Database Query Results : Apigenin (mainly Parsley), , ERK

Api, Apigenin (mainly Parsley): Click to Expand ⟱
Features:

Apigenin — a plant-derived flavone (4′,5,7-trihydroxyflavone) abundant in parsley/celery/chamomile and other dietary sources, often abbreviated APG (or “Api” in some indexes). It is a small-molecule polyphenol classified as a dietary phytochemical/nutraceutical candidate with broad pleiotropic signaling effects in oncology models (cell-cycle control, apoptosis, inflammatory signaling, metabolic stress, and invasion/angiogenesis programs), but with important translation constraints driven by low aqueous solubility and extensive phase-II conjugation.

Primary mechanisms (ranked):

  1. Pleiotropic pro-apoptotic / cell-cycle checkpoint engagement (mitochondrial apoptosis, caspases; CDK/cyclin suppression; p53 context-dependent)
  2. PI3K–AKT–MAPK signaling suppression with downstream anti-proliferative and anti-migration effects
  3. Inflammation axis suppression (NF-κB; COX-2 and pro-inflammatory cytokine programs)
  4. Redox stress reprogramming (often ROS↑ in cancer models; antioxidant/NRF2 effects are context-dependent and can diverge between cancer vs normal cells)
  5. HIF-1α–glycolysis downshift with ATP stress (model-dependent)
  6. Anti-invasive / anti-EMT programs (FAK/integrins; MMP/uPA; EMT markers)
  7. Epigenetic modulation (HDAC/DNMT/EZH2 axes; context-dependent)
  8. Anti-angiogenic signaling (VEGF/related programs; model-dependent)
  9. Stemness pathway pressure (Hh/GLI, CK2; model-dependent)
  10. Chemo-/death-ligand sensitization (e.g., TRAIL sensitization reported in preclinical systems)

Bioavailability / PK relevance: Oral apigenin exposure is commonly limited by poor water solubility and extensive first-pass metabolism (glucuronidation/sulfation). Human data indicate circulating apigenin is largely present as conjugated metabolites, and dietary intake can yield only low (typically sub-µM) systemic levels; lipidic/self-emulsifying formulations can increase exposure in vivo (formulation-dependent). Reported half-life/kinetic parameters vary widely across studies and matrices.

In-vitro vs systemic exposure relevance: Many anti-cancer in vitro studies use ~10–50+ µM apigenin, which can exceed typical achievable free aglycone systemic levels after oral intake; some effects may therefore be high-concentration or formulation-enabled rather than diet-achievable. Tissue-local exposure (GI lumen, local mucosa) may be higher than plasma, and conjugate biology may contribute (context-dependent).

Clinical evidence status: Predominantly preclinical oncology evidence (cell and animal models) with limited, non-definitive human cancer interventional data; at least one pilot clinical study concept exists/has been registered (status-dependent). Strongest human evidence base is for non-cancer indications and general bioactivity rather than oncology efficacy.

Apigenin present in parsley, celery, chamomile, oranges and beverages such as tea, beer and wine.
"It exhibits cell growth arrest and apoptosis in different types of tumors such as breast, lung, liver, skin, blood, colon, prostate, pancreatic, cervical, oral, and stomach, by modulating several signaling pathways."
-Note half-life reports vary 2.5-90hrs?.
-low solubility of apigenin in water : BioAv (improves when mixed with oil/dietary fat or lipid based formulations)
-best oil might be MCT oils (medium-chain fatty acids)


Pathways:
- Often considered an antioxidant, in cancer cells it can paradoxically induce ROS production
(one report that goes against most others, by lowering ROS in cancer cells but still effective)
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, UPR↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓ (Conflicting evidence about Nrf2)
        - Combined with Metformin (reduces Nrf2) amplifies ROS production in cancer cells while sparing normal cells.
- Raises AntiOxidant defense in Normal Cells: NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : , MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, FAK↓, ERK↓,
- inhibits glycolysis and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓,
- Others: PI3K↓, AKT↓, JAK↓, 1, 2, 3, STAT↓, 1, 2, 3, 4, 5, 6, Wnt↓, β-catenin↓, AMPK↓,, α↓,, ERK↓, 5↓, JNK↓,
- Shown to modulate the nuclear translocation of SREBP-2 (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes)
        -Ex: other flavonoids(chrysin, Luteolin, querectin) curcumin, metformin, sulforaphane, ASA
Neuroprotective, Renoprotection, Hepatoprotective, CardioProtective,
- Selectivity: Cancer Cells vs Normal Cells

Apigenin exhibits biological effects (anticancer, anti-inflammatory, antioxidant, neuroprotective, etc.) typically at concentrations roughly in the range of 1–50 µM.

Parsley microgreens can contain up to 2-3 times more apigenin than mature parsley.
Apigenin is typically measured in the range of 1-10 μM for biological activity. Assuming a molecular weight of 270 g/mol for apigenin, we can estimate the following μM concentrations:
10uM*5L(blood)*270g/mol=13.5mg apigenin (assumes 100% bioavailability)
then an estimated 10-20 mg of apigenin per 100 g of fresh weight parlsey
2.2mg/g of apigenin fresh parsley
45mg/g of apigenin in dried parsley (wikipedia)
so 100g of parsley might acheive 10uM blood serum level (100% bioavailability)
BUT bioavailability is only 1-5%
(Supplements available in 75mg liposomal)( Apigenin Pro Liposomal, 200 mg from mcsformulas.com)

A study had 2g/kg bw (meaning 160g for 80kg person) delivered a maximum 0.13uM of plasma concentration @ 7.2hrs.
Assuming parsley is 90-95% water, then that would be ~16g of dried parsley
Conclusion: to reach 10uM would seem very difficult by oral ingestion of parsley.
Other quotes:
      “4g of dried parsley will be enough for 50kg adult”
      5mg/kg BW yields 16uM, so 80Kg person means 400mg (if dried parsley is 130mg/g, then would need 3g/d)
In many cancer cell lines, concentrations in the range of approximately 20–40 µM have been reported to shift apigenin’s activity from mild antioxidant effects (or negligible ROS changes) toward a clear pro-oxidant effect with measurable ROS increases.

Low doses: At lower concentrations, apigenin is more likely to exhibit its antioxidant properties, scavenging ROS and protecting cells from oxidative stress.
In normal cells with robust antioxidant systems, apigenin’s antioxidant effects might prevail, whereas cancer cells—often characterized by an already high level of basal ROS—can be pushed over the oxidative threshold by increased ROS production induced by apigenin.
In environments with lower free copper levels, this pro-oxidant activity is less pronounced, and apigenin may tilt the balance toward its antioxidant function.

Apigenin — cancer-relevant mechanistic pathway matrix

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Mitochondrial apoptosis program ΔΨm ↓, Cyt-c ↑, Caspase cascade ↑, apoptosis ↑ ↔ to protective (model-dependent) R Pro-apoptotic stress commitment Frequently reported core phenotype across tumor models; may be downstream of ROS and kinase-network suppression.
2 Cell-cycle control Cyclin D1/E ↓, CDK2/4/6 ↓, arrest ↑ ↔ G Anti-proliferative checkpointing Often couples to p53/p21 context and growth-factor signaling downshift.
3 PI3K / AKT / MAPK PI3K ↓, AKT ↓, ERK ↓ (model-dependent) ↔ R Growth and survival signaling suppression High industry relevance; provides a convergent explanation for anti-growth and anti-migration phenotypes.
4 NF-κB / COX-2 inflammatory axis NF-κB ↓, COX-2 ↓, inflammatory cytokine programs ↓ Inflammatory tone ↓ G Anti-inflammatory microenvironment pressure Relevant to tumor-promoting inflammation and stromal signaling (context-dependent).
5 ROS modulation ROS ↑ (often), DNA damage ↑, ER stress ↑ (model-dependent) ROS injury ↓ / antioxidant support ↑ (context-dependent) P Redox stress bifurcation (tumor vs normal) Frequently described “paradox”: pro-oxidant stress in tumors while normal cells may show antioxidant protection; not universal.
6 NRF2 / antioxidant defense NRF2 ↓, GSH ↓ (often) ↔ (conflicting) NRF2 ↑, SOD ↑, GSH ↑ (context-dependent) G Antioxidant program reprogramming Direction is context- and model-dependent; important for interpreting chemo-compatibility and ROS claims.
7 HIF-1α / glycolysis HIF-1α ↓, glycolysis ↓, ATP ↓ (model-dependent) ↔ G Metabolic stress / Warburg pressure Reported suppression of glycolysis nodes (e.g., GLUT1/LDHA/HK2/PKM2/PDK1) in some models; may be concentration-sensitive.
8 Migration / invasion and EMT EMT ↓, FAK ↓, integrin signaling ↓, MMPs ↓, uPA ↓ ↔ G Anti-metastatic phenotypes Often downstream of kinase-network suppression and inflammatory tone changes.
9 Angiogenesis programs VEGF ↓ (model-dependent) ↔ G Anti-angiogenic signaling pressure Usually indirect via HIF-1α / inflammatory signaling and tumor-stromal coupling.
10 Epigenetic regulation HDAC ↓, DNMTs ↓, EZH2 ↓ (model-dependent) ↔ G Transcriptional reprogramming Mechanistically plausible but often secondary to upstream stress/kinase changes; evidence varies by model.
11 Cancer stemness pathways Hh/GLI ↓, CK2 ↓, CSC phenotypes ↓ (model-dependent) ↔ G Stemness pressure Typically preclinical; may matter for recurrence-resistance hypotheses.
12 Chemosensitization / death-ligand sensitization Sensitization ↑ (model-dependent) ↔ R Combination leverage Examples include TRAIL sensitization in vitro; translation depends on achievable exposure and interaction risk.
13 Clinical Translation Constraint Low solubility; conjugation-heavy PK; in-vitro concentration gap; potential CYP/UGT/SULT interactions Drug–supplement interaction risk relevant to both — Delivery and interaction limitations Oral free-aglycone systemic levels are often low; formulation can change exposure. In vitro CYP inhibition is reported (notably CYP3A4/2C9); apigenin can also inhibit conjugation pathways in models—caution with narrow-therapeutic-index drugs.

TSF

P: 0–30 min
R: 30 min–3 hr
G: >3 hr
ERK, ERK signaling: Click to Expand ⟱
Source:
Type:
MAPK3 (ERK1)
ERK proteins are kinases that activate other proteins by adding a phosphate group. An overactivation of these proteins causes the cell cycle to stop.
The extracellular signal-regulated kinase (ERK) signaling pathway is a crucial component of the mitogen-activated protein kinase (MAPK) signaling cascade, which plays a significant role in regulating various cellular processes, including proliferation, differentiation, and survival. high levels of phosphorylated ERK (p-ERK) in tumor samples may indicate active ERK signaling and could correlate with aggressive tumor behavior

EEk singaling is frequently activated and is often associated with aggressive tumor behavior, treatment resistance, and poor outcomes.
Scientific Papers found: Click to Expand⟱
1545- Api,    The Potential Role of Apigenin in Cancer Prevention and Treatment
- Review, NA, NA
TNF-α↓, Apigenin downregulates the TNFα
IL6↓,
IL1α↓,
P53↑,
Bcl-xL↓,
Bcl-2↓,
BAX↑,
Hif1a↓, Apigenin inhibited HIF-1alpha and vascular endothelial growth factor expression
VEGF↓,
TumCCA↑, Apigenin exposure induces G2/M phase cell cycle arrest, DNA damage, apoptosis and p53 accumulation
DNAdam↑,
Apoptosis↑,
CycB/CCNB1↓,
cycA1/CCNA1↓,
CDK1↓,
PI3K↓,
Akt↓,
mTOR↓,
IKKα↓, , decreases IKKα kinase activity,
ERK↓,
p‑Akt↓,
p‑P70S6K↓,
p‑S6↓,
p‑ERK↓, decreased the expression of phosphorylated (p)-ERK1/2 proteins, p-AKT and p-mTOR
p‑P90RSK↑,
STAT3↓,
MMP2↓, Apigenin down-regulated Signal transducer and activator of transcription 3target genes MMP-2, MMP-9 and vascular endothelial growth factor
MMP9↓,
TumCP↓, Apigenin significantly suppressed colorectal cancer cell proliferation, migration, invasion and organoid growth through inhibiting the Wnt/β-catenin signaling
TumCMig↓,
TumCI↓,
Wnt/(β-catenin)↓,

1539- Api,  LT,    Dietary flavones counteract phorbol 12-myristate 13-acetate-induced SREBP-2 processing in hepatic cells
- in-vitro, Liver, HepG2
SREBP2↓, ecreased transcription of SREBP-2 upon the apigenin treatment
eff↑, 25 lM of both flavones could significantly bring down the induced pMEK and pERK.
p‑MEK↓,
p‑ERK↓,

2633- Api,    Apigenin induces ROS-dependent apoptosis and ER stress in human endometriosis cells
- in-vitro, EC, NA
TumCP↓, Apigenin reduced proliferation and induced cell cycle arrest and apoptosis in the both endometriosis cell lines
TumCCA↑,
MMP↓, In addition, it disrupted mitochondrial membrane potential (MMP) which was accompanied by an increase in concentration of calcium ions in the cytosol and in pro-apoptotic proteins including Bax and cytochrome c in the VK2/E6E7 and End1/E6E7 cells
Ca+2↑,
BAX↑,
Cyt‑c↑,
ROS↑, Moreover, apigenin treated cells accumulated excessive reactive oxygen species (ROS), and experienced lipid peroxidation and endoplasmic reticulum (ER) stress with activation of the unfolded protein response (UPR) regulatory proteins.
lipid-P↑,
ER Stress↑,
UPR↑,
p‑ERK↓, Apigenin inhibited the phosphorylation of ERK1/2
ERK↓, Similar to previous studies, apigenin-induced apoptosis was also mediated by inactivation of ERK1/2 and JNK proteins and regulation of AKT protein in human endometriosis cells.
JNK↑,

3884- Api,    Neuroprotective, Anti-Amyloidogenic and Neurotrophic Effects of Apigenin in an Alzheimer’s Disease Mouse Model
- in-vivo, AD, NA
*memory↑, Three-month oral treatment with apigenin rescued learning deficits and relieved memory retention in APP/PS1 mice.
*Aβ↓, Apigenin also showed effects affecting APP processing and preventing Aβ burden due to the down-regulation of BACE1 and β-CTF levels, the relief of Aβ deposition, and the decrease of insoluble Aβ levels.
*BACE↓, we observed BACE1 level reduction treated with apigenin.
*antiOx↑, apigenin exhibited superoxide anion scavenging effects and improved antioxidative enzyme activity of superoxide dismutase and glutathione peroxidase.
*BDNF↑, apigenin restored neurotrophic ERK/CREB/BDNF pathway in the cerebral cortex.
*p‑CREB↑, After long-term apigenin treatment, coupled with the elevation of BDNF level, enhanced phosphorylated ERK1/2 and CREB expression were detected in the cerebral cortex
*p‑ERK↑,
*ROS↓, apigenin exhibited superoxide anion scavenging effects and improved antioxidative enzyme activity of superoxide dismutase (SOD) and GSH-Px.
*SOD↑,
*GPx↑,
*neuroP↑, observations are correlated with a prospective neuroprotective, anti-amyloidogenic and neurotrophic effects in AD deficits.

2640- Api,    Apigenin: A Promising Molecule for Cancer Prevention
- Review, Var, NA
chemoPv↑, considerable potential for apigenin to be developed as a cancer chemopreventive agent.
ITGB4↓, apigenin inhibits hepatocyte growth factor-induced MDA-MB-231 cells invasiveness and metastasis by blocking Akt, ERK, and JNK phosphorylation and also inhibits clustering of β-4-integrin function at actin rich adhesive site
TumCI↓,
TumMeta↓,
Akt↓,
ERK↓,
p‑JNK↓,
*Inflam↓, The anti-inflammatory properties of apigenin are evident in studies that have shown suppression of LPS-induced cyclooxygenase-2 and nitric oxide synthase-2 activity and expression in mouse macrophages
*PKCδ↓, Apigenin has been reported to inhibit protein kinase C activity, mitogen activated protein kinase (MAPK), transformation of C3HI mouse embryonic fibroblasts and the downstream oncogenes in v-Ha-ras-transformed NIH3T3 cells (43, 44).
*MAPK↓,
EGFR↓, Apigenin treatment has been shown to decrease the levels of phosphorylated EGFR tyrosine kinase and of other MAPK and their nuclear substrate c-myc, which causes apoptosis in anaplastic thyroid cancer cells
CK2↓, apigenin has been shown to inhibit the expression of casein kinase (CK)-2 in both human prostate and breast cancer cells
TumCCA↑, apigenin induces a reversible G2/M and G0/G1 arrest by inhibiting p34 (cdc2) kinase activity, accompanied by increased p53 protein stability
CDK1↓, inhibiting p34 (cdc2) kinase activity
P53↓,
P21↑, Apigenin has also been shown to induce WAF1/p21 levels resulting in cell cycle arrest and apoptosis in androgen-responsive human prostate cancer
Bax:Bcl2↑, Apigenin treatment has been shown to alter the Bax/Bcl-2 ratio in favor of apoptosis, associated with release of cytochrome c and induction of Apaf-1, which leads to caspase activation and PARP-cleavage
Cyt‑c↑,
APAF1↑,
Casp↑,
cl‑PARP↑,
VEGF↓, xposure of endothelial cells to apigenin results in suppression of the expression of VEGF, an important factor in angiogenesis via degradation of HIF-1α protein
Hif1a↓,
IGF-1↓, oral administration of apigenin suppresses the levels of IGF-I in prostate tumor xenografts and increases levels of IGFBP-3, a binding protein that sequesters IGF-I in vascular circulation
IGFBP3↑,
E-cadherin↑, apigenin exposure to human prostate carcinoma DU145 cells caused increase in protein levels of E-cadherin and inhibited nuclear translocation of β-catenin and its retention to the cytoplasm
β-catenin/ZEB1↓,
HSPs↓, targets of apigenin include heat shock proteins (61), telomerase (68), fatty acid synthase (69), matrix metalloproteinases (70), and aryl hydrocarbon receptor activity (71) HER2/neu (72), casein kinase 2 alpha
Telomerase↓,
FASN↓,
MMPs↓,
HER2/EBBR2↓,
CK2↓,
eff↑, The combination of sulforaphane and apigenin resulted in a synergistic induction of UGT1A1
AntiAg↑, Apigenin inhibit platelet function through several mechanisms including blockade of TxA
eff↑, ex vivo anti-platelet effect of aspirin in the presence of apigenin, which encourages the idea of the combined use of aspirin and apigenin in patients in which aspirin fails to properly suppress the TxA
FAK↓, Apigenin inhibits expression of focal adhesion kinase (FAK), migration and invasion of human ovarian cancer A2780 cells.
ROS↑, Apigenin generates reactive oxygen species, causes loss of mitochondrial Bcl-2 expression, increases mitochondrial permeability, causes cytochrome C release, and induces cleavage of caspase 3, 7, 8, and 9 and the concomitant cleavage of the inhibitor
Bcl-2↓,
Cyt‑c↑,
cl‑Casp3↑,
cl‑Casp7↑,
cl‑Casp8↑,
cl‑Casp9↑,
cl‑IAP2↑,
AR↓, significant decrease in AR protein expression along with a decrease in intracellular and secreted forms of PSA. Apigenin treatment of LNCaP cells
PSA↓,
p‑pRB↓, apigenin inhibited hyperphosphorylation of the pRb protein
p‑GSK‐3β↓, Inhibition of p-Akt by apigenin resulted in decreased phosphorylation of GSK-3beta.
CDK4↓, both flavonoids exhibited cell growth inhibitory effects which were due to cell cycle arrest and downregulation of the expression of CDK4
ChemoSen↑, Combination therapy of gemcitabine and apigenin enhanced anti-tumor efficacy in pancreatic cancer cells (MiaPaca-2, AsPC-1)
Ca+2↑, apigenin in neuroblastoma SH-SY5Y cells resulted in increased apoptosis, which was associated with increases in intracellular free [Ca(2+)] and Bax:Bcl-2 ratio, mitochondrial release of cytochrome c and activation of caspase-9, calpain, caspase-3,12
cal2↑,

243- Api,    Apigenin Attenuates Melanoma Cell Migration by Inducing Anoikis through Integrin and Focal Adhesion Kinase Inhibition
- in-vitro, Melanoma, A375 - in-vitro, Melanoma, A2058
p‑FAK↓, Apigenin reduced integrin protein levels and inhibited the phosphorylation of focal adhesion kinase (FAK)
ERK↓, ERK1/2
Casp3↑,
PARP↑,
ITGA5↓, revealed that integrin subunits α4, α5, αV, and β3 were clearly downregulated in cell lysates of melanoma cells after apigenin treatment

242- Api,    Apigenin inhibits proliferation and invasion, and induces apoptosis and cell cycle arrest in human melanoma cells
- in-vitro, Melanoma, A375 - in-vitro, Melanoma, C8161
ERK↓,
PI3k/Akt/mTOR↓, Akt/mTOR
Casp3↑, cleaved
PARP↑, cleaved
p‑mTOR↓,
p‑Akt↓,

171- Api,    Apigenin in cancer therapy: anti-cancer effects and mechanisms of action
- Review, Var, NA
PI3K/Akt↓,
NF-kB↓,
CK2↓,
FOXO↓,
MAPK↝, modulation of MAPKs by apigenin contributed to apigenin-induced cell cycle arrest at G0/G1 phase
ERK↓, p-ERK1/2,
p‑JAK↓, phosphorylation
Wnt/(β-catenin)↓,
ROS↑, accumulation of reactive oxygen species (ROS) production, leading to induction of DNA damage
CDC25↓,
p‑STAT↓,
DNAdam↑,

416- Api,    In Vitro and In Vivo Anti-tumoral Effects of the Flavonoid Apigenin in Malignant Mesothelioma
- vitro+vivo, NA, NA
Bax:Bcl2↑,
P53↑,
ROS↑,
Casp9↑,
Casp8↑,
cl‑PARP1↑, cleavage
p‑ERK⇅, Here, we demonstrated that API treatment was able to increase ERK1/2 phosphorylation in MM-B1, H-Meso-1, and #40a cells while induced a decrease of ERK1/2 activation in MM-F1 cells.
p‑JNK↓,
p‑p38↑,
p‑Akt↓,
cJun↓,
NF-kB↓,
EGFR↓,
TumCCA↑, increase of the percentage of cells in subG1 phase


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

lipid-P↑, 1,   ROS↑, 4,  

Mitochondria & Bioenergetics ⓘ

CDC25↓, 1,   p‑MEK↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

FASN↓, 1,   PI3K/Akt↓, 1,   PI3k/Akt/mTOR↓, 1,   p‑S6↓, 1,   SREBP2↓, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 3,   APAF1↑, 1,   Apoptosis↑, 1,   BAX↑, 2,   Bax:Bcl2↑, 2,   Bcl-2↓, 2,   Bcl-xL↓, 1,   Casp↑, 1,   Casp3↑, 2,   cl‑Casp3↑, 1,   cl‑Casp7↑, 1,   Casp8↑, 1,   cl‑Casp8↑, 1,   Casp9↑, 1,   cl‑Casp9↑, 1,   CK2↓, 3,   Cyt‑c↑, 3,   cl‑IAP2↑, 1,   JNK↑, 1,   p‑JNK↓, 2,   MAPK↝, 1,   p‑p38↑, 1,   Telomerase↓, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

cJun↓, 1,   p‑pRB↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   HSPs↓, 1,   UPR↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↓, 1,   P53↑, 2,   PARP↑, 2,   cl‑PARP↑, 1,   cl‑PARP1↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 2,   CDK4↓, 1,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 1,   P21↑, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 6,   p‑ERK↓, 3,   p‑ERK⇅, 1,   FOXO↓, 1,   p‑GSK‐3β↓, 1,   IGF-1↓, 1,   IGFBP3↑, 1,   mTOR↓, 1,   p‑mTOR↓, 1,   p‑P70S6K↓, 1,   p‑P90RSK↑, 1,   PI3K↓, 1,   p‑STAT↓, 1,   STAT3↓, 1,   Wnt/(β-catenin)↓, 2,  

Migration ⓘ

AntiAg↑, 1,   Ca+2↑, 2,   cal2↑, 1,   E-cadherin↑, 1,   FAK↓, 1,   p‑FAK↓, 1,   ITGA5↓, 1,   ITGB4↓, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 2,   Hif1a↓, 2,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

IKKα↓, 1,   IL1α↓, 1,   IL6↓, 1,   p‑JAK↓, 1,   NF-kB↓, 2,   PSA↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 3,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 2,   HER2/EBBR2↓, 1,   IL6↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,  
Total Targets: 102

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GPx↑, 1,   ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

p‑CREB↑, 1,  

Cell Death ⓘ

MAPK↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↑, 1,  

Migration ⓘ

PKCδ↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,   BACE↓, 1,  

Functional Outcomes ⓘ

memory↑, 1,   neuroP↑, 1,  
Total Targets: 14

Scientific Paper Hit Count for: ERK, ERK signaling
9 Apigenin (mainly Parsley)
1 Luteolin
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

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