Database Query Results : Boswellia (frankincense), , TumCI

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)

-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

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 NF-κB axis (IKK → NF-κB; NF-κB-regulated genes) NF-κB ↓; downstream targets ↓ (COX-2, Cyclin D1, Bcl-2/Bcl-xL/IAPs, MMP-9, VEGF, CXCR4 etc.) Anti-inflammatory tone (context) R, G Anti-survival / anti-inflammatory transcription AKBA-class compounds suppress NF-κB signaling and reduce multiple NF-κB-regulated tumor programs in vitro and in vivo models.
2 5-LOX (leukotriene pathway) / eicosanoid signaling 5-LOX activity ↓ (context); pro-inflammatory eicosanoid signaling ↓ Anti-inflammatory support P, R Direct enzymatic / lipid-mediator suppression Boswellic acids are widely discussed as 5-LOX–linked anti-inflammatory agents; cancer relevance often tracks inflammation-driven growth signals.
3 Apoptosis (extrinsic + intrinsic; caspases; PARP) Apoptosis ↑; Caspase-8/3 ↑; cl-PARP ↑ (context) ↔ G Cell death execution Reported apoptosis induction includes death-receptor (e.g., DR5-associated) and caspase/PARP cleavage patterns in multiple tumor models.
4 Cell-cycle control (Cyclin D1 / checkpoints) Cyclin D1 ↓; proliferation ↓; arrest ↑ (context) ↔ G Cytostasis Often presented as downstream of NF-κB/survival signaling suppression and stress adaptation.
5 Invasion / metastasis programs (MMP-9, ICAM-1, CXCR4) Invasion markers ↓; MMP-9 ↓; ICAM-1 ↓; CXCR4 ↓ (context) ↔ G Anti-invasive phenotype In vivo tumor models report reductions in invasive and chemokine/migration biomarkers alongside NF-κB suppression.
6 Angiogenesis signaling (VEGF; VEGFR2-mediated angiogenesis) VEGF ↓; angiogenic outputs ↓ (context) ↔ G Anti-angiogenic support AKBA has been reported to suppress angiogenesis programs including VEGF signaling, with VEGFR2-mediated angiogenesis discussed in prostate cancer contexts.
7 PI3K → AKT (± mTOR) survival axis PI3K/AKT ↓ (reported; model-dependent) ↔ R, G Growth/survival suppression Commonly listed as a downstream survival pathway impacted by boswellic acids; keep as “reported” (not universal across all models).
8 MAPK re-wiring (ERK / JNK / p38) Stress-MAPK modulation (context-dependent) ↔ P, R, G Signal reprogramming MAPK direction varies by tumor type/dose and whether the experimental system is inflammatory vs cytotoxic.
9 Chemo-/radio-sensitization (combination relevance) Sensitization ↑ (context) — G Combination leverage Combination studies report enhanced tumor control when AKBA-class compounds are paired with other therapies (context and regimen dependent).
10 Bioavailability constraint (oral exposure; formulation dependence) Systemic exposure often limited without enhanced delivery — — Translation constraint Poor pharmacokinetics are a common limitation; multiple strategies (e.g., micellar delivery, bioenhancers) are studied to improve absorption.

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)
TumCI, Tumor Cell invasion: Click to Expand ⟱
Source:
Type:
Tumor cell invasion is a critical process in cancer progression and metastasis, where cancer cells spread from the primary tumor to surrounding tissues and distant organs. This process involves several key steps and mechanisms:

1.Epithelial-Mesenchymal Transition (EMT): Many tumors originate from epithelial cells, which are typically organized in layers. During EMT, these cells lose their epithelial characteristics (such as cell-cell adhesion) and gain mesenchymal traits (such as increased motility). This transition is crucial for invasion.

2.Degradation of Extracellular Matrix (ECM): Tumor cells secrete enzymes, such as matrix metalloproteinases (MMPs), that degrade the ECM, allowing cancer cells to invade surrounding tissues. This degradation facilitates the movement of cancer cells through the tissue.

3.Cell Migration: Once the ECM is degraded, cancer cells can migrate. They often use various mechanisms, including amoeboid movement and mesenchymal migration, to move through the tissue. This migration is influenced by various signaling pathways and the tumor microenvironment.

4.Angiogenesis: As tumors grow, they require a blood supply to provide nutrients and oxygen. Tumor cells can stimulate the formation of new blood vessels (angiogenesis) through the release of growth factors like vascular endothelial growth factor (VEGF). This not only supports tumor growth but also provides a route for cancer cells to enter the bloodstream.

5.Invasion into Blood Vessels (Intravasation): Cancer cells can invade nearby blood vessels, allowing them to enter the circulatory system. This step is crucial for metastasis, as it enables cancer cells to travel to distant sites in the body.

6.Survival in Circulation: Once in the bloodstream, cancer cells must survive the immune response and the shear stress of blood flow. They can form clusters with platelets or other cells to evade detection.

7.Extravasation and Colonization: After traveling through the bloodstream, cancer cells can exit the circulation (extravasation) and invade new tissues. They may then establish secondary tumors (metastases) in distant organs.

8.Tumor Microenvironment: The surrounding microenvironment plays a significant role in tumor invasion. Factors such as immune cells, fibroblasts, and signaling molecules can either promote or inhibit invasion and metastasis.
Scientific Papers found: Click to Expand⟱
2767- Bos,    The potential role of boswellic acids in cancer prevention and treatment
- Review, Var, NA
*Inflam↓, profound application as a traditional remedy for various ailments, especially inflammatory diseases including asthma, arthritis, cerebral edema, chronic pain syndrome, chronic bowel diseases, cancer
AntiCan↑,
*MAPK↑, 11-keto-BAs can stimulate Mitogen-activated protein kinases (MAPK) and mobilize the intracellular Ca(2+) that are important for the activation of human polymorphonuclear leucocytes (PMNL)
*Ca+2↝,
p‑ERK↓, AKBA prohibited the phosphorylation of extracellular signal-regulated kinase-1 and -2 (Erk-1/2) and impaired the motility of meningioma cells stimulated with platelet-derived growth factor BB
TumCI↓,
cycD1/CCND1↓, In the case of colon cancer, BA treatment on HCT-116 cells led to a decrease in cyclin D, cyclin E, and Cyclin-dependent kinases such as CDK2 and CDK4, along with significant reduction in phosphorylated Rb (pRb)
cycE/CCNE↓,
CDK2↓,
CDK4↓,
p‑RB1↓,
*NF-kB↓, convey inhibition of NF-kappaB and subsequent down-regulation of TNF-alpha expression in activated human monocytes
*TNF-α↓,
NF-kB↓, PC-3 prostate cancer cells in vitro and in vivo by inhibiting constitutively activated NF-kappaB signaling by intercepting the activity of IkappaB kinase (IKK
IKKα↓,
MCP1↓, LPS-challenged ApoE-/- mice via inhibition of NF-κB and down regulation of MCP-1, MCP-3, IL-1alpha, MIP-2, VEGF, and TF
IL1α↓,
MIP2↓,
VEGF↓,
Tf↓,
COX2↓, pancreatic cancer cell lines, AKBA inhibited the constitutive expression of NF-kB and caused suppression of NF-kB regulated genes such as COX-2, MMP-9, CXCR4, and VEGF
MMP9↓,
CXCR4↓,
VEGF↓,
eff↑, AKBA and aspirin revealed that AKBA has higher potential via modulation of the Wnt/β-catenin pathway, and NF-kB/COX-2 pathway in adenomatous polyps
PPARα↓, AKBA is also responsible for down-regulation of PPAR-alpha and C/EBP-alpha in a dose and temporal dependent manner in mature adipocytes, ultimately leading to pparlipolysis
lipid-P?,
STAT3↓, activation of STAT-3 in human MM cells could be inhibited by AKBA
TOP1↓, (PKBA; a semisynthetic analogue of 11-keto-β-boswellic acid), had been reported to influence the activity of topoisomerase I & II,
TOP2↑,
5HT↓, (5-LO), responsible for catalyzing the synthesis of leukotrienes from arachidonic acid and human leucocyte elastase (HLE), and serine proteases involved in several inflammatory processes, is considered to be a potent molecular target of BA derivative
p‑PDGFR-BB↓, BA up-regulates SHP-1 with subsequent dephosphorylation of PDGFR-β and downregulation of PDGF-dependent signaling after PDGF stimulation, thereby exerting an anti-proliferative effect on HSCs hepatic stellate cells
PDGF↓,
AR↓, AKBA targets different receptors that include androgen receptor (AR), death receptor 5 (DR5), and vascular endothelial growth factor receptor 2 (VEGFR2), and leads to the inhibition of proliferation of prostate cancer cells
DR5↑, induced expression of DR4 and DR5.
angioG↓, via apoptosis induction and suppression of angiogenesis
DR4↑,
Casp3↑, AKBA resulted in activation of caspase-3 and caspase-8, and initiation of poly (ADP) ribose polymerase (PARP) cleavage.
Casp8↑,
cl‑PARP↑,
eff↑, AKBA was preincubated with LY294002 or wortmannin (inhibitors of PI3K), it caused a significant enhancement of apoptosis in HT-29 cells
chemoPv↑, chemopreventive response of AKBA was estimated against intestinal adenomatous polyposis through the inhibition of the Wnt/β-catenin and NF-κB/cyclooxygenase-2 signaling pathway
Wnt↓,
β-catenin/ZEB1↓,
ascitic↓, AKBA by the suppression of ascites,
Let-7↑, AKBA could up-regulate the expression of let-7 and miR-200
miR-200b↑,
eff↑, anti-tumorigenic effects of curcumin and AKBA on the regulation of specific cancer-related miRNAs in colorectal cancer cells, and confirmed their protective action
MMP1↓, . It can inhibit the expression of MMP-1, MMP-2, and MMP-9 mRNAs along with secretions of TNF-α and IL-1β in THP-1 cells.
MMP2↓,
eff↑, combined administration of metformin, an anti-diabetic drug, and boswellic acid nanoparticles exhibited significant synergism through the inhibition of MiaPaCa-2 pancreatic cancer cell proliferation
BioAv↓, BA as a therapeutic drug is its poor bioavailability
BioAv↑, administration of BSE-018 concomitantly with a high-fat meal led to several-fold increased areas under the plasma concentration-time curves as well as peak concentrations of beta-boswellic acid (betaBA)
Half-Life↓, drug needs to be given orally at the interval of six hours due to its calculated half- life, which was around 6 hrs.
toxicity↓, BSE has been found to be a safe drug without any adverse side reactions, and is well tolerated on oral administration.
Dose↑, Boswellia serrata extract to the maximum amount of 4200 mg/day is not toxic and it is safe to use though it shows poor bioavailability
BioAv↑, Approaches like lecithin delivery form (Phytosome®), nanoparticle delivery systems like liposomes, emulsions, solid lipid nanoparticles, nanostructured lipid carriers, micelles and poly (lactic-co-glycolic acid) nanoparticles
ChemoSen↑, Like any other natural products BA can also be effective as chemosensitizer

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↓, AKBA is a novel inhibitor of CXCR4 expression
TumCI↓,
HER2/EBBR2↓, AKBA downregulated the expression of HER2 in all pancreatic cancer cells, but not in all breast cancer cell lines.
NF-kB↓,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

lipid-P?, 1,  

Metal & Cofactor Biology ⓘ

Tf↓, 1,  

Core Metabolism/Glycolysis ⓘ

PPARα↓, 1,  

Cell Death ⓘ

Casp3↑, 1,   Casp8↑, 1,   DR4↑, 1,   DR5↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   p‑RB1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↓, 1,   Let-7↑, 1,   STAT3↓, 1,   TOP1↓, 1,   TOP2↑, 1,   Wnt↓, 1,  

Migration ⓘ

miR-200b↑, 1,   MMP1↓, 1,   MMP2↓, 1,   MMP9↓, 1,   PDGF↓, 1,   TumCI↓, 2,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   p‑PDGFR-BB↓, 1,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CXCR4↓, 2,   IKKα↓, 1,   IL1α↓, 1,   MCP1↓, 1,   MIP2↓, 1,   NF-kB↓, 2,  

Synaptic & Neurotransmission ⓘ

5HT↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   ChemoSen↑, 1,   Dose↑, 1,   eff↑, 4,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   ascitic↓, 1,   HER2/EBBR2↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoPv↑, 1,   toxicity↓, 1,  
Total Targets: 51

Pathway results for Effect on Normal Cells:


Cell Death ⓘ

MAPK↑, 1,  

Migration ⓘ

Ca+2↝, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  
Total Targets: 5

Scientific Paper Hit Count for: TumCI, Tumor Cell invasion
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#:324  State#:%  Dir#:%
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