Apigenin (mainly Parsley) Cancer Research Results

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
Scientific Papers found: Click to Expand⟱
2596- Api,  LT,    Natural Nrf2 Inhibitors: A Review of Their Potential for Cancer Treatment
- Review, Var, NA
NRF2↓, chemoPv↑, ChemoSen↑,
2594- Api,  docx,    Targeted hyaluronic acid-based lipid nanoparticle for apigenin delivery to induce Nrf2-dependent apoptosis in lung cancer cells
- in-vitro, Lung, A549
NRF2↓, ChemoSen↑,
2593- Api,    Apigenin promotes apoptosis of 4T1 cells through PI3K/AKT/Nrf2 pathway and improves tumor immune microenvironment in vivo
- in-vivo, BC, 4T1
TumCP↓, TumCMig↓, TumCI↓, Apoptosis↑, MMP↑, ROS↑, p‑PI3K↓, PI3K↓, Akt↓, NRF2↓, AntiTum↑, OS↑,
2586- Api,  doxoR,    Apigenin sensitizes doxorubicin-resistant hepatocellular carcinoma BEL-7402/ADM cells to doxorubicin via inhibiting PI3K/Akt/Nrf2 pathway
- in-vitro, HCC, Bel-7402
NRF2↓, ChemoSen↑,
2585- Api,    Apigenin inhibits the proliferation of adenoid cystic carcinoma via suppression of glucose transporter-1
- in-vitro, ACC, NA
GLUT1↓, TumCG↓,
2584- Api,  Chemo,    The versatility of apigenin: Especially as a chemopreventive agent for cancer
- Review, Var, NA
ChemoSen↑, RadioS↑, eff↝, DR5↑, selectivity↑, angioG↓, selectivity↑, chemoP↑, MAPK↓, PI3K↓, Akt↓, mTOR↓, Wnt↓, β-catenin/ZEB1↓, GLUT1↓, radioP↑, BioAv↓, chemoPv↑,
2583- Api,  Rad,    The influence of apigenin on cellular responses to radiation: From protection to sensitization
- Review, Var, NA
radioP↑, RadioS↑, *COX2↓, *ROS↓, VEGF↓, MMP2↓, STAT3↓, AMPK↑, Apoptosis↑, MMP9↓, glucose↓,
2319- Api,    Apigenin sensitizes radiotherapy of mouse subcutaneous glioma through attenuations of cell stemness and DNA damage repair by inhibiting NF-κB/HIF-1α-mediated glycolysis
- in-vitro, GBM, NA
Glycolysis↓, NF-kB↓, p65↓, Hif1a↓, GLUT1↓, GLUT3↓, PKM2↓, RadioS↑, TumVol↓, TumW↓,
2318- Api,    Apigenin as a multifaceted antifibrotic agent: Therapeutic potential across organ systems
- Review, Nor, NA
*ROS↓, *PKM2↓, *Hif1a↓, *TGF-β↓, *AMPK↑, *Inflam↓, *PI3K↓, *Akt↑, *NRF2↑, *NF-kB↓,
2317- Api,    Apigenin intervenes in liver fibrosis by regulating PKM2-HIF-1α mediated oxidative stress
- in-vivo, Nor, NA
*hepatoP↑, *PKM2↓, *Hif1a↓, *MDA↓, *Catalase↓, *GSH↑, *SOD↑, *GPx↑, *TAC↑, *α-SMA↓, *Vim↓, *ROS↓,
2316- Api,    The interaction between apigenin and PKM2 restrains progression of colorectal cancer
- in-vitro, CRC, LS174T - in-vitro, CRC, HCT8 - in-vivo, CRC, NA
TumCP↓, PKM2↓, Glycolysis↓, TumCG↑, selectivity↑,
2314- Api,    Apigenin Restrains Colon Cancer Cell Proliferation via Targeted Blocking of Pyruvate Kinase M2-Dependent Glycolysis
- in-vitro, Colon, HCT116 - in-vitro, Colon, HT29 - in-vitro, Colon, DLD1
Glycolysis↓, PKM2:PKM1↓, β-catenin/ZEB1↓, cMyc↓,
210- Api,    Apigenin inhibits migration and invasion via modulation of epithelial mesenchymal transition in prostate cancer
- in-vitro, Pca, DU145
EMT↓, E-cadherin↑, Snail↓, Vim↓,
310- Api,    Apigenin inhibits renal cell carcinoma cell proliferation
- vitro+vivo, RCC, ACHN - in-vitro, RCC, 786-O - in-vitro, RCC, Caki-1 - in-vitro, RCC, HK-2
TumCCA↑, p‑ATM↑, p‑CHK1↑, p‑CDC25↑, p‑cDC2↑, P53↑, BAX↑, Casp9↑, Casp3↑,
308- Api,    Apigenin Inhibits Cancer Stem Cell-Like Phenotypes in Human Glioblastoma Cells via Suppression of c-Met Signaling
- in-vitro, GBM, U87MG - in-vitro, GBM, U373MG
cMET↓, Akt↓, Nanog↓, SOX2↓,
307- Api,    Flavonoids inhibit angiogenic cytokine production by human glioma cells
- in-vitro, GBM, GL-15
TGF-β↓,
275- Api,    Apigenin inhibits the self-renewal capacity of human ovarian cancer SKOV3‑derived sphere-forming cells
- in-vitro, Ovarian, SKOV3
HH↓, CK2↓, Gli1↓,
273- Api,    Apigenin inhibited migration and invasion of human ovarian cancer A2780 cells through focal adhesion kinase
- in-vivo, Ovarian, A2780S
FAK↓,
270- Api,    Apigenin induces apoptosis in human leukemia cells and exhibits anti-leukemic activity in vivo via inactivation of Akt and activation of JNK
- in-vivo, AML, U937
Akt↓, JNK↑, Mcl-1↓, cl‑Bcl-2↓, Casp3↑, Casp7↑, Casp9↑, cl‑PARP↑, mTOR↓, GSK‐3β↓,
269- Api,    Cytotoxicity of apigenin on leukemia cell lines: implications for prevention and therapy
- in-vitro, AML, HL-60 - in-vitro, AML, K562 - in-vitro, AML, TF1
JAK↓, PI3K↓, cDC2↓, STAT↓,
268- Api,    Induction of apoptosis by apigenin and related flavonoids through cytochrome c release and activation of caspase-9 and caspase-3 in leukaemia HL-60 cells
- in-vitro, AML, HL-60
Casp3↑, PARP↑,
244- Api,    Inhibition of the STAT3 signaling pathway contributes to apigenin-mediated anti-metastatic effect in melanoma
- in-vivo, Melanoma, B16-F10 - in-vivo, Melanoma, A375 - in-vivo, Melanoma, G361
STAT3↓, MMP2↓, MMP9↓, VEGF↓, Twist↓, E-cadherin↑, N-cadherin↓, EMT↓,
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↓, ERK↓, Casp3↑, PARP↑, ITGA5↓,
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↓, Casp3↑, PARP↑, p‑mTOR↓, p‑Akt↓,
240- Api,    The flavonoid apigenin reduces prostate cancer CD44(+) stem cell survival and migration through PI3K/Akt/NF-κB signaling
- in-vitro, Pca, PC3 - in-vitro, Pca, CD44+
P21↑, p27↑, Casp3↑, Casp8↑, Slug↓, Snail↓, NF-kB↓, PI3K↓, Akt↓,
238- Api,    Apigenin inhibits TGF-β-induced VEGF expression in human prostate carcinoma cells via a Smad2/3- and Src-dependent mechanism
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, C4-2B
VEGF↓, TGF-β↓, Src↓, FAK↓, Akt↓, SMAD2↓, SMAD3↓,
237- Api,    Apigenin blocks IKKα activation and suppresses prostate cancer progression
- in-vivo, Pca, PC3 - in-vivo, Pca, 22Rv1 - in-vivo, Pca, LNCaP - in-vivo, Pca, DU145
IKKα↓, NF-kB↓,
211- Api,    Suppression of NF-κB and NF-κB-Regulated Gene Expression by Apigenin through IκBα and IKK Pathway in TRAMP Mice
- in-vivo, Pca, NA
IKKα↓, NF-kB↓, cycD1/CCND1↓, COX2↓, Bcl-2↓, Bcl-xL↓, VEGF↓, PCNA↓, BAX↑,
311- Api,    Apigenin inhibits the proliferation of adenoid cystic carcinoma via suppression of glucose transporter-1
- in-vitro, ACC, NA
GLUT1↓, CC(CDKs/cyclins)↓, TumCCA↑,
208- Api,    Apigenin induces apoptosis by targeting inhibitor of apoptosis proteins and Ku70–Bax interaction in prostate cancer
- in-vivo, Pca, PC3 - in-vivo, Pca, DU145
XIAP↓, survivin↓, Bcl-xL↓, Bcl-2↓, BAX↑,
207- Api,    Involvement of nuclear factor-kappa B, Bax and Bcl-2 in induction of cell cycle arrest and apoptosis by apigenin in human prostate carcinoma cells
- in-vitro, Pca, LNCaP
PSA↓, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4/6↓, P21↑, AR↓,
206- Api,    Inhibition of glutamine utilization sensitizes lung cancer cells to apigenin-induced apoptosis resulting from metabolic and oxidative stress
- in-vitro, Lung, H1299 - in-vitro, Lung, H460 - in-vitro, Lung, A549 - in-vitro, CRC, HCT116 - in-vitro, Melanoma, A375 - in-vitro, Lung, H2030 - in-vitro, CRC, SW480
Glycolysis↓, lactateProd↓, PGK1↓, ALDOA↓, GLUT1↓, ENO1↓, ATP↓, Casp9↑, Casp3↑, cl‑PARP↑, PI3K/Akt↓, HK1↓, HK2↓, ROS↑, Apoptosis↑, eff↓, NADPH↓, PPP↓,
180- Api,    Induction of caspase-dependent apoptosis by apigenin by inhibiting STAT3 signaling in HER2-overexpressing MDA-MB-453 breast cancer cells
- in-vitro, BC, MDA-MB-231
cl‑Casp8↑, cl‑Casp3↑, cl‑PARP↑, BAX∅, Bcl-2∅, Bcl-xL∅, p‑STAT3↓, P53↑, P21↑, p‑JAK2↓, VEGF↓,
179- Api,    Apigenin induces caspase-dependent apoptosis by inhibiting signal transducer and activator of transcription 3 signaling in HER2-overexpressing SKBR3 breast cancer cells
- in-vitro, BC, SkBr3
cl‑Casp8↑, cl‑Casp3↑, VEGF↓, TumCG↓, TumCCA↑, cl‑PARP↑, p‑STAT3↓, p‑JAK2↓,
178- Api,    Autophagy inhibition enhances apigenin-induced apoptosis in human breast cancer cells
- in-vivo, BC, MDA-MB-231 - in-vitro, BC, T47D
Casp3↑, cl‑PARP↑, Bcl-2↓, Bcl-xL↓, BAX↑,
177- Api,    Inhibition of MDA-MB-231 breast cancer cell proliferation and tumor growth by apigenin through induction of G2/M arrest and histone H3 acetylation-mediated p21WAF1/CIP1 expression
- in-vitro, BC, MDA-MB-231
Cyc↓, CycB/CCNB1↓, CDK1↓, P21↑, PCNA↝, HDAC↓, TumCP↓, TumCCA↑, ac‑H3↑, TumW↓, TumVol↓,
176- Api,    Induction of caspase-dependent extrinsic apoptosis by apigenin through inhibition of signal transducer and activator of transcription 3 (STAT3) signalling in HER2-overexpressing BT-474 breast cancer cells
- in-vitro, BC, BT474
cl‑Casp8↑, cl‑Casp3↑, p‑JAK1↓, p‑JAK2↓, p‑STAT3↓, P53↑, VEGF↓, Hif1a↓, MMP9↓, TumCG↓, TumCCA↑, cl‑PARP↑,
175- Api,    Apigenin up-regulates transgelin and inhibits invasion and migration of colorectal cancer through decreased phosphorylation of AKT
- vitro+vivo, CRC, SW480 - vitro+vivo, CRC, DLD1 - vitro+vivo, CRC, LS174T
MMP↓, p‑Akt↓, TumCP↓, TumCI↓, NADH↓, HSP90↓, other↑, talin?,
174- Api,    Downregulation of NEDD9 by apigenin suppresses migration, invasion, and metastasis of colorectal cancer cells
- in-vitro, CRC, SW480 - in-vitro, CRC, DLD1
NEDD9↓, TumCMig↓, TumCI↓,
173- Api,    Apigenin-induced apoptosis is enhanced by inhibition of autophagy formation in HCT116 human colon cancer cells
- in-vitro, Colon, HCT116
CycB/CCNB1↓, cDC2↓, CDC25↓, P53↑, P21↑, cl‑PARP↑, proCasp8↓, proCasp9↓, proCasp3↓,
172- Api,    Apigenin suppresses colorectal cancer cell proliferation, migration and invasion via inhibition of the Wnt/β-catenin signaling pathway
- in-vitro, CRC, SW480 - in-vitro, CRC, HTC15
Wnt/(β-catenin)↓, TCF↓, LEF1↓, TumCP↓, TumCMig↓, TumCI↓,
171- Api,    Apigenin in cancer therapy: anti-cancer effects and mechanisms of action
- Review, Var, NA
PI3K/Akt↓, NF-kB↓, CK2↓, FOXO↓, MAPK↝, ERK↓, p‑JAK↓, Wnt/(β-catenin)↓, ROS↑, CDC25↓, p‑STAT↓, DNAdam↑,
5- Api,    Common Botanical Compounds Inhibit the Hedgehog Signaling Pathway in Prostate Cancer
- in-vitro, Pca, NA
HH↓, Gli1↓,
589- Api,  5-FU,    Interactions between dietary flavonoids apigenin or luteolin and chemotherapeutic drugs to potentiate anti-proliferative effect on human pancreatic cancer cells, in vitro
- in-vitro, PC, Bxpc-3
GSK‐3β↓, NF-kB↓,
4279- Api,    The Beneficial Role of Apigenin against Cognitive and Neurobehavioural Dysfunction: A Systematic Review of Preclinical Investigations
- Review, NA, NA
*antiOx↑, *Inflam↓, *BBB↑, *5HT↑, *CREB↑, *BDNF↑, *memory↑, *motorD↑, *Mood↑, *cognitive↑, *ROS↓,
1301- Api,    Bcl-2 inhibitor and apigenin worked synergistically in human malignant neuroblastoma cell lines and increased apoptosis with activation of extrinsic and intrinsic pathways
- in-vitro, neuroblastoma, NA
BAX↑, Bcl-2↓, Cyt‑c↑, cal2↑, Casp3↑,
1152- Api,    Does Oral Apigenin Have Real Potential for a Therapeutic Effect in the Context of Human Gastrointestinal and Other Cancers?
- Analysis, Nor, NA
*BioAv↓, Half-Life∅, *BioAv↓, Dose∅, eff↑, CYP1A2↓, CYP2C9↓, CYP3A4↓,
1151- Api,    Plant flavone apigenin inhibits HDAC and remodels chromatin to induce growth arrest and apoptosis in human prostate cancer cells: In vitro and in vivo study
- in-vitro, Pca, PC3 - in-vitro, Pca, 22Rv1 - in-vivo, NA, NA
TumCCA↑, Apoptosis↑, HDAC↓, P21↑, BAX↑, TumCG↓, Bcl-2↓, Bax:Bcl2↑, HDAC1↓, HDAC3↓,
1150- Api,    Apigenin inhibits the TNFα-induced expression of eNOS and MMP-9 via modulating Akt signalling through oestrogen receptor engagement
- in-vitro, Lung, EAhy926
eNOS↓, MMP9↓, Akt↓, p38↓, JNK↓,
1149- Api,    Apigenin inhibits colonic inflammation and tumorigenesis by suppressing STAT3-NF-κB signaling
- vitro+vivo, IBD, NA
COX2↓, MPO↓, NF-kB↓, STAT3↓, Inflam↓,

Showing Research Papers: 51 to 100 of 129
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 129

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HK1↓, 1,   MPO↓, 1,   NADH↓, 1,   NRF2↓, 4,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   CDC25↓, 2,   p‑CDC25↑, 1,   MMP↓, 1,   MMP↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALDOA↓, 1,   AMPK↑, 1,   cMyc↓, 1,   CYP3A4↓, 1,   ENO1↓, 1,   glucose↓, 1,   Glycolysis↓, 4,   HK2↓, 1,   lactateProd↓, 1,   NADPH↓, 1,   PGK1↓, 1,   PI3K/Akt↓, 2,   PI3k/Akt/mTOR↓, 1,   PKM2↓, 2,   PKM2:PKM1↓, 1,   PPP↓, 1,  

Cell Death ⓘ

Akt↓, 7,   p‑Akt↓, 2,   Apoptosis↑, 4,   BAX↑, 6,   BAX∅, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 5,   Bcl-2∅, 1,   cl‑Bcl-2↓, 1,   Bcl-xL↓, 3,   Bcl-xL∅, 1,   Casp3↑, 9,   cl‑Casp3↑, 3,   proCasp3↓, 1,   Casp7↑, 1,   Casp8↑, 1,   cl‑Casp8↑, 3,   proCasp8↓, 1,   Casp9↑, 3,   proCasp9↓, 1,   CK2↓, 2,   Cyt‑c↑, 1,   DR5↑, 1,   JNK↓, 1,   JNK↑, 1,   MAPK↓, 1,   MAPK↝, 1,   Mcl-1↓, 1,   p27↑, 1,   p38↓, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   other↑, 1,  

Protein Folding & ER Stress ⓘ

HSP90↓, 1,  

DNA Damage & Repair ⓘ

p‑ATM↑, 1,   p‑CHK1↑, 1,   DNAdam↑, 1,   P53↑, 4,   PARP↑, 3,   cl‑PARP↑, 7,   PCNA↓, 1,   PCNA↝, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   Cyc↓, 1,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   P21↑, 6,   TumCCA↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

cDC2↓, 2,   p‑cDC2↑, 1,   cMET↓, 1,   EMT↓, 2,   ERK↓, 3,   FOXO↓, 1,   Gli1↓, 2,   GSK‐3β↓, 2,   HDAC↓, 2,   HDAC1↓, 1,   HDAC3↓, 1,   HH↓, 2,   mTOR↓, 2,   p‑mTOR↓, 1,   Nanog↓, 1,   PI3K↓, 4,   p‑PI3K↓, 1,   SOX2↓, 1,   Src↓, 1,   STAT↓, 1,   p‑STAT↓, 1,   STAT3↓, 3,   p‑STAT3↓, 3,   TCF↓, 1,   TumCG↓, 4,   TumCG↑, 1,   Wnt↓, 1,   Wnt/(β-catenin)↓, 2,  

Migration ⓘ

cal2↑, 1,   CC(CDKs/cyclins)↓, 1,   CDK4/6↓, 1,   E-cadherin↑, 2,   FAK↓, 2,   p‑FAK↓, 1,   ITGA5↓, 1,   LEF1↓, 1,   MMP2↓, 2,   MMP9↓, 4,   N-cadherin↓, 1,   NEDD9↓, 1,   Slug↓, 1,   SMAD2↓, 1,   SMAD3↓, 1,   Snail↓, 2,   talin?, 1,   TGF-β↓, 2,   TumCI↓, 4,   TumCMig↓, 3,   TumCP↓, 5,   Twist↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   eNOS↓, 1,   Hif1a↓, 2,   VEGF↓, 7,  

Barriers & Transport ⓘ

GLUT1↓, 5,   GLUT3↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IKKα↓, 2,   Inflam↓, 1,   JAK↓, 1,   p‑JAK↓, 1,   p‑JAK1↓, 1,   p‑JAK2↓, 3,   NF-kB↓, 7,   p65↓, 1,   PSA↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 4,   CYP1A2↓, 1,   CYP2C9↓, 1,   Dose∅, 1,   eff↓, 1,   eff↑, 1,   eff↝, 1,   Half-Life∅, 1,   RadioS↑, 3,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

AR↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,   chemoP↑, 1,   chemoPv↑, 2,   OS↑, 1,   radioP↑, 2,   TumVol↓, 2,   TumW↓, 2,  
Total Targets: 166

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↓, 1,   GPx↑, 1,   GSH↑, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 4,   SOD↑, 1,   TAC↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   CREB↑, 1,   PKM2↓, 2,  

Cell Death ⓘ

Akt↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,  

Migration ⓘ

TGF-β↓, 1,   Vim↓, 1,   α-SMA↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 2,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 2,   NF-kB↓, 1,  

Synaptic & Neurotransmission ⓘ

5HT↑, 1,   BDNF↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,  

Functional Outcomes ⓘ

cognitive↑, 1,   hepatoP↑, 1,   memory↑, 1,   Mood↑, 1,   motorD↑, 1,  
Total Targets: 30

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#:32  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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