Sulforaphane (mainly Broccoli) / Casp3 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


Casp3, CPP32, Cysteinyl aspartate specific proteinase-3: Click to Expand ⟱
Source:
Type:
Also known as CP32.
Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death.
As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression.
Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy.
Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent.
On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer.
Procaspase-3 is a apoptotic marker protein.
Prognostic significance:
• High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers.
• Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers.
Scientific Papers found: Click to Expand⟱
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↝,
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
CSCs↓, Shh↓, Gli↓, Nanog↓, OCT4↓, PDGFRA↓, cycD1/CCND1↑, Apoptosis↑, Casp↑, Smo↓, Gli1↓, GLI2↓, Bcl-2↓, Casp3↑, Casp7↑,
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
Casp8↑, MMP↓, Casp3↑, Apoptosis↑, GSH↓, GSH↑,
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↑,
1463- SFN,    Sulforaphane induces reactive oxygen species-mediated mitotic arrest and subsequent apoptosis in human bladder cancer 5637 cells
- in-vitro, Bladder, 5637
tumCV↓, CycB/CCNB1↑, p‑CDK1↑, Apoptosis↑, Casp8↑, Casp9↑, Casp3↑, cl‑PARP↑, ROS↑, eff↓,
1456- SFN,    Sulforaphane regulates cell proliferation and induces apoptotic cell death mediated by ROS-cell cycle arrest in pancreatic cancer cells
- in-vitro, PC, MIA PaCa-2 - in-vitro, PC, PANC1
tumCV↓, TumCP↓, cl‑PARP↑, cl‑Casp3↑, TumCCA↑, ROS↑, MMP↓, γH2AX↑, eff↓, *toxicity↓,
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↓,
1459- SFN,  AF,    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↑, TumCCA↑, Apoptosis↑, MMP↓, BAX↑, cl‑PARP↑, Casp3↑, Casp8↑, Casp9↑, ROS↑, eff↓, PI3K↓, Akt↓, TrxR↓, BAX↑, Bcl-2∅,
1464- SFN,    d,l-Sulforaphane Induces ROS-Dependent Apoptosis in Human Gliomablastoma Cells by Inactivating STAT3 Signaling Pathway
- in-vitro, GBM, NA
Apoptosis↑, Casp3↑, BAX↑, Bcl-2↓, ROS↑, p‑STAT3↓, JAK2↓, eff↓,
1467- SFN,    Sulforaphane generates reactive oxygen species leading to mitochondrial perturbation for apoptosis in human leukemia U937 cells
- in-vitro, AML, U937
Apoptosis↑, ROS↑, MMP↓, Casp3↑, Bcl-2↓, eff↓,
1469- SFN,    Sulforaphane enhances the therapeutic potential of TRAIL in prostate cancer orthotopic model through regulation of apoptosis, metastasis, and angiogenesis
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vivo, Pca, NA
eff↑, ROS↑, MMP↓, Casp3↑, Casp9↑, DR4↑, DR5↑, BAX↑, Bak↑, BIM↑, NOXA↑, Bcl-2↓, Bcl-xL↓, Mcl-1↓, eff↓, TumCG↓, TumCP↓, eff↑, NF-kB↓, PI3K↓, Akt↓, MEK↓, ERK↓, angioG↓, FOXO3↑,
1315- SFN,    Sulforaphane Induces Apoptosis of Acute Human Leukemia Cells Through Modulation of Bax, Bcl-2 and Caspase-3
- in-vitro, AML, K562
TumCP↓, BAX↑, Casp3↑, Bcl-2↓,
1434- SFN,  GEM,    Sulforaphane Potentiates Gemcitabine-Mediated Anti-Cancer Effects against Intrahepatic Cholangiocarcinoma by Inhibiting HDAC Activity
- in-vitro, CCA, HuCCT1 - in-vitro, CCA, HuH28 - in-vivo, NA, NA
HDAC↓, ac‑H3↑, ChemoSen↑, tumCV↓, TumCP↓, TumCCA↑, Apoptosis↑, cl‑Casp3↑, TumCI↓, VEGF↓, VEGFR2↓, Hif1a↓, eNOS↓, EMT?, TumCG↓, Ki-67↓, TUNEL↑, P21↑, p‑Chk2↑, CDC25↓, BAX↑, *ROS↓, NQO1?,
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↓,
1726- SFN,    Sulforaphane: A Broccoli Bioactive Phytocompound with Cancer Preventive Potential
- Review, Var, NA
Dose↝, eff↝, IL1β↓, IL6↓, IL12↓, TNF-α↓, COX2↓, CXCR4↓, MPO↓, HSP70/HSPA5↓, HSP90↓, VCAM-1↓, IKKα↓, NF-kB↓, HO-1↑, Casp3↑, Casp7↑, Casp8↑, Casp9↑, cl‑PARP↑, Cyt‑c↑, Diablo↑, CHOP↑, survivin↓, XIAP↓, p38↑, Fas↑, PUMA↑, VEGF↓, Hif1a↓, Twist↓, Zeb1↓, Vim↓, MMP2↓, MMP9↓, E-cadherin↑, N-cadherin↓, Snail↓, CD44↓, cycD1/CCND1↓, cycA1/CCNA1↓, CycB/CCNB1↓, cycE/CCNE↓, CDK4↓, CDK6↓, p50↓, P53↑, P21↑, GSH↑, SOD↑, GSTs↑, mTOR↓, Akt↓, PI3K↓, β-catenin/ZEB1↓, IGF-1↓, cMyc↓, CSCs↓,
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↑,
1474- SFN,    Sulforaphane induces p53‑deficient SW480 cell apoptosis via the ROS‑MAPK signaling pathway
- in-vitro, Colon, SW480
TumCG↓, Apoptosis↑, MMP↓, Bax:Bcl2↑, Casp3↑, Casp7↑, Casp9↑, ROS↑, e-ERK↑, p38↑, P53∅, eff↓, ChemoSen↑,
1477- SFN,    Sulforaphane Induces Oxidative Stress and Death by p53-Independent Mechanism: Implication of Impaired Glutathione Recycling
- in-vitro, OS, MG63
tumCV↓, Apoptosis↑, Casp3↑, ROS↑, GSR↓, GPx↓,
1481- SFN,  docx,    Combination of Low-Dose Sulforaphane and Docetaxel on Mitochondrial Function and Metabolic Reprogramming in Prostate Cancer Cell Lines
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
ChemoSen↑, Casp3↑, ROS↑, Casp8↑, Cyt‑c↑, Glycolysis↓, GSH↓, GSH/GSSG↓, *toxicity↓,
1732- SFN,    Sulforaphane, a Dietary Component of Broccoli/Broccoli Sprouts, Inhibits Breast Cancer Stem Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, SUM159 - in-vivo, NA, NA
TumCD↑, CSCs↓, Wnt↓, β-catenin/ZEB1↓, *BioAv↑, angioG↓, VEGF↓, Hif1a↓, MMP2↓, MMP9↓, Casp3↑, *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?,

Showing Research Papers: 1 to 22 of 22

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 22

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GPx↓, 1,   GSH↓, 2,   GSH↑, 2,   GSH/GSSG↓, 1,   GSR↓, 1,   GSTA1↑, 1,   GSTs↑, 1,   HO-1↑, 2,   MPO↓, 1,   NQO1?, 1,   NRF2↑, 4,   NRF2∅, 1,   p‑NRF2↑, 1,   mt-OXPHOS↓, 1,   ROS?, 1,   ROS↑, 14,   SOD↑, 1,   TrxR↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 1,   CDC25↓, 1,   MEK↓, 1,   MMP↓, 9,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AKT1↓, 1,   cMyc↓, 1,   glucoNG↓, 1,   Glycolysis↓, 2,   HK2↓, 1,  

Cell Death ⓘ

Akt↓, 3,   p‑Akt↓, 1,   Apoptosis↑, 12,   Bak↑, 1,   BAX↑, 7,   Bax:Bcl2↑, 4,   Bcl-2↓, 7,   Bcl-2∅, 1,   Bcl-xL↓, 1,   BIM↑, 1,   Casp↑, 1,   Casp12?, 1,   Casp3↑, 20,   cl‑Casp3↑, 2,   Casp7↑, 4,   Casp8↑, 6,   Casp8∅, 2,   Casp9↑, 10,   p‑Chk2↑, 1,   Cyt‑c↓, 1,   Cyt‑c↑, 5,   Diablo↑, 1,   DR4↑, 1,   DR5↑, 2,   Fas↑, 1,   hTERT/TERT↓, 2,   IAP1↓, 1,   Mcl-1↓, 1,   NOXA↑, 1,   p27↑, 1,   p38↑, 2,   PUMA↑, 1,   survivin↓, 2,   Telomerase↓, 1,   TRAIL↑, 1,   TumCD↑, 1,   TUNEL↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 2,   p70S6↓, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   HATs↓, 1,   tumCV↓, 5,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 2,   HSP70/HSPA5↓, 1,   HSP90↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMT1↓, 1,   DNMT3A↓, 1,   DNMTs↓, 2,   P53↑, 1,   P53∅, 1,   cl‑PARP↑, 8,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↑, 1,   p‑CDK1↑, 1,   CDK4↓, 1,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 1,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 1,   cycD1/CCND1↑, 2,   cycE/CCNE↓, 1,   p19↑, 1,   P21↑, 4,   TumCCA?, 1,   TumCCA↓, 1,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   ALDH1A1↓, 1,   CD133↓, 1,   CD44↓, 4,   cMYB↓, 1,   CSCs↓, 5,   EMT?, 1,   EMT↓, 2,   ERK↓, 2,   ERK↑, 1,   e-ERK↑, 1,   FOXO3↑, 1,   Gli↓, 1,   Gli1↓, 2,   HDAC↓, 6,   IGF-1↓, 1,   mTOR↓, 1,   p‑mTOR↓, 1,   Nanog↓, 2,   NOTCH↓, 1,   OCT4↓, 2,   PDGFRA↓, 1,   PI3K↓, 3,   Shh↓, 2,   Smo↓, 2,   p‑STAT3↓, 1,   TumCG↓, 4,   Wnt↓, 3,  

Migration ⓘ

AP-1↑, 1,   E-cadherin↑, 2,   ER-α36↓, 1,   GLI2↓, 1,   Ki-67↓, 1,   MMP1↓, 1,   MMP2↓, 6,   MMP9↓, 4,   N-cadherin↓, 1,   Snail↓, 2,   TumCI↓, 2,   TumCP↓, 4,   TumMeta↓, 1,   Twist↓, 1,   VCAM-1↓, 1,   Vim↓, 1,   Zeb1↓, 2,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature ⓘ

angioG↓, 4,   EGFR↓, 2,   eNOS↓, 1,   Hif1a↓, 5,   VEGF↓, 4,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   CXCR4↓, 1,   IFN-γ↑, 1,   IKKα↓, 1,   IL12↓, 1,   IL1β↓, 3,   IL2↑, 1,   IL6↓, 2,   JAK2↓, 1,   NF-kB↓, 5,   p50↓, 1,   TNF-α↓, 3,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

EGFR↓, 2,   GutMicro↝, 1,   HER2/EBBR2↓, 2,   hTERT/TERT↓, 2,   IL6↓, 2,   Ki-67↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   CardioT↓, 1,   ChemoSideEff↓, 1,   Remission↑, 1,   TumW↓, 2,  
Total Targets: 184

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↑, 1,   NRF2↑, 2,   ROS↓, 2,  

Cell Death ⓘ

MAPK↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   HDAC↓, 1,   HDAC3↓, 1,   STAT3↓, 1,  

Migration ⓘ

Ki-67↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   Half-Life∅, 1,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   cardioP↑, 1,   toxicity↓, 3,  
Total Targets: 17

Scientific Paper Hit Count for: Casp3, CPP32, Cysteinyl aspartate specific proteinase-3
22 Sulforaphane (mainly Broccoli)
1 Auranofin
1 Gemcitabine (Gemzar)
1 Docetaxel
1 doxorubicin
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#:42  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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