TXA2 Cancer Research Results

TXA2, thromboxane A2: Click to Expand ⟱
Source:
Type:
TXA2 is a bioactive lipid mediator primarily produced via the action of cyclooxygenases (COX-1/COX-2) and thromboxane synthase (TXA2S, gene TBXAS1), and it plays a role in regulating platelet aggregation, vasoconstriction, and cellular signaling that may contribute to tumor progression.

TXA2 is a bioactive lipid mediator that, beyond its role in platelet aggregation and vascular regulation, is involved in several tumor-promoting processes such as inflammation, angiogenesis, and metastasis. In various cancers—such as breast, prostate, colorectal, lung, ovarian, and head and neck cancers—elevated TXA2 levels or enhanced signaling have been associated with more aggressive disease and poorer clinical outcomes.
Scientific Papers found: Click to Expand⟱
5415- ASA,    The Anti-Metastatic Role of Aspirin in Cancer: A Systematic Review
- Review, Var, NA
TumMeta↓, The included studies demonstrated that aspirin suppresses metastatic dissemination across multiple cancer types through coordinated platelet-dependent and tumor-intrinsic mechanisms.
COX1↓, Aspirin consistently inhibited platelet aggregation and COX-1-dependent TXA2 production, disrupting platelet–tumor cell interactions, intravascular metastatic niche formation, and platelet-mediated immune suppression.
TXA2↓,
AntiAg↑, Beyond platelet effects, aspirin suppressed EMT, migration, and invasion through modulation of EMT transcriptional regulators and inflammatory signaling pathways.
EMT↓,
TumCMig↓,
TumCI↓,
AMPK↑, Additional mechanisms included activation of AMPK, inhibition of c-MYC signaling, regulation of redox-responsive pathways and impairment of anoikis resistance.
cMyc↓,
PGE2↓, Importantly, oral aspirin (20 mg/kg/day; human-equivalent ≈ 150 mg/day), administered before tumor cell injection, prevented platelet-induced metastatic enhancement and suppressed TXA2 and PGE2 production.
Dose↑, medium and high doses of aspirin reduced pulmonary metastatic burden by more than 50%, whereas low-dose aspirin was ineffective.
RadioS↑, Wang et al. [45] demonstrated that low-dose aspirin suppresses radiotherapy-induced release of immunosuppressive exosomes in breast cancer, restoring NK-cell proliferation and enhancing antitumor immunity in vivo.
PD-L1↓, Similarly, Xiao et al. [46] showed that aspirin epigenetically downregulates PD-L1 expression by inhibiting KAT5-dependent histone acetylation, thereby restoring T-cell activation
E-cadherin↑, Aspirin restored E-cadherin expression and suppressed EMT regulators, including Slug, vimentin, Twist, MMP-2, and MMP-9.
EMT↓,
Slug↓,
Vim↓,
Twist↓,
MMP2↓,
MMP9↓,
other↑, definitive conclusions regarding clinical efficacy across cancer types cannot yet be drawn. Nevertheless, the consistency of mechanistic signals across experimental systems supports further investigation of aspirin as a low-cost adjunct in oncology

5413- ASA,    Drug Resistance and Pseudoresistance: An Unintended Consequence of Enteric Coating Aspirin
- Trial, Nor, NA
*cardioP↑, Low dose aspirin reduces the secondary incidence of myocardial infarction and stroke.
*other↝, Pseudoresistance, reflecting delayed and reduced drug absorption, complicates enteric coated but not immediate release aspirin administration.
*COX1↓, irreversible acetylation of Ser530 in the enzyme prostaglandin G/H synthase-1 (commonly termed cyclooxygenase [COX]-1) and the consequent suppression of thromboxane (Tx) A2 (TxA2) formation.
*TXA2↓,

5408- ASA,    An aspirin a day keeps cancer at bay
- Review, Var, NA
TumMeta↓, It has long been hypothesised that aspirin prevents cancer deaths by preventing metastasis.
TXA2↓, A recent study demonstrates this to be mediated through inhibition of Thromboxane A2 (TXA2) leading to reversal of suppression of T cell immunity.
*AntiAg↑, It was therefore hypothesised [3, 5] that aspirin prevents cancer metastasis, very likely through its anti-platelet action but the exact mechanism of action remained unclear.
COX1↓, anti-platelet activity through inhibition of cyclooxygenase-1 (COX-1) remains the main plausible mechanism.

5402- ASA,    Aspirin prevents metastasis by limiting platelet TXA2 suppression of T cell immunity
- Review, Var, NA
COX1↓, Here we show that inhibitors of cyclooxygenase 1 (COX-1), including aspirin, enhance immunity to cancer metastasis by releasing T cells from suppression by platelet-derived thromboxane A2 (TXA2).
TumMeta↓, Moreover, low-dose (75–300 mg) aspirin treatment is associated with a reduction in the rate of cancer death in individuals without metastasis at the time of cancer diagnosis
*Half-Life↓, Aspirin has a short half-life (around 20 min), such that only frequent high doses of aspirin can achieve sustained pharmacological inhibition of COX-1 and COX-2 in nucleated cells
*COX2↓, Aspirin can inhibit both COX-1 and COX-2
*TXA2↓, suppression by platelet-derived thromboxane A2 (TXA2).

4342- CA,    Antiplatelet effects of caffeic acid due to Ca(2＋) mobilizationinhibition via cAMP-dependent inositol-1, 4, 5-trisphosphate receptor phosphorylation
- in-vitro, NA, NA
*AntiAg↑, CAFA dose-dependently inhibited collagen-induced platelet aggregation and suppressed the production of TXA2, an aggregation-inducing autacoid associated with the strong inhibition of COX-1 in platelet microsomes exhibiting cytochrome C reductase acti
*TXA2↓, prevention of platelet aggregation-mediated thrombotic diseases.
*COX1↓,

6013- CGA,    Advances in Pharmacological Properties, Molecular Mechanisms, and Bioavailability Strategies of Chlorogenic Acid in Cardiovascular Diseases Therapy
- Review, CardioV, NA
*BioAv↝, As a dietary component, CGA exhibits moderate oral bioavailability [9], and its molecular structure remains largely intact during oral digestion
*BioAv↝, The composition of gut microbiota plays a critical role in CGA’s metabolism and absorption, producing 11 key metabolites, with the most primary products dihydrocaffeic acid, dihydroferulic acid, and 3-(3-hydroxyphenyl) propionic acid [
*BP↓, eported that CGA lowers blood pressure by relaxing vascular smooth muscle and improving endothelial function
*ROS↓, inhibiting the sources of reactive oxygen species (ROS), such as NADPH oxidase,
*NADPH↓,
*AntiAg↑, he downregulation of thromboxane A2 plays a crucial role in CGA-mediated inhibition of platelet aggregation
*TXA2↓,
*antiOx↑, cCGA exhibited the strongest antioxidant effect, which may be related to improved mitochondrial function [
*cardioP↑, CGA exerts significant cardioprotective effects by modulating multiple signaling pathways.
*Inflam↓, reduce infarct size in MI induced by left anterior descending artery (LAD) ligation in rats. It achieves this by suppressing inflammation and enhancing the activity of antioxidant enzymes, such as SOD and CAT, thereby improving cardiac function
*SOD↑,
*Catalase↑,
*Ferroptosis↓, CGA’s ability to alleviate ferroptosis
*NF-kB↓, inhibiting the NF-κB and JNK signaling pathways, highlighting its cardioprotective potential in a TAC mouse model
*JNK↓,
*NRF2↑, CGA reduces oxidative stress and ROS-induced damage by upregulating the Nrf2/HO-1 pathway, thereby mitigating doxorubicin-induced cardiotoxicity and improving cardiac tissue integrity
*HO-1↑,
*toxicity↓, which are widely used in traditional Chinese medicine [60,61], it is generally considered safe.
*BioAv↓, CGA struggles to cross lipophilic membranes, resulting in poor absorption and bioavailability [69]. Simply increasing the oral dose is not an advisable solution, as it carries significant risks.
*BioAv↑, in vitro study reported that the covalent bonding between CGA and soluble oat β-glucan significantly improved CGA’s structural stability and maximized its pharmacological potential
*BioAv↑, Studies have reported that CGA-loaded liposomes, prepared from cholesterol and phosphatidylcholine, showed a relative oral bioavailability of 129.38% compared to free CGA.
eff↑, bovine serum albumin (BSA)-decorated chlorogenic acid silver nanoparticles (AgNPs-CGA-BSA) exhibited significant antioxidant and anticancer effects both in vitro and in vivo.

4337- CUR,    Inhibitory effect of curcumin, a food spice from turmeric, on platelet-activating factor- and arachidonic acid-mediated platelet aggregation through inhibition of thromboxane formation and Ca2+ signaling
- in-vitro, NA, NA
*AntiAg↑, We show that curcumin inhibited platelet aggregation mediated by the platelet agonists epinephrine (200 μM), ADP (4 μM), platelet-activating factor (PAF; 800 nM), collagen (20 μg/mL), and arachidonic acid (AA: 0.75 mM).
*TXA2↓, results suggest that the curcumin-mediated preferential inhibition of PAF- and AA-induced platelet aggregation involves inhibitory effects on TXA2 synthesis and Ca2+ signaling, but without the involvement of PKC.

1162- PI,    Piperine Inhibits the Activities of Platelet Cytosolic Phospholipase A2 and Thromboxane A2 Synthase without Affecting Cyclooxygenase-1 Activity: Different Mechanisms of Action Are Involved in the Inhibition of Platelet Aggregation and Macrophage Inflammatory Response
- in-vitro, NA, NA
*cPLA2↓, attenuating cPLA2 activity in collagen-stimulated platelets.
TXA2↓, results suggest that piperine inhibits platelet aggregation by attenuating cPLA2 and TXA2 synthase activities, rather than through the inhibition of COX-1 activity
COX2↓,
PGE2↓,
PGD2↓,


Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   cMyc↓, 1,  

Transcription & Epigenetics ⓘ

other↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 2,  

Migration ⓘ

AntiAg↑, 1,   E-cadherin↑, 1,   MMP2↓, 1,   MMP9↓, 1,   Slug↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumMeta↓, 3,   Twist↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

TXA2↓, 3,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 3,   COX2↓, 1,   PD-L1↓, 1,   PGD2↓, 1,   PGE2↓, 2,  

Drug Metabolism & Resistance ⓘ

Dose↑, 1,   eff↑, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

PD-L1↓, 1,  
Total Targets: 24

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   Ferroptosis↓, 1,   HO-1↑, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

cPLA2↓, 1,   NADPH↓, 1,  

Cell Death ⓘ

Ferroptosis↓, 1,   JNK↓, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Migration ⓘ

AntiAg↑, 4,  

Angiogenesis & Vasculature ⓘ

TXA2↓, 5,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 2,   COX2↓, 1,   Inflam↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   BioAv↝, 2,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

BP↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 2,   toxicity↓, 1,  
Total Targets: 25

Scientific Paper Hit Count for: TXA2, thromboxane A2
4 Aspirin -acetylsalicylic acid
1 Caffeic acid
1 Chlorogenic acid
1 Curcumin
1 Piperine
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#:%  Target#:1028  State#:%  Dir#:1
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