Boswellia (frankincense) Cancer Research Results

Bos, Boswellia (frankincense): Click to Expand ⟱
Features:
Boswellia is an herbal extract from the Boswellia serrata tree that may help reduce inflammation.
May help with rheumatoid arthritis, inflammatory bowel disease, asthma, and cancer.
-Naturally occurring pentacyclic triterpenoids include ursolic acid (UA), oleanolic acid (OA), betulinic acid (BetA), bosewellic acid (BA), Asiatic acid (AA), α-amyrin, celastrol, glycyrrhizin, 18-β-glycyrrhetinic acid, lupeol, escin, madecassic acid, momordin I, platycodon D, pristimerin, saikosaponins, soyasapogenol B, and avicin
Boswellia refers to a group of resinous extracts obtained from Boswellia trees (e.g., Boswellia serrata). Traditionally used in Ayurvedic and traditional Chinese medicine, Boswellia is reputed for its anti-inflammatory, analgesic, and immunomodulatory properties. Its bioactive components—such as boswellic acids.
Boswellic acids belong to the pentacyclic triterpenoid class (a broader chemical family that includes compounds such as ursolic acid and betulinic acid found in other plants) 
      3-acetyl-11-keto-β-boswellic acid (AKBA) 
      11-keto-β-boswellic acid (KBA) 
      α-boswellic acid (αBA) 
      β-boswellic acid (βBA) 
      3-acetyl-α-boswellic acid (AαBA) 
      3-acetyl-β-boswellic acid (AβBA)
-Anti-inflammatory Activity (blocking the enzyme 5-lipoxygenase) 5LOX↓,.
-AKBA inhibits methionine adenosyltransferase 2A (MAT2A)***** (help in Methionine reduced diet?)
Boswellia extracts are often administered in doses ranging from 300 mg to 1,200 mg per day

AKBA (Acetyl-11-keto-β-boswellic acid) is a bioactive compound derived from Boswellia serrata, a plant used traditionally for its anti-inflammatory properties. (upto 30% AKBA in Boswellia MEGA AKBA)
AKBA also available in Inflasanum @ 90% AKDA (MCSformulas)

Boswellia (frankincense) — Boswellia refers to oleo-gum-resin extracts from Boswellia species, most commonly Boswellia serrata, enriched in pentacyclic triterpenes known as boswellic acids. It is best classified as a botanical extract / natural-product mixture rather than a single drug entity, although much of the mechanistic cancer literature focuses on specific constituents such as 3-acetyl-11-keto-β-boswellic acid (AKBA) and 11-keto-β-boswellic acid (KBA). Standard abbreviations include Bos, BS, BA, KBA, and AKBA. The dominant translational theme is anti-inflammatory and anti-edema activity with broader preclinical anticancer signaling effects; however, extract composition, formulation, and exposure vary substantially across studies.

Primary mechanisms (ranked):

  1. 5-lipoxygenase-linked leukotriene suppression and broader inflammatory eicosanoid downregulation
  2. NF-κB pathway suppression with downstream reduction of COX-2, cytokines, survival factors, and pro-metastatic genes
  3. Mitochondrial apoptosis and cell-cycle arrest in cancer models, including caspase activation, PARP cleavage, and cyclin/CDK suppression
  4. PI3K/Akt, ERK/MAPK, STAT3, Wnt/β-catenin, and related growth-signaling attenuation
  5. Anti-invasive / anti-angiogenic signaling, including MMP, VEGF, CXCR4, and EMT-related effects
  6. MAT2A inhibition by AKBA with one-carbon / SAM metabolism disruption
  7. Context-dependent redox modulation, with pro-apoptotic oxidative stress in some cancer models but antioxidant / NRF2-supportive effects reported in normal or inflamed tissues

Bioavailability / PK relevance: Boswellic acids are lipophilic and have poor oral bioavailability with marked formulation dependence. Human studies show food, especially a high-fat meal, substantially increases exposure, and reported half-life data are generally compatible with multi-hour persistence but not with reliably high systemic levels from standard extracts. Enhanced-delivery systems may improve exposure, but classic oral preparations remain PK-limited.

In-vitro vs systemic exposure relevance: Many mechanistic cancer studies use boswellic-acid concentrations in the roughly 10–50 µM range, which commonly exceed plasma exposure expected from standard oral Boswellia extracts. That makes direct translation of apoptosis, invasion, and signaling data uncertain unless high-exposure formulations, tissue accumulation, or local-compartment effects are demonstrated. Extract-level anti-inflammatory and edema effects are clinically more plausible than broad direct cytotoxic anticancer effects at routine oral dosing.

Clinical evidence status: Cancer-directed evidence remains limited. There is meaningful human evidence for adjunctive anti-edema use during/after brain tumor irradiation and a small phase Ia presurgical breast-cancer window study showing reduced proliferation markers, but there is no established oncologic approval and no robust phase III anticancer efficacy program. Overall status is preclinical-heavy with small human adjunct / early translational signals.


-Note half-life reports vary 2.5-90hrs?.
BioAv (bio availability increases with high fat meal)
Pathways:
- induce or lower ROS production (not consistant increase for cancer cells)
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑,
- may Raise AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓ (context-dependent; stress/inflammatory MAPK modulation), Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓,
- inhibit Growth/Metastases : , MMPs↓, MMP2↓, MMP9↓, VEGF↓, NF-κB↓, CXCR4↓, ERK↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, TOP1↓,
- inhibits angiogenesis↓ : VEGF↓, Notch↓, PDGF↓,
- Others: PI3K↓, AKT↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK(JNK is activated under stress)
- Synergies: chemo-sensitization, chemoProtective, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Hepatoprotective,

- Selectivity: Cancer Cells vs Normal Cells

Mechanistic profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 5-LOX eicosanoid signaling ↓ leukotriene-linked inflammatory drive ↓ inflammatory tone P, R Anti-inflammatory leverage Most historically grounded Boswellia mechanism; strongest at extract / boswellic-acid anti-inflammatory level and likely central to edema-control relevance.
2 NF-κB inflammatory survival axis ↓ NF-κB, COX-2, TNF-α, IL-1β, IL-6, VEGF, MMPs ↓ inflammatory stress R, G Anti-survival transcriptional suppression Supported across multiple tumor models; likely more translationally plausible as inflammation-modulating adjunct action than as stand-alone tumor cytotoxicity.
3 Mitochondrial apoptosis ↑ caspases, ↑ Cyt-c, ↓ MMP, ↑ cl-PARP ↔ / protective (context-dependent) R, G Programmed cell death Common in AKBA-focused in-vitro studies; robust mechanistically, but often demonstrated at concentrations that may exceed routine oral exposure.
4 Cell-cycle control ↓ cyclin D1, ↓ cyclin E, ↓ CDK2/4/6, ↑ arrest ↔ G Antiproliferative restraint Frequently accompanies apoptosis in colon, lung, breast, and hematologic models.
5 PI3K Akt ERK STAT growth signaling ↓ PI3K, ↓ Akt, ↓ ERK, ↓ STAT3 (context-dependent) ↔ / cytoprotective inflammatory dampening R, G Growth-signaling attenuation Plausible multi-target effect, but much of the literature is model-specific and extract-dependent.
6 EMT invasion angiogenesis axis ↓ EMT, ↓ MMP2/9, ↓ CXCR4, ↓ VEGF, ↓ migration / invasion ↔ G Anti-metastatic phenotype Consistent preclinical theme; clinically unproven as a direct antimetastatic therapy.
7 One-carbon metabolism MAT2A ↓ MAT2A activity (AKBA-specific), ↓ SAM flux (context-dependent) ↔ / uncertain R, G Metabolic / epigenetic stress Mechanistically important for AKBA, but direct evidence is strongest outside oncology; relevant as a credible target, not yet a clinically established Boswellia cancer mechanism.
8 Mitochondrial ROS increase ↑ ROS (context-dependent) ↓ ROS (context-dependent) R Redox bifurcation Cancer-cell oxidative push and normal-tissue antioxidant support can both appear in the literature; this is not a uniformly one-directional axis.
9 NRF2 antioxidant response ↔ / variable ↑ NRF2, ↑ SOD, ↑ GSH, ↑ catalase (context-dependent) G Normal-tissue cytoprotection More relevant for anti-inflammatory / tissue-protective use than for direct tumor kill; should be treated as secondary, not core, in cancer framing.
10 Chemosensitization or radiotherapy adjunct ↑ treatment response (context-dependent) ↑ edema control / possible steroid sparing G Adjunctive translational utility Human evidence is strongest for cerebral-edema reduction around brain tumor radiotherapy rather than for proven direct tumor response enhancement.
11 Clinical Translation Constraint Low systemic exposure from standard oral extracts Generally mild GI tolerability profile G PK-limited translation Poor solubility, food dependence, extract heterogeneity, and formulation variability are major reasons preclinical potency does not cleanly translate into established anticancer efficacy.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (primary/physical–chemical effects; rapid enzymatic/kinase shifts)
  • R: 30 min–3 hr (acute redox + stress-response signaling)
  • G: >3 hr (gene-regulatory adaptation and phenotype-level outcomes)
Scientific Papers found: Click to Expand⟱
2777- Bos,    Boswellia serrata Preserves Intestinal Epithelial Barrier from Oxidative and Inflammatory Damage
- in-vitro, IBD, NA
*p‑NF-kB↓, *ROS↓, Inflam↓,
2024- Bos,    Antiproliferative and cell cycle arrest potentials of 3-O-acetyl-11-keto-β-boswellic acid against MCF-7 cells in vitro
- in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
MMP↓, Cyt‑c↑, ROS↑, Casp8↑, Casp9↑, AntiTum↑, selectivity↑, TumCCA↑,
2767- Bos,    The potential role of boswellic acids in cancer prevention and treatment
- Review, Var, NA
*Inflam↓, AntiCan↑, *MAPK↑, *Ca+2↝, p‑ERK↓, TumCI↓, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, p‑RB1↓, *NF-kB↓, *TNF-α↓, NF-kB↓, IKKα↓, MCP1↓, IL1α↓, MIP2↓, VEGF↓, Tf↓, COX2↓, MMP9↓, CXCR4↓, VEGF↓, eff↑, PPARα↓, lipid-P?, STAT3↓, TOP1↓, TOP2↑, 5HT↓, p‑PDGFR-BB↓, PDGF↓, AR↓, DR5↑, angioG↓, DR4↑, Casp3↑, Casp8↑, cl‑PARP↑, eff↑, chemoPv↑, Wnt↓, β-catenin/ZEB1↓, ascitic↓, Let-7↑, miR-200b↑, eff↑, MMP1↓, MMP2↓, eff↑, BioAv↓, BioAv↑, Half-Life↓, toxicity↓, Dose↑, BioAv↑, ChemoSen↑,
2768- Bos,    Boswellic acids as promising agents for the management of brain diseases
- Review, Var, NA - Review, AD, NA - Review, Park, NA
*neuroP↑, *ROS↓, *cognitive↓, TumCP↓, TumCMig↓, TumMeta↓, angioG↓, Apoptosis↑, *Inflam↓, IL1↓, IL2↓, IL4↓, IL6↓, TNF-α↓, P53↑, Akt↓, NF-kB↓, DNAdam↑, Casp↑, COX2↓, MMP9↓, CXCR4↓, VEGF↓, *SOD↑, *Catalase↑, *GPx↑, *NRF2↑,
2772- Bos,    Mechanistic role of boswellic acids in Alzheimer’s disease: Emphasis on anti-inflammatory properties
- Review, AD, NA
*neuroP↑, *Inflam↓, *AChE↓, *Choline↑, *NRF2↑, *NF-kB↑, *BBB↑, *BioAv↑, *Half-Life↓, *Dose↝, *PGE2↓, *ROS↓, *cognitive↑, *antiOx↑, 5LO↓, *TNF-α↓, *IL6↓, *HO-1↑,
2773- Bos,    Targeted inhibition of tumor proliferation, survival, and metastasis by pentacyclic triterpenoids: Potential role in prevention and therapy of cancer
- Review, Var, NA
Inflam↓, TumCCA↑, Casp3↑, Casp8↑, Casp9↑, STAT3↑, SHP1↓, NF-kB↓, cycD1/CCND1↓, COX2↓, Ki-67↓, CD31↓, IAP1↓, MMPs↓, Bcl-2↓, Bcl-xL↓,
2774- Bos,    Boswellia ovalifoliolata abrogates ROS mediated NF-κB activation, causes apoptosis and chemosensitization in Triple Negative Breast Cancer cells
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-453
ChemoSen↑, Casp3↑, ROS↓, NF-kB↓,
2775- Bos,    The journey of boswellic acids from synthesis to pharmacological activities
- Review, Var, NA - Review, AD, NA - Review, PSA, NA
ROS↑, ER Stress↑, TumCG↓, Apoptosis↑, Inflam↓, ChemoSen↑, Casp↑, ERK↓, cl‑PARP↑, AR↓, cycD1/CCND1↓, VEGFR2↓, CXCR4↓, radioP↑, NF-kB↓, VEGF↓, P21↑, Wnt↓, β-catenin/ZEB1↓, Cyt‑c↑, MMP2↓, MMP1↓, MMP9↓, PI3K↓, MAPK↓, JNK↑, *5LO↓, *NRF2↑, *HO-1↑, *MDA↓, *SOD↑, *hepatoP↑, *ALAT↓, *AST↓, *LDH↑, *CRP↓, *COX2↓, *GSH↑, *ROS↓, *Imm↑, *Dose↝, *eff↑, *neuroP↑, *cognitive↑, *IL6↓, *TNF-α↓,
2776- Bos,    Anti-inflammatory and anti-cancer activities of frankincense: Targets, treatments and toxicities
- Review, Var, NA
*5LO↓, *TNF-α↓, *MMP3↓, *COX1↓, *COX2↓, *PGE2↓, *Th2↑, *Catalase↑, *SOD↑, *NO↑, *PGE2↑, *IL1β↓, *IL6↓, *Th1 response↓, *Th2↑, *iNOS↓, *NO↓, *p‑JNK↓, *p38↓, GutMicro↑, p‑Akt↓, GSK‐3β↓, cycD1/CCND1↓, Akt↓, STAT3↓, CSCs↓, AR↓, P21↑, DR5↑, CHOP↑, Casp3↑, Casp8↑, cl‑PARP↑, DNAdam↑, p‑RB1↓, FOXM1↓, TOP2↓, CDC25↓, p‑CDK1↓, p‑ERK↓, MMP9↓, VEGF↓, angioG↓, ROS↑, Cyt‑c↑, AIF↑, Diablo↑, survivin↓, ICAD↓, ChemoSen↑, SOX9↓, ER Stress↑, GRP78/BiP↑, cal2↓, AMPK↓, mTOR↓, ROS↓,
1451- Bos,    Phytochemical Analysis and Anti-cancer Investigation of Boswellia serrata Bioactive Constituents In Vitro
- in-vitro, CRC, HepG2 - in-vitro, CRC, HCT116
eff↑,
2778- Bos,    Development, Analytical Characterization, and Bioactivity Evaluation of Boswellia serrata Extract-Layered Double Hydroxide Hybrid Composites
- in-vitro, Nor, NA
*ATP↓, *ROS↓,
2779- Bos,    Identification of a natural inhibitor of methionine adenosyltransferase 2A regulating one-carbon metabolism in keratinocytes
- in-vitro, Nor, HaCaT - in-vitro, PSA, NA
*MATs↓, *SAM-e↓,
3866- Bos,    Mechanistic role of boswellic acids in Alzheimer's disease: Emphasis on anti-inflammatory properties
- Review, AD, NA
*neuroP↑, *Inflam↓, *AChE↓, *Ach↑, *NRF2↑, *NF-kB↓, *Aβ↓,
3867- Bos,    Effect of food intake on the bioavailability of boswellic acids from a herbal preparation in healthy volunteers
- Human, Nor, NA
*eff↑, BioAv↝,
3868- Bos,    Enhanced absorption of boswellic acids by a lecithin delivery form (Phytosome(®)) of Boswellia extract
*Inflam↓, *BioAv↓, *BioAv↑, *eff↑,
4269- Bos,    Boswellia serrata gum resin aqueous extract upregulatesBDNF but not CREB expression in adult male rat hippocampus
- in-vivo, NA, NA
*BDNF↑, *CREB∅,
4270- Bos,    Boswellic acids ameliorate neurodegeneration induced by AlCl3: the implication of Wnt/β-catenin pathway
- in-vivo, AD, NA
*memory↑, *AChE↓, *Aβ↓, *TNF-α↓, *IL1β↓, *lipid-P↓, *TAC↑, *BDNF↑, *β-catenin/ZEB1↑, *Dose↑,
5675- Bos,    Modulation of Pgp function by boswellic acids
- in-vitro, Nor, NA
*P-gp↑,
1423- Bos,    Acetyl-11-keto-β-Boswellic Acid Suppresses Invasion of Pancreatic Cancer Cells Through The Downregulation of CXCR4 Chemokine Receptor Expression
- in-vitro, Melanoma, U266 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, SkBr3 - in-vitro, PC, PANC1
CXCR4↓, TumCI↓, HER2/EBBR2↓, NF-kB↓,
1185- Bos,    The journey of boswellic acids from synthesis to pharmacological activities
- Review, NA, NA
BAX↑, NF-kB↓, cl‑PARP↑, Casp3↑, Casp8↑,
1248- Bos,    The anti-proliferative effects of a frankincense extract in a window of opportunity phase ia clinical trial for patients with breast cancer
- Trial, BC, NA
TumCP↓,
1416- Bos,    Anti-cancer properties of boswellic acids: mechanism of action as anti-cancerous agent
- Review, NA, NA
5LO↓, TumCCA↑, LC3B↓, PI3K↓, Akt↓, Glycolysis↓, AMPK↑, mTOR↓, Let-7↑, COX2↓, VEGF↓, CXCR4↓, MMP2↓, MMP9↓, HIF-1↓, angioG↓, TumCP↓, TumCMig↓, NF-kB↓,
1417- Bos,    Potential complementary and/or synergistic effects of curcumin and boswellic acids for management of osteoarthritis
- Review, Arthritis, NA
5LO↓, COX2↓, PGE2↓,
1419- Bos,    Enhanced Bioavailability of Boswellic Acid by Piper longum: A Computational and Pharmacokinetic Study
- in-vivo, Nor, NA
*BioAv↑,
1420- Bos,    Acetyl-11-keto-β-boswellic acid inhibits proliferation and induces apoptosis of gastric cancer cells through the phosphatase and tensin homolog /Akt/ cyclooxygenase-2 signaling pathway
- vitro+vivo, GC, BGC-823
TumCP↓, TumCG↓, PTEN↑, BAX↑, Bcl-2↓, p‑Akt↓, COX2↓,
1421- Bos,    Coupling of boswellic acid-induced Ca2+ mobilisation and MAPK activation to lipid metabolism and peroxide formation in human leucocytes
- in-vitro, AML, HL-60 - in-vitro, Nor, NA
ROS↑, NADPH↝, 5LO↓, Ca+2↑, p38↑, p42↑,
1422- Bos,    Boswellic acid exerts antitumor effects in colorectal cancer cells by modulating expression of the let-7 and miR-200 microRNA family
- in-vitro, CRC, NA - in-vivo, NA, NA
5LO↓, TumCG↓, Let-7↑, miR-200b↑, NF-kB↓, cMyc↓, cycD1/CCND1↓, MMP9↓, CXCR4↓, VEGF↓, Bcl-xL↓, survivin↓, IAP1↓, XIAP↓, TumCG↓, CDK6↓, Vim↓, E-cadherin↑,
1169- Bos,    Boswellic Acid Inhibits Growth and Metastasis of Human Colorectal Cancer in Orthotopic Mouse Model By Downregulating Inflammatory, Proliferative, Invasive, and Angiogenic Biomarkers
- in-vivo, CRC, NA
TumCG↓, TumVol↓, Weight∅, ascitic↓, TumMeta↓, Ki-67↓, CD31↓, NF-kB↓, COX2↓, Bcl-2↓, Bcl-xL↓, IAP1↓, survivin↓, cycD1/CCND1↓, ICAM-1↓, MMP9↓, CXCR4↓, VEGF↓,
1424- Bos,    Boswellia sacra essential oil induces tumor cell-specific apoptosis and suppresses tumor aggressiveness in cultured human breast cancer cells
- in-vitro, BC, T47D - in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
tumCV↓, Apoptosis↑, cl‑Casp8↑, cl‑Casp9↑, cl‑PARP↑,
1425- Bos,    Protective Effect of Boswellic Acids against Doxorubicin-Induced Hepatotoxicity: Impact on Nrf2/HO-1 Defense Pathway
- in-vivo, Nor, NA
*ChemoSen↑, *NRF2↑, *HO-1↑, *ROS↓, *lipid-P↓, *DNAdam↓,
1426- Bos,  CUR,  Chemo,    Novel evidence for curcumin and boswellic acid induced chemoprevention through regulation of miR-34a and miR-27a in colorectal cancer
- in-vivo, CRC, NA - in-vitro, CRC, HCT116 - in-vitro, CRC, RKO - in-vitro, CRC, SW480 - in-vitro, RCC, SW-620 - in-vitro, RCC, HT-29 - in-vitro, CRC, Caco-2
miR-34a↑, miR-27a-3p↓, TumCG↓, BAX↑, Bcl-2↓, PARP1↓, TumCCA↑, Apoptosis↑, cMyc↓, CDK4↓, CDK6↓, cycD1/CCND1↓, ChemoSen↑, miR-34a↑, miR-27a-3p↓,
1427- Bos,    Acetyl-keto-β-boswellic acid inhibits cellular proliferation through a p21-dependent pathway in colon cancer cells
- in-vitro, CRC, HT-29 - in-vitro, CRC, HCT116 - in-vitro, CRC, LS174T
TumCG↓, TumCCA↑, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, p‑RB1↓, P21↑,
1447- Bos,    Boswellia carterii n-hexane extract suppresses breast cancer growth via induction of ferroptosis by downregulated GPX4 and upregulated transferrin
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vivo, BC, 4T1 - in-vitro, Nor, MCF10
tumCV↓, AntiCan↑, *toxicity↓, Ferroptosis↑, i-Iron↑, GPx4↓, ROS↑, lipid-P↑, Tf↑, TumCG↓,
1448- Bos,    A triterpenediol from Boswellia serrata induces apoptosis through both the intrinsic and extrinsic apoptotic pathways in human leukemia HL-60 cells
- in-vitro, AML, HL-60
TumCP↓, Apoptosis↑, ROS↑, NO↑, cl‑Bcl-2↑, BAX↑, MMP↓, Cyt‑c↑, AIF↑, Diablo↑, survivin↓, ICAD↓, Casp↑, cl‑PARP↑, DR4↑, TNFR 1↑,
1449- Bos,  Chemo,    Anti-proliferative, Pro-apoptotic, and Chemosensitizing Potential of 3-Acetyl-11-keto-β-boswellic Acid (AKBA) Against Prostate Cancer Cells
- in-vitro, Pca, PC3
TumCP↓, ChemoSen↑, MMP↝, ROS↝, Apoptosis↑,
1450- Bos,  Cisplatin,    3-Acetyl-11-keto-β-boswellic acid (AKBA) induced antiproliferative effect by suppressing Notch signaling pathway and synergistic interaction with cisplatin against prostate cancer cells
- in-vitro, Pca, DU145
ROS↑, MMP↓, Casp↑, Apoptosis↑, Bax:Bcl2↑, TumCCA?, cycD1/CCND1↓, CDK4↓, P21↑, p27↑, NOTCH↓, ChemoSen↑,

Showing Research Papers: 1 to 36 of 36

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 36

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GPx4↓, 1,   i-Iron↑, 1,   lipid-P?, 1,   lipid-P↑, 1,   ROS↓, 2,   ROS↑, 7,   ROS↝, 1,  

Metal & Cofactor Biology ⓘ

Tf↓, 1,   Tf↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 2,   CDC25↓, 1,   MMP↓, 3,   MMP↝, 1,   p42↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↓, 1,   AMPK↑, 1,   cMyc↓, 2,   Glycolysis↓, 1,   NADPH↝, 1,   PPARα↓, 1,  

Cell Death ⓘ

Akt↓, 3,   p‑Akt↓, 2,   Apoptosis↑, 7,   BAX↑, 4,   Bax:Bcl2↑, 1,   Bcl-2↓, 4,   cl‑Bcl-2↑, 1,   Bcl-xL↓, 3,   Casp↑, 4,   Casp3↑, 5,   Casp8↑, 5,   cl‑Casp8↑, 1,   Casp9↑, 2,   cl‑Casp9↑, 1,   Cyt‑c↑, 4,   Diablo↑, 2,   DR4↑, 2,   DR5↑, 2,   Ferroptosis↑, 1,   IAP1↓, 3,   ICAD↓, 2,   JNK↑, 1,   MAPK↓, 1,   p27↑, 1,   p38↑, 1,   survivin↓, 4,   TNFR 1↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   SOX9↓, 1,  

Transcription & Epigenetics ⓘ

miR-27a-3p↓, 2,   tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 2,   GRP78/BiP↑, 1,  

Autophagy & Lysosomes ⓘ

LC3B↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 1,   cl‑PARP↑, 6,   PARP1↓, 1,  

Cell Cycle & Senescence ⓘ

p‑CDK1↓, 1,   CDK2↓, 2,   CDK4↓, 4,   cycD1/CCND1↓, 9,   cycE/CCNE↓, 2,   P21↑, 4,   p‑RB1↓, 3,   TumCCA?, 1,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   ERK↓, 1,   p‑ERK↓, 2,   FOXM1↓, 1,   GSK‐3β↓, 1,   Let-7↑, 3,   miR-34a↑, 2,   mTOR↓, 2,   NOTCH↓, 1,   PI3K↓, 2,   PTEN↑, 1,   SHP1↓, 1,   STAT3↓, 2,   STAT3↑, 1,   TOP1↓, 1,   TOP2↓, 1,   TOP2↑, 1,   TumCG↓, 8,   Wnt↓, 2,  

Migration ⓘ

5LO↓, 5,   Ca+2↑, 1,   cal2↓, 1,   CD31↓, 2,   E-cadherin↑, 1,   Ki-67↓, 2,   miR-200b↑, 2,   MMP1↓, 2,   MMP2↓, 3,   MMP9↓, 7,   MMPs↓, 1,   PDGF↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 6,   TumMeta↓, 2,   Vim↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 4,   HIF-1↓, 1,   NO↑, 1,   p‑PDGFR-BB↓, 1,   VEGF↓, 8,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 7,   CXCR4↓, 7,   ICAM-1↓, 1,   IKKα↓, 1,   IL1↓, 1,   IL1α↓, 1,   IL2↓, 1,   IL4↓, 1,   IL6↓, 1,   Inflam↓, 3,   MCP1↓, 1,   MIP2↓, 1,   NF-kB↓, 10,   PGE2↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

5HT↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 3,   CDK6↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   BioAv↝, 1,   ChemoSen↑, 7,   Dose↑, 1,   eff↑, 5,   Half-Life↓, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 3,   ascitic↓, 2,   FOXM1↓, 1,   GutMicro↑, 1,   HER2/EBBR2↓, 1,   IL6↓, 1,   Ki-67↓, 2,  

Functional Outcomes ⓘ

AntiCan↑, 2,   AntiTum↑, 1,   chemoPv↑, 1,   radioP↑, 1,   toxicity↓, 1,   TumVol↓, 1,   Weight∅, 1,  
Total Targets: 153

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 2,   GPx↑, 1,   GSH↑, 1,   HO-1↑, 3,   lipid-P↓, 2,   MDA↓, 1,   NRF2↑, 5,   ROS↓, 6,   SAM-e↓, 1,   SOD↑, 3,   TAC↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   CREB∅, 1,   LDH↑, 1,   MATs↓, 1,  

Cell Death ⓘ

iNOS↓, 1,   p‑JNK↓, 1,   MAPK↑, 1,   p38↓, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

Choline↑, 1,  

Migration ⓘ

5LO↓, 2,   Ca+2↝, 1,   MMP3↓, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,   NO↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,   P-gp↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 2,   CRP↓, 1,   IL1β↓, 2,   IL6↓, 3,   Imm↑, 1,   Inflam↓, 5,   NF-kB↓, 2,   NF-kB↑, 1,   p‑NF-kB↓, 1,   PGE2↓, 2,   PGE2↑, 1,   Th1 response↓, 1,   Th2↑, 2,   TNF-α↓, 5,  

Synaptic & Neurotransmission ⓘ

AChE↓, 3,   BDNF↑, 2,  

Protein Aggregation ⓘ

Aβ↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 3,   ChemoSen↑, 1,   Dose↑, 1,   Dose↝, 2,   eff↑, 3,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   CRP↓, 1,   IL6↓, 3,   LDH↑, 1,  

Functional Outcomes ⓘ

cognitive↓, 1,   cognitive↑, 2,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 4,   toxicity↓, 1,  
Total Targets: 68

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

 

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