟱

3175-

Ash,

SFN,

Withaferin A and sulforaphane regulate breast cancer cell cycle progression through epigenetic mechanisms

in-vitro,

BC,

MDA-MB-231

in-vitro,

BC,

MCF-7

"highlight2" >DNMTs↓, Withaferin A (WA), found in the Indian winter cherry and documented as a DNA methyl transferase (DNMT) inhibitor,
"highlight2" >HDAC↓, sulforaphane (SFN), a well-known histone deacetylase (HDAC) inhibitor
"highlight2" >eff↑, SFN + WA synergistically promote breast cancer cell death

1433-

Ash,

SFN,

A Novel Combination of Withaferin A and Sulforaphane Inhibits Epigenetic Machinery, Cellular Viability and Induces Apoptosis of Breast Cancer Cells

in-vitro,

BC,

MCF-7

1.0 µM WA and 5.0 µM SFN

in-vitro,

BC,

MDA-MB-231

"highlight2" >eff↑, synergistic inhibition of cellular viability in MCF-7
"highlight2" >Bcl-2↓,
"highlight2" >BAX↑,
"highlight2" >tumCV↓,
"highlight2" >DNMT1↓,
"highlight2" >DNMT3A↓, DNMT3A and DNMT3B mRNA expression is down-regulated
"highlight2" >HDAC↓, significant decreases in HDAC activity

2703-

BBR,

CUR,

SFN,

UA,

GamB

Naturally occurring anti-cancer agents targeting EZH2

Review,

Var,

"highlight2" >EZH2↓, In fact, several natural products such as curcumin, triptolide, ursolic acid, sulforaphane, davidiin, tanshindiols, gambogic acid, berberine and Alcea rosea have been shown to serve as EZH2 modulators.

1473-

BCA,

SFN,

An Insight on Synergistic Anti-cancer Efficacy of Biochanin A and Sulforaphane Combination Against Breast Cancer

in-vitro,

BC,

MCF-7

"highlight2" >eff↑, cytotoxicity of BCA and SFN was found to be around 24.5 µM and 27.2 µM respectively, while the combination of BCA and SFN had shown an inhibitory activity at about 20.1 µM.
"highlight2" >ROS↑,
"highlight2" >other↑, profound increase in apoptogenic activity of compounds when treated in combination at lower dose.
"highlight2" >ERK↓,
"highlight2" >Apoptosis↑,

5397-

CUR,

SFN,

RES,

EGCG,

Ash

Targeting Cancer Stem Cells with Phytochemicals: Molecular Mechanisms and Therapeutic Potential

Review,

Var,

"highlight2" >CSCs↓, curcumin, sulforaphane, resveratrol, EGCG, genistein, quercetin, parthenolide, berberine, and withaferin A. Collectively, these compounds suppress CSC self-renewal,

4881-

CUR,

SFN,

RES,

EGCG,

Lyco

An update of Nrf2 activators and inhibitors in cancer prevention/promotion

Review,

Var,

"highlight2" >*NRF2↑, natural Nrf2 activators include curcumin, sulforaphane (SF), kahweol, resveratrol, garlic oganosulfur compounds, zerumbone, epigallocatechin-3-gallate, carnosol, cinnamonyl-based compounds, lycopene, and cafestol
"highlight2" >*antiOx↑, these chemopreventive agents can activate the antioxidants, phase II detoxification factors, and transducers, and protect the cells from carcinogenic exposure

162-

CUR,

EGCG,

SFN,

Shattering the underpinnings of neoplastic architecture in LNCap: synergistic potential of nutraceuticals in dampening PDGFR/EGFR signaling and cellular proliferation

in-vitro,

Pca,

LNCaP

"highlight2" >p‑PDGF↓, phosphorylation

2165-

dietP,

SFN,

Broccoli sprout supplementation in patients with advanced pancreatic cancer is difficult despite positive effects—results from the POUDER pilot study

Trial,

PC,

"highlight2" >Dose↝, Fifteen capsules with pulverized broccoli sprouts containing 90 mg/508 μmol sulforaphane and 180 mg/411 μmol glucoraphanin or methylcellulose were administered daily for up to 1 year.
"highlight2" >OS↑, Compared to those of the placebo group, the mean death rate was lower in the treatment group during the first 6 months after intake
"highlight2" >eff↝, broccoli sprouts sometimes increased digestive problems, nausea and emesis.

2163-

dietP,

SFN,

Intake of Cruciferous Vegetables Modifies Bladder Cancer Survival

Human,

Bladder,

"highlight2" >OS↑, a strong and significant inverse association was observed between bladder cancer mortality and broccoli intake
"highlight2" >OS∅, There were no significant associations for total vegetables, total fruits, or other individual cruciferous vegetables.

685-

EGCG,

CUR,

SFN,

RES,

GEN

The “Big Five” Phytochemicals Targeting Cancer Stem Cells: Curcumin, EGCG, Sulforaphane, Resveratrol and Genistein

Analysis,

NA,

"highlight2" >Bcl-2↓,
"highlight2" >survivin↓,
"highlight2" >XIAP↓,
"highlight2" >EMT↓,
"highlight2" >Apoptosis↑,
"highlight2" >Nanog↓,
"highlight2" >cMyc↓,
"highlight2" >OCT4↓,
"highlight2" >Snail↓,
"highlight2" >Slug↓,
"highlight2" >Zeb1↓,
"highlight2" >TCF↓,

4664-

GEN,

CUR,

RES,

EGCG,

SFN

Targeting cancer stem cells by nutraceuticals for cancer therapy

Review,

Var,

"highlight2" >CSCs↓, we will describe the some natural chemopreventive agents that target CSCs in a variety of human malignancies, including soy isoflavone, curcumin, resveratrol, tea polyphenols, sulforaphane, quercetin, indole-3-carbinol, 3,3′-diindolylmethane, withafe
"highlight2" >other↝, Because chemotherapy and radiotherapy cannot effectively remove CSCs
"highlight2" >eff↑, Curcumin and EGCG combination attenuated the CD44+ cell population via inhibition of pSTAT3 and retaining the crosstalk between STAT3 and NF-κB in breast cancer cells [233]
"highlight2" >CD44↓,
"highlight2" >p‑STAT3↓,

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

"highlight2" >DNMTs↓, GEN extensively studied for its role as DNA methyltransferase (DNMT) inhibitor
"highlight2" >HDAC↓, SFN), is known as a histone deacetylase (HDAC) inhibitor
"highlight2" >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
"highlight2" >TumCCA↑, G2 phase in MDA-MB-231 and G1 phase in MCF-7
"highlight2" >HMTs↓, histone methyltransferase (HMT) inhibitor
"highlight2" >HDAC2↓, combination downregulates the levels of HDAC2 and HDAC3 both at the mRNA and protein levels
"highlight2" >HDAC3↓,
"highlight2" >KLF4↓, potential to downregulate KLF4 levels, which plays an important role in stem cell formation.
"highlight2" >hTERT/TERT↓,

5185-

PEITC,

SFN,

Suppression of NF-kappaB and NF-kappaB-regulated gene expression by sulforaphane and PEITC through IkappaBalpha, IKK pathway in human prostate cancer PC-3 cells

in-vitro,

Pca,

PC3

"highlight2" >NF-kB↓, treatment with SFN (20 and 30 microM) and PEITC (5 and 7.5 microM) significantly inhibited NF-kappaB transcriptional activity, nuclear transloction of p65, and gene expression of NF-kappaB-regulated VEGF, cylcin D1, and Bcl-X(L) in PC-3 C4 cells.
"highlight2" >p65↓,
"highlight2" >VEGF↓,
"highlight2" >cycD1/CCND1↓,
"highlight2" >Bcl-xL↓,
"highlight2" >IKKα↓, mainly mediated through the inhibition of IKK phosphorylation, particularly IKKbeta

911-

QC,

SFN,

Pilot study evaluating broccoli sprouts in advanced pancreatic cancer (POUDER trial) - study protocol for a randomized controlled trial

"highlight2" >TumCG↓,
"highlight2" >Risk↓, decreased risk of extra-prostatic manifestation of prostate cancer: cruciferous vegetables, in particular broccoli which is rich in sulforaphane and quercetin

4667-

RES,

CUR,

SFN,

Physiological modulation of cancer stem cells by natural compounds: Insights from preclinical models

Review,

Var,

"highlight2" >CSCs↓, phytochemicals such as resveratrol, curcumin, sulforaphane, and others suppress CSC-associated pathways as well as sensitize CSCs to chemotherapy and radiotherapy
"highlight2" >ChemoSen↑,
"highlight2" >RadioS↑,
"highlight2" >ALDH↓, deplete ALDH+ or CD44+ CSC pools, which ultimately decrease tumor initiation and recurrence.
"highlight2" >CD44↓,
"highlight2" >Wnt↓, graphical abstract
"highlight2" >β-catenin/ZEB1↓,
"highlight2" >NOTCH↓,
"highlight2" >HH↓,
"highlight2" >NF-kB↓,

5002-

Sal,

SFN,

Salinomycin and Sulforaphane Exerted Synergistic Antiproliferative and Proapoptotic Effects on Colorectal Cancer Cells by Inhibiting the PI3K/Akt Signaling Pathway in vitro and in vivo

in-vivo,

CRC,

Caco-2

vitro+vivo,

CRC,

CX-1

"highlight2" >Apoptosis↑, we evaluated the molecular mechanism behind SAL- and SFN-mediated CRC cell apoptosis.
"highlight2" >PI3K↓, The combination treatment induced apoptosis in Caco-2 and CX-1 cells by inhibiting the PI3K/Akt pathway, which increased the expression of the tumor suppressor protein p53.
"highlight2" >Akt↓,
"highlight2" >P53↑,
"highlight2" >BAX↑, The treatment also decreased the expression of the survival protein Bcl-2 and increased the expression of the proapoptotic protein Bax, which increased the Bax/Bcl-2 ratio
"highlight2" >Bax:Bcl2↑,
"highlight2" >p‑PARP↑, as well as enhanced poly ADP-ribose polymerase (PARP) cleavage.
"highlight2" >TumCMig↓, Cotreatment also significantly decreased migration and invasion compared to that of the control and SAL or SFN monotherapies.

4736-

Se,

SFN,

Synergy between sulforaphane and selenium in protection against oxidative damage in colonic CCD841 cells

in-vitro,

Nor,

CCD841

"highlight2" >*TrxR1↑, Treatment of cells with SFN and Se significantly induced TrxR-1 expression.
"highlight2" >*H2O2↓, Pretreatment of cells with SFN protects against H2O2-induced cell death; this protection was enhanced by cotreatment with Se.
"highlight2" >*NRF2↑, SFN activates the Nrf2 signaling pathway and protects against H2O2-mediated oxidative damage in normal colonic cells.

2447-

SFN,

Sulforaphane Bioavailability from Glucoraphanin-Rich Broccoli: Control by Active Endogenous Myrosinase

Review,

Nor,

"highlight2" >*BioAv↓, when either broccoli sprouts or seeds are administered directly to subjects without prior extraction and consequent inactivation of endogenous myrosinase, the sulforaphane in those preparations is 3-4-fold more bioavailable than sulforaphane from gl
"highlight2" >*BioAv↓, sulforaphane is only moderately stable over time, especially in aqueous solution
"highlight2" >*BioAv↓, their useful shelf-life is limited unless chemically stabilized, kept cold, or made frequently during the study
"highlight2" >*BioAv↝, see Table 1 for interesing bioavailable information of different forms

2449-

SFN,

Optimization of a blanching step to maximize sulforaphane synthesis in broccoli florets

Study,

Nor,

"highlight2" >BioAv↑, Optimal blanching condition was immersion in water at 57° for 13 min.coinciding with the minimum glucosinolates and glucoraphanin content, and with the maximum myrosinase. Sulforaphane content was increased by 237% compared with fresh broccoli.

2448-

SFN,

Sulforaphane and bladder cancer: a potential novel antitumor compound

Review,

Bladder,

"highlight2" >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
"highlight2" >TumCG↓,
"highlight2" >TumCI↓,
"highlight2" >TumMeta↓,
"highlight2" >glucoNG↓, Additionally, it can inhibit BC gluconeogenesis
"highlight2" >ChemoSen↑, demonstrate definite effects when combined with chemotherapeutic drugs/carcinogens.
"highlight2" >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
"highlight2" >Casp3↑,
"highlight2" >Casp7↑,
"highlight2" >cl‑PARP↑,
"highlight2" >survivin↓,
"highlight2" >EGFR↓,
"highlight2" >HER2/EBBR2↓,
"highlight2" >ATP↓, SFN inhibits the production of ATP by inhibiting glycolysis and mitochondrial oxidative phosphorylation in BC cells in a dose-dependent manner
"highlight2" >Glycolysis↓,
"highlight2" >mt-OXPHOS↓,
"highlight2" >AKT1↓, dysregulation of glucose metabolism by inhibiting the AKT1-HK2 axis
"highlight2" >HK2↓,
"highlight2" >Hif1a↓, Sulforaphane inhibits glycolysis by down-regulating hypoxia-induced HIF-1α
"highlight2" >ROS↑, SFN can upregulate ROS production and Nrf2 activity
"highlight2" >NRF2↑,
"highlight2" >EMT↓, inhibiting EMT process through Cox-2/MMP-2, 9/ ZEB1 and Snail and miR-200c/ZEB1 pathways
"highlight2" >COX2↓,
"highlight2" >MMP2↓,
"highlight2" >MMP9↓,
"highlight2" >Zeb1↓,
"highlight2" >Snail↓,
"highlight2" >HDAC↓, FN modulates the histone status in BC cells by regulating specific HDAC and HATs,
"highlight2" >HATs↓,
"highlight2" >MMP↓, SFN upregulates ROS production, induces mitochondrial oxidative damage, mitochondrial membrane potential depolarization, cytochrome c release
"highlight2" >Cyt‑c↓,
"highlight2" >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
"highlight2" >Smo↓,
"highlight2" >Gli1↓,
"highlight2" >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
"highlight2" >BioAv↝, It has been reported that the ability of individuals to use gut myrosinase to convert glucoraphanin into SFN varies widely
"highlight2" >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

2552-

SFN,

Chemo,

Chemopreventive activity of sulforaphane

Review,

Var,

"highlight2" >chemoPv↑, chemopreventive activity of SFN
"highlight2" >TumCG↓, SFN can inhibit the initiation of tumor development or halt the progression of cancer
"highlight2" >*ROS↓, SFN can also exhibit chemopreventive behavior by interfering with various signaling pathways that regulate oxidative stress, inflammation, cell proliferation, differentiation, and apoptosis
"highlight2" >*Inflam↓,
"highlight2" >*Dose↝, In rats, the pharmacokinetics of SFN was assessed following an oral dose of 50 μmol of SFN. The plasma concentration of SFN can be detected at 1 hour and it peaks at 20 μM at 4 hours.
"highlight2" >*NRF2↑, epigenetic reactivation of Nrf2 and subsequent induction of downstream target genes HO-1, NQO1, and UGT1A1
"highlight2" >*HO-1↑,
"highlight2" >*NQO1↑,
"highlight2" >NF-kB↓, inactivation of NF-κB is an important chemopreventive mechanism of SFN
"highlight2" >ROS↑, It was demonstrated that SFN-induced apoptosis is mediated by reactive oxygen species (ROS)-mediated activation of AMPK in human gastric cancer cells.

2553-

SFN,

Mechanistic review of sulforaphane as a chemoprotective agent in bladder cancer

Review,

Bladder,

"highlight2" >antiOx↓, SFN is a bioactive compound with both antioxidant and anti-inflammatory properties.
"highlight2" >Inflam↓,
"highlight2" >ChemoSen↑, SFN also improves the efficacy of certain traditional chemotherapeutic regimens
"highlight2" >ROS⇅, A lesser established mechanism proposed by Li, et al. is that SFN induces mild increases ROS, leading to transcription factor EB (TFEB) activation. TFEB plays a role in activating antioxidant response elements and...ultimately reducing overall oxidat
"highlight2" >*NRF2↑, SFN treatment increased Nrf2 and, therefore, glutathione levels
"highlight2" >*GSH↑,
"highlight2" >Catalase↑, Cancer cells treated with SFN showed higher catalase levels, heme oxygenase 1, and NAD(P)
"highlight2" >HO-1↑,
"highlight2" >NAD↑,
"highlight2" >chemoP↑, Taken together, these studies provide strong evidence for the chemoprotective nature of SFN in various human epithelial cancers, including those of the bladder.

2554-

SFN,

Sulforaphane (SFN): An Isothiocyanate in a Cancer Chemoprevention Paradigm

Review,

Var,

"highlight2" >Dose↝, In human subjects given single doses of 200 μmol broccoli sprouts ITC preparation, ITC plasma concentrations peaked between 0.943 and 2.27 μmol/L 1 h after feeding, with half-life of 1.77 ± 0.13 h suggesting the possibility of clinical intervention a
"highlight2" >chemoPv↑, present review provides the current understanding of the cancer chemopreventive pharmacology of sulforaphane towards its potential as an anticancer agent.
"highlight2" >*NQO1↑, sulforaphane upregulated the expression of NQO1, GST and GCL in the small intestine of wildtype mice
"highlight2" >*GSTA1↑,
"highlight2" >HDAC↓, Sulforaphane as Inhibitor of HDACs Challenges the Pro-Oncogenic Epigenetic Pattern in Cancer Cells
"highlight2" >NF-kB↓, In a study on prostate cancer cells, treatment with SFN (20 and 30 μM) significantly inhibited NF-κB

2555-

SFN,

Chemopreventive functions of sulforaphane: A potent inducer of antioxidant enzymes and apoptosis

Review,

Var,

"highlight2" >chemoPv↑, induction of Metallothioneins MT by sulforaphane as a strategy for achieving chemoprevention and chemoprotection.
"highlight2" >HDAC↓, sulforaphane supplementation resulted in slower tumor growth and significant histone deacetylase (HDAC) inhibition in the xenografts,
"highlight2" >TumCCA↑, HDAC inhibition represents a novel chemoprevention mechanism by which sulforaphane can promote cell cycle arrest and apoptosis.
"highlight2" >Apoptosis↑,
"highlight2" >Mets↑, induction of Metallothioneins MT by sulforaphane
"highlight2" >*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.
"highlight2" >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.

2556-

SFN,

The role of Sulforaphane in cancer chemoprevention and health benefits: a mini-review

Review,

Var,

"highlight2" >chemoPv↑, sulforaphane (SFN) has surfaced as a particularly potent chemopreventive agent based on its ability to target multiple mechanisms within the cell to control carcinogenesis
"highlight2" >HDAC↓, SFN's chemopreventative properties was also demonstrated in another study, where through its HDACi activity,
"highlight2" >Hif1a↓, SFN inhibits hypoxia inducible factor-1 Î± (HIF-1Î±) and c-Myc, two angiogenesis- associated transcription factors
"highlight2" >angioG↓,
"highlight2" >CYP1A1↓, CYP1A1 reduction, MFC7
"highlight2" >eff↑, Kallifatidis et al. reported SFN to potentiate the anti-cancer effects of cisplatin, gemcitabine, doxorubicin or 5-flurouracil on prostate cancer cell line MIA-PaCa2 while also increasing cytotoxicity of cancer stem cells
"highlight2" >BioAv↑, Shapiro et al. reported that the chewing of fresh broccoli sprouts increases the interaction of glucosinolates with myrosinase and consequently, increases the bioavailability of SFN in the body (Shapiro et al. 2001).

3183-

SFN,

Sulforaphane potentiates the efficacy of chemoradiotherapy in glioblastoma by selectively targeting thioredoxin reductase 1

in-vitro,

GBM,

"highlight2" >RadioS↑, SFN synergistically improves chemoradiotherapy efficacy in GBM cells
"highlight2" >TrxR1↓, Herein, we demonstrate that sulforaphane (SFN), an isothiocyanate phytochemical with anti-cancer effects, inhibits the activity of thioredoxin reductase 1 (TrxR1)
"highlight2" >ROS↑, This inhibition of TrxR1 leads to the accumulation of reactive oxygen species (ROS), thereby enhancing chemoradiotherapy-induced apoptosis in GBM cells.
"highlight2" >ChemoSen↑,
"highlight2" >Prx↓, Impaired/reduced function(ai)

3180-

SFN,

Exploring the therapeutic effects of sulforaphane: an in-depth review on endoplasmic reticulum stress modulation across different disease contexts

Review,

Var,

"highlight2" >*cardioP↑, broad range of protective functions of sulforaphane, improving various diseases, such as cardiovascular, central nervous system, liver, eye, and reproductive diseases, as well as diabetes, cancer, gastroenteritis, and osteoarthritis,
"highlight2" >*ER Stress↓, through the amelioration of ER stress in both in vivo and in vitro studies.
"highlight2" >GRP78/BiP↑, Sulforaphane significantly increased the level of Bip/GRP78, and XBP-1 protein expression and enhanced the rate of HepG2 cells apoptosis.
"highlight2" >XBP-1↑,
"highlight2" >Apoptosis↑,
"highlight2" >*NRF2↑, Mitigates oxidative stress and ER stress in vascular cells, contributing to cardioprotection
"highlight2" >UPR↑, SFN can drive the UPR into an overactivated state(ai)

3181-

SFN,

Effect of sulforaphane on protein expression of Bip/GRP78 and caspase-12 in human hapetocelluar carcinoma HepG-2 cells

in-vitro,

HCC,

HepG2

"highlight2" >GRP78/BiP↑, SFN can up-regulate the expression of Bip/GRP78 and caspase-12,by which induce apoptosis of HepG-2 cells through the endoplasmic reticulum pathway.
"highlight2" >Casp12↑,
"highlight2" >Apoptosis↑,
"highlight2" >ER Stress↑,

3182-

SFN,

Sulforaphane Modulates AQP8-Linked Redox Signalling in Leukemia Cells

in-vitro,

AML,

 10 and 30 μM SFN

B1647 cell line

"highlight2" >Prx↓, The results show that the cell treatment with 10 μM SFN for 24 h significantly decreased Prx-1 expression.
"highlight2" >AQPs↓, Results indicated that sulforaphane inhibited both aquaporin-8 and Nox2 expression, thus decreasing B1647 cells viability.
"highlight2" >NOX↓,
"highlight2" >tumCV↓,
"highlight2" >AntiCan↑, In addition to its well-known anticancer activity [2], SFN has been demonstrated to possess cardioprotective [3], neuroprotective [4], and anti-inflammatory activities
"highlight2" >cardioP↑,
"highlight2" >neuroP↑,
"highlight2" >Inflam↓,
"highlight2" >chemoPv↑, potent chemopreventive effect of SFN is based on its ability to target multiple mechanisms within the cell to control carcinogenesis
"highlight2" >angioG↓, SFN prevents uncontrolled cancer cell proliferation through the modulation of genes involved in apoptosis and cell cycle arrest [5, 8], angiogenesis [9, 10], and metastasis
"highlight2" >TumMeta↓,
"highlight2" >selectivity↑, SFN is able to selectively exert cytotoxic effects in many human cancer cells without affecting normal cells
"highlight2" >ROS↓, Results in Figure 4 show that only 10 μM SFN treatment causes a significant decrease of ROS intracellular levels in respect to control cells,

1733-

SFN,

Sonic Hedgehog Signaling Inhibition Provides Opportunities for Targeted Therapy by Sulforaphane in Regulating Pancreatic Cancer Stem Cell Self-Renewal

in-vitro,

PC,

PanCSC

in-vitro,

Nor,

HPNE

in-vitro,

Nor,

HNPSC

"highlight2" >CSCs↓, In an in vitro model, human pancreatic CSCs derived spheres were significantly inhibited on treatment with SFN
"highlight2" >Shh↓, SFN inhibited the components of Shh pathway and Gli transcriptional activity
"highlight2" >Gli↓,
"highlight2" >Nanog↓, suppressing the expression of pluripotency maintaining factors (Nanog and Oct-4) as well as PDGFRα and Cyclin D1
"highlight2" >OCT4↓,
"highlight2" >PDGFRA↓,
"highlight2" >cycD1/CCND1↑,
"highlight2" >Apoptosis↑, SFN induced apoptosis by inhibition of BCL-2 and activation of caspases
"highlight2" >Casp↑,
"highlight2" >Smo↓, SFN inhibited the expression of Smo, Gli1 and Gli2.
"highlight2" >Gli1↓,
"highlight2" >GLI2↓,
"highlight2" >Bcl-2↓, SFN induced apoptosis in pancreatic CSCs by inhibiting Bcl-2 expression and through the activation of caspase 3/7
"highlight2" >Casp3↑,
"highlight2" >Casp7↑,

2446-

SFN,

CAP,

The Molecular Effects of Sulforaphane and Capsaicin on Metabolism upon Androgen and Tip60 Activation of Androgen Receptor

in-vitro,

Pca,

LNCaP

10uM

"highlight2" >AR↓, Sulforaphane and capsaicin decreased nuclear AR, prostate specific antigen and Bcl-XL levels, and cell proliferation induced by androgen and Tip60 in LNCaP cells.
"highlight2" >Bcl-xL↓,
"highlight2" >TumCP↓,
"highlight2" >Glycolysis↓, Sulforaphane at 10 µM reduced the glycolysis and glycolytic capacity by 42% and 39%,
"highlight2" >HK2↓, These bioactive compounds prevented the increase in glycolysis, hexokinase and pyruvate kinase activity, and reduced HIF-1α stabilization induced by androgen and Tip60 in LNCaP cells.
"highlight2" >PKA↓,
"highlight2" >Hif1a↓, Sulforaphane and Capsaicin Reduced the Increased HIF-1α Levels Induced by Androgen Stimulus and Tip60 Overexpression
"highlight2" >PSA↓, Sulforaphane and capsaicin prevented the activation of AR signaling (decreased nuclear AR levels and PSA levels)
"highlight2" >ECAR↓, and glycolysis (decreased EACR; and HK and PK activities) induced by androgen and Tip60.
"highlight2" >BioAv↑, increased sulforaphane bioavailability can be attained after the intake of sulforaphane-enriched broccoli sprout preparation (generated by quick steaming followed by myrosinase treatment) in mice
"highlight2" >BioAv↓, Liposomal and methoxypoly (ethylene glycol)-poly(ε-caprolactone) microencapsulation increase capsaicin bioavailability by 3.34-fold and 6-fold respectively in rats
"highlight2" >*toxicity↓, considering that the minimum lethal oral dose of capsaicin is 100 mg/Kg body weight in mice, its consumption could be safely increased

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

"highlight2" >TumCCA↑, SFN (5-10 µM) promoted cell cycle arrest, elevation in the levels of p21 and p27 and cellular senescence
"highlight2" >P21↑,
"highlight2" >p27↑,
"highlight2" >NO↑, effects were accompanied by nitro-oxidative stress, genotoxicity and diminished AKT signaling
"highlight2" >Akt↓,
"highlight2" >ATP↓, decreased pools of ATP and AMPK activation, and autophagy induction
"highlight2" >AMPK↑,
"highlight2" >TumAuto↑,
"highlight2" >DNMT1↓, decreased levels of DNA methyltransferases (DNMT1, DNMT3B)
"highlight2" >HK2↓, A decrease in HK2 levels was observed in SFN-treated MDA-MB-231 cells
"highlight2" >PKM2↓, and a decrease in PKM2 levels was noticed in SFN-treated MDA-MB-231 and SK-BR-3 cells
"highlight2" >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
"highlight2" >HDAC4↓,
"highlight2" >HDAC8↓,

2444-

SFN,

Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage

in-vitro,

Nor,

MRC-5

Human fetal lung MRC-5 fibroblasts and human foreskin BJ

"highlight2" >*GlucoseCon↓, SFN delayed senescence by decreasing glucose metabolism on the approach to senescence, exhibiting a caloric restriction mimetic-like activity
"highlight2" >*ROS↓, and thereby decreased oxidative damage to cell protein and DNA
"highlight2" >*Trx↓, This was associated with increased expression of thioredoxin-interacting protein, curbing entry of glucose into cells;
"highlight2" >*HK2↓, decreased hexokinase-2
"highlight2" >*NRF2↑, SFN is an activator of transcription factor Nrf2 [14] which regulates antioxidant response element- (ARE-) linked gene expression.
"highlight2" >*Catalase↑, CAT, PDRX1, and GCLM, expression was increased in senescence and treatment with SFN increased the expression further
"highlight2" >*TXNIP↑, increased expression of TXNIP, curbing the entry of glucose into cells
"highlight2" >*PFKFB2↓, decreased PFKFB2 and increased G6PD, downregulating glycolysis.
"highlight2" >*G6PD↑,

2406-

SFN,

Sulforaphane and Its Protective Role in Prostate Cancer: A Mechanistic Approach

Review,

Pca,

"highlight2" >HK2↓, When TRAMP mice were given 6 μmol/mouse (1 mg/mouse) three times a week for 17–19 weeks, the prostate tumor expression of glycolysis-promoting enzymes such as (HKII), 2 (PKM2) and (LDHA) was decreased by 32–45%
"highlight2" >PKM2↓,
"highlight2" >LDHA↓,
"highlight2" >Glycolysis↓, These results provide evidence that sulforaphane suppresses in vivo glycolysis in prostate cancer cells
"highlight2" >LAMP2↑, The study shows that 10–20 μM of sulforaphane significantly increased lysosome-associated membrane protein 2 (LAMP2) in the cell lines
"highlight2" >Hif1a↓, sulforaphane has been shown to suppress HIF-1α
"highlight2" >DNAdam↓, SFN causes DNA damage and prevents DNA repair in prostate cancer cell
"highlight2" >DNArepair↓,
"highlight2" >Dose↝, 5 to 100 mg/kg of sulforaphane reduce tumors in animal models [ 5 , 19]. For a 70 kg human, this translates to 350–7000 mg/kg, which is significantly above the upper threshold of tolerable doses

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

"highlight2" >TumCP↓, Sulforaphane can reduce cell proliferation and PKM2-mediated glycolysis in gastric carcinoma cells, apparently by activating the TBX15/KIF2C pathway.
"highlight2" >Glycolysis↓,
"highlight2" >TBX15↑,
"highlight2" >GlucoseCon↓, Overexpressing TBX15 in SGC7901 and BGC823 cells significantly reduced glucose uptake, lactate production, cell viability, expression of KIF2C, and pyruvate kinase M2-mediated (PKM2) glycolysis. These effects were recapitulated by treatment with sulf
"highlight2" >lactateProd↓,
"highlight2" >tumCV↓,
"highlight2" >PKM2↓,
"highlight2" >KIF2C↓,

2404-

SFN,

Prostate cancer chemoprevention by sulforaphane in a preclinical mouse model is associated with inhibition of fatty acid metabolism

in-vitro,

Pca,

LNCaP

5 and 10 μM

in-vitro,

Pca,

22Rv1

in-vivo,

NA,

TRAMP mice

"highlight2" >ACC1↓, SFN (5 and 10 μM) resulted in downregulation of protein and mRNA levels of acetyl-CoA carboxylase 1 (ACC1) and fatty acid synthase (FASN), but not ATP citrate lyase
"highlight2" >FASN↓,
"highlight2" >CPT1A↓, SFN decreased ACC1, FASN and CPT1A expression in LNCaP and 22Rv1 cells
"highlight2" >β-oxidation↓, SFN treatment decreased expression of β-oxidation dehydrogenases
"highlight2" >SREBP1?, SFN treatment decreased SREBP1 protein level in prostate cancer cells
"highlight2" >HK2↓, Similarly, when Hi-Myc mice were given 1 mg/mouse of sulforaphane three times each week for 5–10 weeks, expression of HKII, PKM2 and LDHA was significantly decreased.
"highlight2" >PKM2↓,
"highlight2" >LDHA↓,
"highlight2" >Glycolysis↓, These results provide evidence that sulforaphane suppresses in vivo glycolysis in prostate cancer cells

2403-

SFN,

Reversal of the Warburg phenomenon in chemoprevention of prostate cancer by sulforaphane

in-vitro,

Pca,

LNCaP

5 and 10 µM SFN

in-vitro,

Pca,

22Rv1

in-vitro,

Pca,

PC3

in-vivo,

NA,

mouse

"highlight2" >ECAR↓, SFN treatment: (i) decreased real-time extracellular acidification rate in LNCaP, but not in PC-3 cell line;
"highlight2" >HK2↓, (ii) significantly downregulated expression of hexokinase II (HKII), pyruvate kinase M2 and/or lactate dehydrogenase A (LDHA) in vitro in cells and in vivo . HKII: 32%
"highlight2" >PKM2↓, PKM2: 45%
"highlight2" >LDHA↓, LDHA: 33%
"highlight2" >Glycolysis↓, (iii) significantly suppressed glycolysis in prostate of Hi-Myc mice
"highlight2" >Warburg↓, Reversal of the Warburg phenomenon

2168-

SFN,

Amelioration of Alzheimer's disease by neuroprotective effect of sulforaphane in animal model

in-vivo,

AD,

Aβ-induced AD acute mouse models

"highlight2" >*NRF2↑, previously been found to stimulate the Nrf2-ARE pathway
"highlight2" >*cognitive↑, ameliorated cognitive function of Aβ-induced AD acute mouse models
"highlight2" >other↓, inhibition of Aβ aggregation

2167-

SFN,

The dietary isothiocyanate sulforaphane targets pathways of apoptosis, cell cycle arrest, and oxidative stress in human pancreatic cancer cells and inhibits tumor growth in severe combined immunodeficient mice

in-vitro,

PC,

MIA PaCa-2

in-vitro,

PC,

PANC1

"highlight2" >Casp8↑, activation of caspase-8, loss of mitochondrial membrane potential, and loss of plasma membrane integrity
"highlight2" >MMP↓,
"highlight2" >Casp3↑, Incubations at higher sulforaphane doses (>10 micromol/L) resulted in cleavage of caspase-3 in the G(1) subpopulation, suggesting that the induction of apoptosis
"highlight2" >Apoptosis↑,
"highlight2" >GSH↓, PANC-1, was positively correlated with a decrease in cellular glutathione levels,
"highlight2" >GSH↑, whereas sustained increases in glutathione observed in MIA PaCa-2 cells

2166-

SFN,

Sulforaphane targets cancer stemness and tumor initiating properties in oral squamous cell carcinomas via miR-200c induction

in-vitro,

Oral,

in-vivo,

NA,

"highlight2" >CSCs↓, sulforaphane dose-dependently eliminated the proliferation rate of OSCC-CSCs
"highlight2" >selectivity↑, whereas the inhibition on SG(normal) cells proliferation was limited.
"highlight2" >TumCMig↓, sulforaphane treatment of OSCC-CSCs decreased the migration, invasion, clonogenicity, and in vivo tumorigenicity of xenograghts.
"highlight2" >TumCI↓,

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,

 mouse prostate (TRAMP) model

"highlight2" >HDAC↓, broccoli sprouts, inhibits epigenetic regulators such as histone deacetylase (HDAC) enzymes. significant decline in HDAC3 protein expression in the epithelial cells of prostate ventral
"highlight2" >Dose↝, TRAMP mice were fed a 15% broccoli sprout
"highlight2" >Risk↓, Broccoli sprouts reduced prostate cancer incidence and progression to invasive cancer by 11- and 2.4-fold at 12 and 28 wk of age, respectively.
"highlight2" >TumCP↓,
"highlight2" >H3↓, Broccoli sprout consumption also decreased histone H3 lysine 9 trimethylation in the ventral lobe (age 12 wk), and decreased histone H3 lysine 18 acetylation in all prostate lobes (age 28 wk).

1736-

SFN,

Antitumor and antimetastatic effects of dietary sulforaphane in a triple-negative breast cancer models

in-vitro,

BC,

in-vivo,

BC,

"highlight2" >TumCG↓, in vivo experiment showed up to 31% tumor growth inhibition after sulforaphane treatment
"highlight2" >selectivity↓, The in vitro study confirmed that SFN inhibited cell migration, but only in cells derived from 3D spheroids, not from 2D in vitro cultures.

1735-

SFN,

Activation of multiple molecular mechanisms for apoptosis in human malignant glioblastoma T98G and U87MG cells treated with sulforaphane

in-vitro,

GBM,

T98G

 20 μM and 40 μM SFN for 24 h

in-vitro,

GBM,

U87MG

"highlight2" >Apoptosis↑, confirmed apoptosis in glioblastoma cells treated with sulforaphane
"highlight2" >Ca+2↑, Increase in intracellular free Ca2+ was detected by fura-2 assay, suggesting activation of Ca2+-dependent pathways for apoptosis.
"highlight2" >Bax:Bcl2↑, increased Bax:Bcl-2 ratio
"highlight2" >cal2↑, Upregulation of calpain, a Ca2+-dependent cysteine protease, activated caspase-12 that in turn caused activation of caspase-9.
"highlight2" >Casp12↑,
"highlight2" >Casp9↑,
"highlight2" >Cyt‑c↑, cytochrome c was released from mitochondria to cytosol

1734-

SFN,

Sulforaphane Inhibits Nonmuscle Invasive Bladder Cancer Cells Proliferation through Suppression of HIF-1α-Mediated Glycolysis in Hypoxia

in-vitro,

Bladder,

RT112

"highlight2" >selectivity↑, sulforaphane, a natural chemical which was abundant in cruciferous vegetables, could suppress bladder cancer cells proliferation in hypoxia significantly stronger than in normoxia
"highlight2" >TumCP↓,
"highlight2" >Glycolysis↓, sulforaphane decreased glycolytic metabolism in a hypoxia microenvironment by downregulating hypoxia-induced HIF-1α and blocking HIF-1α t
"highlight2" >Hif1a↓,

1729-

SFN,

Discovery and development of sulforaphane as a cancer chemopreventive phytochemical

Review,

Nor,

"highlight2" >eff↑, but mild heating of broccoli (60–70 °C) inactivated ESP and preserved myrosinase and increased SF yield 3–7-fold
"highlight2" >angioG↓,
"highlight2" >VEGF↓,
"highlight2" >MMP9↓,
"highlight2" >MMP2↓,

3199-

SFN,

Sulforaphane improves chemotherapy efficacy by targeting cancer stem cell-like properties via the miR-124/IL-6R/STAT3 axis

in-vitro,

GC,

"highlight2" >CSCs↓, It also plays important roles in mediating CSCs. For example, overexpression of miR-124 reduced neurosphere formation, CD133+ cell subpopulations, and stem cell markers such as BMI1, Nanog, and nestin in glioma cells
"highlight2" >CD133↓,
"highlight2" >BMI1↓,
"highlight2" >Nanog↓,
"highlight2" >Nestin↓,

4202-

SFN,

Regulation of BDNF transcription by Nrf2 and MeCP2 ameliorates MPTP-induced neurotoxicity

Review,

Park,

"highlight2" >*NRF2↑, Repeated administration of sulforaphane (SFN, an Nrf2 activator) attenuated dopaminergic neurotoxicity in MPTP-treated mice through activation of BDNF and suppression of MeCP2 expression
"highlight2" >*BDNF↑,

4201-

SFN,

Activation of BDNF by transcription factor Nrf2 contributes to antidepressant-like actions in rodents

in-vivo,

NA,

mice

"highlight2" >*NRF2↑, Activation of Nrf2 by sulforaphane (SFN) showed fast-acting antidepressant-like effects in mice by activating BDNF as well as by inhibiting the expression of its transcriptional repressors (HDAC2, mSin3A, and MeCP2)
"highlight2" >*BDNF↑,
"highlight2" >*HDAC2↓,
"highlight2" >*Mood↑,

4200-

SFN,

Sulforaphane activates anti-inflammatory microglia, modulating stress resilience associated with BDNF transcription

in-vitro,

NA,

mice

"highlight2" >*NRF2↑, SFN activated Nrf2 to promote BDNF transcription by binding to the exon I promoter, which is associated with increased Nrf2
"highlight2" >*BDNF↑,
"highlight2" >*Inflam↓, SFN inhibited the pro-inflammatory phenotype and activated the anti-inflammatory phenotype of microglia, which was associated with increased Nrf2 and decreased MeCP2 expression in microglia of stressed mice.

4199-

SFN,

Sulforaphane and Brain Health: From Pathways of Action to Effects on Specific Disorders

Review,

AD,

Review,

Park,

"highlight2" >*BBB↑, SF is able to cross the blood–brain barrier as well as to protect it
"highlight2" >*BDNF↑, SF can protect against neuronal cell death by inhibiting apoptosis, by upregulating brain-derived neurotrophic factor (BDNF) it can enhance neuronal function and plasticity, and support neurogenesis.
"highlight2" >*neuroG↑,
"highlight2" >*NRF2↑, , Nrf2 inducers like SF that have no direct redox activity are often referred to as “indirect antioxidants”
"highlight2" >*HO-1↑, (NQO1) (HO-1 or HMOX), as well as (Cat), (SOD), (Prx), (HSP), glutathione S-transferases (GST), thioredoxin reductase (Trx), glutathione synthetase (GS), glutathione peroxidases (GPx) and glutathione reductase in the brain
"highlight2" >*Catalase↑,
"highlight2" >*SOD↑,
"highlight2" >*HSPs↑, It enhances the expression of HSP70, HSP90, and HSP40 in normal human fibroblasts
"highlight2" >*GSTs↑,
"highlight2" >*Trx↑,
"highlight2" >*GPx↑,
"highlight2" >*GSR↑,
"highlight2" >*GSH↑, ability of SF to upregulate GSH in the brain is critical for antioxidant protection in youth but may become even more important with age.
"highlight2" >*NQO1↑, SF administration to astrocytes increased NQO1 concentrations and protected against oxygen and glucose-induced astrocyte cell death
"highlight2" >*GutMicro↑, the fact that SF modulates microbiome composition
"highlight2" >*Inflam↓, reduces inflammation and enhances gut barrier integrity,
"highlight2" >*neuroP↑, The effect of SF on the gut microbiome may also affect the production of short-chain fatty acids (SCFA) like butyrate, which have neuroprotective effects

Showing Research Papers: 1 to 50 of 146
Page 1 of 3 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 146

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, Catalase↑, 2, GPx↑, 1, GSH↑, 2, GSR↑, 1, GSTA1↑, 1, GSTs↑, 1, H2O2↓, 1, HO-1↑, 2, NQO1↑, 3, NRF2↑, 12, ROS↓, 2, SOD↑, 1, Trx↓, 1, Trx↑, 1, TrxR1↑, 1,

Core Metabolism/Glycolysis ⓘ

G6PD↑, 1, GlucoseCon↓, 1, HK2↓, 1, PFKFB2↓, 1,

Protein Folding & ER Stress ⓘ

ER Stress↓, 1, HSPs↑, 1,

Proliferation, Differentiation & Cell State ⓘ

HDAC2↓, 1, neuroG↑, 1,

Migration ⓘ

TXNIP↑, 1,

Barriers & Transport ⓘ

BBB↑, 1,

Immune & Inflammatory Signaling ⓘ

Inflam↓, 3,

Synaptic & Neurotransmission ⓘ

BDNF↑, 4,

Drug Metabolism & Resistance ⓘ

BioAv↓, 3, BioAv↝, 1, Dose↝, 1,

Clinical Biomarkers ⓘ

GutMicro↑, 1,

Functional Outcomes ⓘ

cardioP↑, 1, cognitive↑, 1, Mood↑, 1, neuroP↑, 1, toxicity↓, 1,
Total Targets: 37

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#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

Sulforaphane (mainly Broccoli) Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Protein Folding & ER Stress ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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