condition found tbRes List
PBG, Propolis -bee glue: Click to Expand ⟱
Features: Compound
Brazilian Green Propolis often considered best
• Derived from Baccharis dracunulifolia, this type is rich in artepillin C.
• It has been widely researched for its anticancer, anti-inflammatory, and antioxidant properties.
-Propolis common researched flavonoids :chrysin, pinocembrin, galangin, pinobanksin(Pinocembrin)
-most representative phenolic acids were caffeic acid, p-coumaric acid, and ferulic acid, as well as their derivatives, DMCA and caffeic acid prenyl, benzyl, phenylethyl (CAPE), and cinnamyl esters
-One of the most studied active compounds of a poplar-type propolis is caffeic acid phenethyl ester (CAPE)
-caffeic acid phenethyl ester (CAPE), galangin, chrysin, nemorosone, propolin G, artepillin C, cardanol, pinocembrin, pinobanksin, chicoric acid, and phenolic acids (caffeic acid, ferulic acid, and coumaric acid), as well as luteolin, apigenin, myricetin, naringenin, kaempferol, quercetin, polysaccharides, tannins, terpenes, sterols, and aldehydes -content highly variable based on location and extraction
Two main factors of interest:
1. affects interstitual fluild pH
2. high concentration raises ROS (Reactive Oxygen Species), while low concentration may reduce ROS

- Artepillin-C (major phenolic compounds found in Brazilian green propolis (BGP))
- caffeic acid major source

Do not combine with 2DG

Pathways:
-Propolis compounds (e.g., artepillin C, caffeic acid phenethyl ester [CAPE]) can trigger apoptosis (programmed cell death) in cancer cells.
-Propolis has been shown to inhibit NF‑κB activation.
-Propolis extracts can cause cell cycle arrest at specific checkpoints (e.g., G0/G1 or G2/M phases).
-Enhance the body’s antitumor immune responses, for example by activating natural killer (NK) cells and modulating cytokine profiles.

-Note half-life no standard, high variablity of content.
BioAv poor water solubility, and low oral bioavailability.
Pathways:
- high concentration may induce ROS production, while low concentrations mya low it. This may apply to both normal and cancer cells. Normal Cells Example. (Also not sure if high level are acheivable in vivo due to bioavailability)
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
SOD↓, GSH↓ Catalase↓ HO1↓ GPx↓ -->
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : NLRP3↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, P53↑,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓,
- Others: PI3K↓, AKT↓, STAT↓, β-catenin↓, AMPK, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells


Akt, PKB-Protein kinase B: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
Akt1 is involved in cellular survival pathways, by inhibiting apoptotic processes; Akt2 is an important signaling molecule in the insulin signaling pathway. It is required to induce glucose transport.

Inhibitors:
-Curcumin: downregulate AKT phosphorylation and signaling.
-Resveratrol
-Quercetin: inhibit the PI3K/AKT pathway.
-Epigallocatechin Gallate (EGCG)
-Luteolin and Apigenin: inhibit AKT phosphorylation


Scientific Papers found: Click to Expand⟱
2781- CHr,  PBG,    Chrysin a promising anticancer agent: recent perspectives
- Review, Var, NA
PI3K↓, It can block Phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) and Mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling in different animals against various cancers
Akt↓,
mTOR↓,
MMP9↑, Chrysin strongly suppresses Matrix metalloproteinase-9 (MMP-9), Urokinase plasminogen activator (uPA) and Vascular endothelial growth factor (VEGF), i.e. factors that can cause cancer
uPA↓,
VEGF↓,
AR↓, Chrysin has the ability to suppress the androgen receptor (AR), a protein necessary for prostate cancer development and metastasis
Casp↑, starts the caspase cascade and blocks protein synthesis to kill lung cancer cells
TumMeta↓, Chrysin significantly decreased lung cancer metastasis i
TumCCA↑, Chrysin induces apoptosis and stops colon cancer cells in the G2/M cell cycle phase
angioG↓, Chrysin prevents tumor growth and cancer spread by blocking blood vessel expansion
BioAv↓, Chrysin’s solubility, accessibility and bioavailability may limit its medical use.
*hepatoP↑, As chrysin reduced oxidative stress and lipid peroxidation in rat liver cells exposed to a toxic chemical agent.
*neuroP↑, Protecting the brain against oxidative stress (GPx) may be aided by increasing levels of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx).
*SOD↑,
*GPx↑,
*ROS↓, A decrease in oxidative stress and an increase in antioxidant capacity may result from chrysin’s anti-inflammatory properties
*Inflam↓,
*Catalase↑, Supplementation with chrysin increased the activity of antioxidant enzymes like SOD and catalase and reduced the levels of oxidative stress markers like malondialdehyde (MDA) in the colon tissue of the rats.
*MDA↓, Antioxidant enzyme activity (SOD, CAT) and oxidative stress marker (MDA) levels were both enhanced by chrysin supplementation in mouse liver tissue
ROS↓, reduction of reactive oxygen species (ROS) and oxidative stress markers in the cancer cells further indicated the antioxidant activity of chrysin
BBB↑, After crossing the blood-brain barrier, it has been shown to accumulate there
Half-Life↓, The half-life of chrysin in rats is predicted to be close to 2 hours.
BioAv↑, Taking chrysin with food may increase the effectiveness of the supplement: increased by a factor of 1.8 when taken with a high-fat meal
ROS↑, In contrast to 5-FU/oxaliplatin, chrysin increases the production of reactive oxygen species (ROS), which in turn causes autophagy by stopping Akt and mTOR from doing their jobs
eff↑, mixture of chrysin and cisplatin caused the SCC-25 and CAL-27 cell lines to make more oxygen free radicals. After treatment with chrysin, cisplatin, or both, the amount of reactive oxygen species (ROS) was found to have gone up.
ROS↑, When reactive oxygen species (ROS) and calcium levels in the cytoplasm rise because of chrysin, OC cells die.
ROS↑, chrysin is the cause of death in both types of prostate cancer cells. It does this by depolarizing mitochondrial membrane potential (MMP), making reactive oxygen species (ROS), and starting lipid peroxidation.
lipid-P↑,
ER Stress↑, when chrysin is present in DU145 and PC-3 cells, the expression of a group of proteins that control ER stress goes up
NOTCH1↑, Chrysin increased the production of Notch 1 and hairy/enhancer of split 1 at the protein and mRNA levels, which stopped cells from dividing
NRF2↓, Not only did chrysin stop Nrf2 and the genes it controls from working, but it also caused MCF-7 breast cancer cells to die via apoptosis.
p‑FAK↓, After 48 hours of treatment with chrysin at amounts between 5 and 15 millimoles, p-FAK and RhoA were greatly lowered
Rho↓,
PCNA↓, Lung histology and immunoblotting studies of PCNA, COX-2, and NF-B showed that adding chrysin stopped the production of these proteins and maintained the balance of cells
COX2↓,
NF-kB↓,
PDK1↓, After the chrysin was injected, the genes PDK1, PDK3, and GLUT1 that are involved in glycolysis had less expression
PDK3↑,
GLUT1↓,
Glycolysis↓, chrysin stops glycolysis
mt-ATP↓, chrysin inhibits complex II and ATPases in the mitochondria of cancer cells
Ki-67↓, the amounts of Ki-67, which is a sign of growth, and c-Myc in the tumor tissues went down
cMyc↓,
ROCK1↓, (ROCK1), transgelin 2 (TAGLN2), and FCH and Mu domain containing endocytic adaptor 2 (FCHO2) were much lower.
TOP1↓, DNA topoisomerases and histone deacetylase were inhibited, along with the synthesis of the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and (IL-1 beta), while the activity of protective signaling pathways was increased
TNF-α↓,
IL1β↓,
CycB↓, Chrysin suppressed cyclin B1 and CDK2 production in order to stop cancerous growth.
CDK2↓,
EMT↓, chrysin treatment can also stop EMT
STAT3↓, chrysin block the STAT3 and NF-B pathways, but it also greatly reduced PD-L1 production both in vivo and in vitro.
PD-L1↓,
IL2↑, chrysin increases both the rate of T cell growth and the amount of IL-2

1682- PBG,    Honey, Propolis, and Royal Jelly: A Comprehensive Review of Their Biological Actions and Health Benefits
- Review, Var, NA
i-LDH↓, cytotoxic activities of Tualang honey in human breast cancer cells were demonstrated by elevated secretion of lactate dehydrogenase (LDH)
Akt↓, figure 2
MAPK↓, figure 2
NF-kB↓, figure 2
IL1β↓, figure 2
IL6↓, figure 2
TNF-α↓, figure 2
iNOS↓, figure 2
COX2↓, figure 2
ROS↓, figure 2
Bcl-2↓, figure 2
PARP↓, figure 2
P53↑, figure 2
BAX↑, figure 2
Casp3↑, figure 2
TumCCA↑, Several components of honey such as chrysin, quercetin, and kaempferol have been shown to arrest cell cycle at various phases such as G0/G1, G1, and G2/M
Cyt‑c↑, hese stimuli cause several proteins located within the intermembrane space (IMS) of the mitochondria, such as cytochrome c, to be released
MMP↓, Honey induces MOMP in cancer cell lines by decreasing the mitochondrial membrane potential
eff↑, amplifying the apoptotic effect of tamoxifen by intensified depolarization of the mitochondrial membrane.

3257- PBG,    The Potential Use of Propolis as a Primary or an Adjunctive Therapy in Respiratory Tract-Related Diseases and Disorders: A Systematic Scoping Review
- Review, Var, NA
CDK4↓, CAPE also induces G1 phase cell arrest by lowering the expression of CDK4, CDK6, Rb, and p-Rb. M
CDK6↓,
pRB↓,
ROS↓, Artepillin C, a bioactive component of Brazilian green propolis, reduces oxidative damage markers, namely 4-HNE-modified proteins, 8-OHdG, malonaldehyde, and thiobarbituric acid reactive substances in lung tissues with pulmonary adenocarcinoma
TumCCA↑, Propolin, a novel component of prenylflavanones in Taiwanese propolis, was demonstrated to have anti-cancer properties. Propolin H induces cell arrest at G1 phase and upregulates the expression of p21
P21↑,
PI3K↓, Propolin C also inhibits PI3K/Akt and ERK-mediated epithelial-to-mesenchymal transition by upregulating E-cadherin (epithelial cell marker) and downregulating vimentin
Akt↓,
EMT↓,
E-cadherin↑,
Vim↓,
*COX2↓, bioactive compounds such as CAPE, galangin significantly reduce the activity of lung cyclooxygenase (COX) and myeloperoxidase (MPO), and malonaldehyde (MDA), TNF-α, and IL-6 levels, while increasing the activity of catalase (CAT) and SOD
*MPO↓,
*MDA↓,
*TNF-α↓,
*IL6↓,
*Catalase↑,
*SOD↑,
*AST↓, Chrysin also reduces the expression of oxidative and inflammatory markers such as aspartate transaminase (AST), alanine aminotransferase (ALT), IL-1β, IL-10, TNF-α, and MDA levels and increases the antioxidant parameters such as SOD, CAT, and GPx
*ALAT↓,
*IL1β↓,
*IL10↓,
*GPx↓,
*TLR4↓, propolis also inhibits the expression of Toll-like receptor 4 (TLR4), macrophage infiltration, MPO activity, and apoptosis of lung tissues in septic animals
*Sepsis↓,
*IFN-γ↑, CAPE also significantly increases IFN-γ
*GSH↑, propolis significantly increased the level of GSH and the histological appearances of propolis-treated bleomycin-induced pulmonary fibrosis rats.
*NRF2↑, CAPE significantly increases the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2)
*α-SMA↓, propolis significantly inhibits the expression of α- SMA, collagen fibers, and TGF-1β.
*TGF-β↓,
*IL5↓, Propolis also inhibits the expression of inflammatory cytokines and chemokines such as TNF-α, IL-5, IL-6, IL-8, IL-10, NF-kB, IFN-γ, PGF2a, and PGE2.
*IL6↓,
*IL8↓,
*PGE2↓,
*NF-kB↓,
*MMP9↓, downregulating the expression of TGF-1β, ICAM-1, α-SMA, MMP-9, IgE, and IgG1.

1660- PBG,    Emerging Adjuvant Therapy for Cancer: Propolis and its Constituents
- Review, Var, NA
MMPs↓, inhibition of matrix metalloproteinases, anti-angiogenesis
angioG↓,
TumMeta↓, prevention of metastasis, cell-cycle arrest
TumCCA↑,
Apoptosis↑,
ChemoSideEff↓, moderation of the chemotherapy-induced deleterious side effects
eff∅, components conferring antitumor potentials have been identified as caffeic acid phenethyl ester, chrysin, artepillin C, nemorosone, galangin, cardanol, etc
HDAC↓, Taiwanese green propolis extract was used to develop an anticancer agent NBM-HD-3, a histone deacetylase inhibitor (HDACis).
PTEN↑, found to increase phosphatase and tensin homolog (PTEN) and protein kinase B (Akt) protein levelssignificantly, while decreasing phospho-PTEN and phospho-Akt levels markedly
p‑PTEN↓,
p‑Akt↓,
Casp3↑, Propolis induced apoptosis and caspase 3 cleavage, increased phosphorylation of extracellular signal regulated kinase 1/2 (ERK1/2), protein kinase B/Akt1 and focal adhesion kinase (FAK).
p‑ERK↑,
p‑FAK↑,
Dose?, When administered orally for 20 weeks at a dose of 100-300 mg/kg, the protective role against the lingual carcinogenesis was observed
Akt↓, treatment reduced the protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1
GSK‐3β↓,
FOXO3↓,
eff↑, Co-treatment with CAPE and 5-fluorouracil exhibited additive anti-proliferation of TW2.6 cells.
IL2↑, Propolis administration stimulated IL-2 and IL-10 production
IL10↑,
NF-kB↓, reduces the expression of growth and transcription factors, including NF-κB.
VEGF↓, CAPE dose-dependently suppresses vascular endothelial growth factor (VEGF) formation by MDA-231 cells,
mtDam↑, Brazilian red propolis significantly reduced the cancer cell viability through the induction of mitochondrial dysfunction, caspase-3 activity and DNA fragmentation.
ER Stress↑, the action was believed to be due to endoplasmic reticulum stress-related signalling induction of CCAAT/enhancer-binding protein homologous protein (CHOP)
AST↓, Rats,(250 mg/kg) thrice a week for 3 weeks
ALAT↓, Rats,(250 mg/kg) thrice a week for 3 weeks
ALP↓, Rats,(250 mg/kg) thrice a week for 3 weeks
COX2↓, Rats,(250 mg/kg) thrice a week for 3 weeks, Expression of COX-2 and NF-kB p65 was significantly lowered
eff↑, co-treatment of cancer cells with 100 ng/mL TRAIL and 50 μg/mL propolis extract increased the percentage of apoptotic cells to about 66% and caused a significant disruption of membrane potential in LNCaP cells (
Bax:Bcl2↑, decreased Bcl-2/Bax ratio

1661- PBG,    Propolis: a natural compound with potential as an adjuvant in cancer therapy - a review of signaling pathways
- Review, Var, NA
JNK↓, downregulating pathways involving Jun-N terminal kinase, ERK1/2, Akt and NF-ƘB
ERK↓,
Akt↓,
NF-kB↓,
FAK↓, inhibiting Wtn2 and FAK, and MAPK and PI3K/AKT signaling pathways
MAPK↓,
PI3K↓,
Akt↓,
P21↑, propolis-induced up-regulation of p21 and p27
p27↑,
TRAIL↑, effects of propolis are mediated through upregulation of TRAIL, Bax, p53, and downregulation of the ERK1/2 signaling
BAX↑,
P53↑,
ERK↓,
ChemoSen↑, effective adjuvant therapy aimed at reducing related side effects associated with chemotherapy and radiotherapy
RadioS↑,
Glycolysis↓, Chinese poplar propolis decreased aerobic glycolysis by reducing the levels of crucial enzymes such as phosphofructokinase (PFK), hexokinase 2 (HK2), pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA)
HK2↓,
PKM2↓,
LDHA↓,
PFK↓,

1664- PBG,    Anticancer Activity of Propolis and Its Compounds
- Review, Var, NA
Apoptosis↑,
TumCMig↓,
TumCCA↑,
TumCP↓,
angioG↓,
P21↑, upregulating p21 and p27 expression
p27↑,
CDK1↓, thanol-extracted Cameroonian propolis increased the amount of DU145 and PC3 cells in G0/G1 phase, down-regulated cell cycle proteins (CDK1, pCDK1, and their related cyclins A and B)
p‑CDK1↓,
cycA1↓,
CycB↓,
P70S6K↓, Caffeic acid phenylethyl ester has been shown to inhibit the S6 beta-1 ribosomal protein kinase (p70S6K),
CLDN2↓, inhibition of NF-κB may be involved in the decrease of claudin-2 mRNA level
HK2↓, Chinese poplar propolis has been shown to significantly reduce the level of glycolysis at the stage of action of hexokinase 2 (HK2), phosphofructokinase (PFK), muscle isozyme pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA)
PFK↓,
PKM2↓,
LDHA↓,
TLR4↓, hinese propolis, as well as CAPE, inhibits breast cancer cell proliferation in the inflammatory microenvironment by inhibiting the Toll-like receptor 4 (TLR4) signal pathway
H3↓, Brazilian red propolis bioactive isoflavonoid, down-regulates the alpha-tubulin, tubulin in microtubules, and histone H3 genes
α-tubulin↓,
ROS↑, CAPE also affects the apoptotic intrinsic pathway by increasing ROS production
Akt↓, CAPE induces apoptosis by decreasing the levels of proteins related to carcinogenesis, including Akt, GSK3b, FOXO1, FOXO3a, NF-kB, Skp2 and cyclin D1
GSK‐3β↓,
FOXO3↓,
NF-kB↓,
cycD1↓,
MMP↓, It was found that chrysin caused a loss of mitochondria membrane potential (MMP) while increasing the production of reactive oxygen species (ROS), cytoplasmic Ca2+ levels, and lipid peroxidation
ROS↑,
i-Ca+2↑,
lipid-P↑,
ER Stress↑, Chrysin also induced endoplasmic reticulum (ER) stress by activating unfolded protein response proteins (UPR) such as PRKR-like ER kinase (PERK), eukaryotic translation initiation factor 2α (eIF2α), and 78 kDa glucose-regulated protein (GRP78)
UPR↑,
PERK↑,
eIF2α↑,
GRP78/BiP↑,
BAX↑, CAPE activated Bax protein
PUMA↑, CAPE also significantly increased PUMA expression
ROS↑, Northeast China causes cell apoptosis in human gastric cancer cells with increased production of reactive oxygen species (ROS) and reduced mitochondrial membrane potential.
MMP↓,
Cyt‑c↑, release of cytochrome C from mitochondria to the cytoplasm is observed, as well as the activation of cleaved caspases (8, 9, and 3) and PARP
cl‑Casp8↑,
cl‑Casp8↑,
cl‑Casp3↑,
cl‑PARP↑,
eff↑, administration of Iranian propolis extract in combination with 5-fluorouracil (5-FU) significantly reduced the number of azaxymethane-induced aberrant crypt foci compared to 5-FU or propolis alone.
eff↑, Propolis may also have a positive effect on the efficacy of photodynamic therapy (PDT). enhances the intracellular accumulation of protoporphyrin IX (PpIX) in human epidermoid carcinoma cells
RadioS↑, breast cancer patients undergoing radiotherapy and supplemented with propolis had a statistically significant longer median disease-free survival time than the control group
ChemoSen↑, confirmed that propolis mouthwash is effective and safe in the treatment of chemo- or radiotherapy-induced oral mucositis in cancer patients.
eff↑, Quercetin, ferulic acid, and CAPE may also influence the MDR of cancer cells by inhibiting P-gp expression

1678- PBG,  5-FU,  sericin,    In vitro and in vivo anti-colorectal cancer effect of the newly synthesized sericin/propolis/fluorouracil nanoplatform through modulation of PI3K/AKT/mTOR pathway
- in-vitro, CRC, Caco-2 - in-vivo, NA, NA
PI3K↓, mechanism of action of the prepared nanoformula revealed that it acts through the inhibition of the PI3K/AKT/mTOR signaling pathway and consequently inhibiting cancerous cells proliferation.
Akt↓,
mTOR↓,
TumCP↓,
Bcl-2↓, downregulated BCL2 (B-cell lymphoma 2) and activated BAX, Caspase 9 and Caspase 3 expression
BAX↑,
Casp3↑,
Casp9↑,
ROS↓, prepared nanoformula decreased the ROS (Reactive Oxygen Species) production in vivo owing to PI3K/AKT/mTOR pathway inhibition and FOXO-1 (Forkhead Box O1) activation
FOXO1↑,
*toxicity∅, LD50 of the prepared nanoformula reached 1 mg/Kg upon oral administration.
eff↑, It is well known that propolis and sericin inhibit PI3K/AKT and ERK pathway


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Results for Effect on Cancer/Diseased Cells:
Akt↓,8,   p‑Akt↓,1,   ALAT↓,1,   ALP↓,1,   angioG↓,3,   Apoptosis↑,2,   AR↓,1,   AST↓,1,   mt-ATP↓,1,   BAX↑,4,   Bax:Bcl2↑,1,   BBB↑,1,   Bcl-2↓,2,   BioAv↓,1,   BioAv↑,1,   i-Ca+2↑,1,   Casp↑,1,   Casp3↑,3,   cl‑Casp3↑,1,   cl‑Casp8↑,2,   Casp9↑,1,   CDK1↓,1,   p‑CDK1↓,1,   CDK2↓,1,   CDK4↓,1,   CDK6↓,1,   ChemoSen↑,2,   ChemoSideEff↓,1,   CLDN2↓,1,   cMyc↓,1,   COX2↓,3,   cycA1↓,1,   CycB↓,2,   cycD1↓,1,   Cyt‑c↑,2,   Dose?,1,   E-cadherin↑,1,   eff↑,8,   eff∅,1,   eIF2α↑,1,   EMT↓,2,   ER Stress↑,3,   ERK↓,2,   p‑ERK↑,1,   FAK↓,1,   p‑FAK↓,1,   p‑FAK↑,1,   FOXO1↑,1,   FOXO3↓,2,   GLUT1↓,1,   Glycolysis↓,2,   GRP78/BiP↑,1,   GSK‐3β↓,2,   H3↓,1,   Half-Life↓,1,   HDAC↓,1,   HK2↓,2,   IL10↑,1,   IL1β↓,2,   IL2↑,2,   IL6↓,1,   iNOS↓,1,   JNK↓,1,   Ki-67↓,1,   i-LDH↓,1,   LDHA↓,2,   lipid-P↑,2,   MAPK↓,2,   MMP↓,3,   MMP9↑,1,   MMPs↓,1,   mtDam↑,1,   mTOR↓,2,   NF-kB↓,5,   NOTCH1↑,1,   NRF2↓,1,   P21↑,3,   p27↑,2,   P53↑,2,   P70S6K↓,1,   PARP↓,1,   cl‑PARP↑,1,   PCNA↓,1,   PD-L1↓,1,   PDK1↓,1,   PDK3↑,1,   PERK↑,1,   PFK↓,2,   PI3K↓,4,   PKM2↓,2,   pRB↓,1,   PTEN↑,1,   p‑PTEN↓,1,   PUMA↑,1,   RadioS↑,2,   Rho↓,1,   ROCK1↓,1,   ROS↓,4,   ROS↑,6,   STAT3↓,1,   TLR4↓,1,   TNF-α↓,2,   TOP1↓,1,   TRAIL↑,1,   TumCCA↑,5,   TumCMig↓,1,   TumCP↓,2,   TumMeta↓,2,   uPA↓,1,   UPR↑,1,   VEGF↓,2,   Vim↓,1,   α-tubulin↓,1,  
Total Targets: 113

Results for Effect on Normal Cells:
ALAT↓,1,   AST↓,1,   Catalase↑,2,   COX2↓,1,   GPx↓,1,   GPx↑,1,   GSH↑,1,   hepatoP↑,1,   IFN-γ↑,1,   IL10↓,1,   IL1β↓,1,   IL5↓,1,   IL6↓,2,   IL8↓,1,   Inflam↓,1,   MDA↓,2,   MMP9↓,1,   MPO↓,1,   neuroP↑,1,   NF-kB↓,1,   NRF2↑,1,   PGE2↓,1,   ROS↓,1,   Sepsis↓,1,   SOD↑,2,   TGF-β↓,1,   TLR4↓,1,   TNF-α↓,1,   toxicity∅,1,   α-SMA↓,1,  
Total Targets: 30

Scientific Paper Hit Count for: Akt, PKB-Protein kinase B
7 Propolis -bee glue
1 Chrysin
1 5-fluorouracil
1 sericin
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:137  Target#:4  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

Home Page