TRPA1 Cancer Research Results

TRPA1, Transient Receptor Potential Ankyrin 1: Click to Expand ⟱
Source:
Type:

Transient Receptor Potential Ankyrin 1, a Ca²⁺-permeable, nonselective cation channel. It is best known as a sensory “irritant/pain” receptor activated by electrophilic/pungent compounds such as allyl isothiocyanate, allicin, cinnamaldehyde, eugenol, and some cannabinoids.

TRPA1 is biphasic/context-dependent in cancer.

Strategy Possible Effect Concern
TRPA1 inhibition May reduce oxidative-stress tolerance and improve chemosensitivity. Most compelling for breast/lung spheroid-type ROS-defense model.
TRPA1 activation In some models, strong activation causes Ca2+ overload, mitochondrial dysfunction, and apoptosis. Could also promote survival if activation is moderate or coupled to Ca2+ extrusion mechanisms.
Natural TRPA1 agonists Could be anticancer in some contexts. Could theoretically support survival in TRPA1-dependent cancers if dose/exposure creates adaptive Ca2+ signaling rather than overload.


Compound/Product TRPA1 Relationship Database Note
Allicin / Garlic TRPA1 agonist(activated) Strong overlap; garlic organosulfur compounds are classic TRPA1 activators.
Allyl isothiocyanate / Mustard / Wasabi / Crucifers Strong TRPA1 agonist Relevant if sulforaphane or crucifer compounds are tracked separately.
Cinnamaldehyde / Cinnamon TRPA1 agonist Good tag under cinnamon or cinnamaldehyde.
Eugenol / Clove TRPA1 agonist/modulator Good tag under eugenol.
Gingerol / Ginger TRPA1 agonist Relevant if ginger or gingerol is in the database.
Cannabidiol / Cannabinoids TRPA1 agonist/modulator Mechanistically relevant, but pharmacology is broad.
Oleocanthal / Olive oil phenolics TRPA1 activation linked to pungency Lower cancer-specific relevance than allicin, allyl isothiocyanate, or cinnamaldehyde.


Scientific Papers found: Click to Expand⟱
6461- 1,8-Cin,    1,8-cineole (eucalyptol): A versatile phytochemical with therapeutic applications across multiple diseases
- Review, AD, NA - Review, Var, NA
*Inflam↓, long history of use in traditional medicine and exhibits an array of biological properties, including anti-inflammatory, antioxidant, antimicrobial, bronchodilatory, analgesic, and pro-apoptotic effects.
*antiOx↑,
*neuroP↑, recent studies have highlighted the neuroprotective, analgesic, and pro-apoptotic properties of 1,8-cineole, underscoring its potential beneficial role in a broad spectrum of conditions such as Alzheimer’s disease, neuropathic pain, and cancer
*BioAv↑, Marked by a logP value of 2.74, 1,8-cineole strikes an optimal equilibrium between solubility and permeability, hinting at its favorable potential for oral bioavailability
*Half-Life↝, In rabbits, oral administration of 200 mg/kg has led to rapid attainment of peak plasma concentration within 1 h, indicating efficient absorption
*toxicity↓, compound’s toxicity profile, the oral acute LD50 value in rats is documented at 2480 mg/kg body weight
*PGE2↓, 1,8-cineole decreased the release of prostaglandin E2 and leukotriene B4 (LTB4) from peripheral blood mononuclear cells in asthmatic patients, and reduced TNF-α, IL-1β, LTB4, and thromboxane B2 in lipopolysaccharide (LPS)-stimulated peripheral blood
*TNF-α↓,
*IL1β↓,
*NO↓, 1,8-cineole hindered LPS-induced nitric oxide (NO) production in mouse macrophage cell lines
*NF-kB↓, inhibition of nuclear translocation of NF-κB p65 and PPARγ, leading to the suppression of immune response genes.
*PPARγ↓,
COX2↓, ,8-cineole has been found to impede UVB-induced COX-2 protein and mRNA production in HaCaT cells
*ROS↓, 1,8-cineole’s antioxidant properties play a crucial role in its therapeutic potential, as it is effective in neutralizing reactive oxygen species (ROS)
*SOD↑, 1,8-cineole treatment enhanced antioxidant enzymes activities, such as superoxide dismutase (SOD) and catalase (CAT), increased total antioxidant capacity, and decreased ROS and malondialdehyde (MDA)
*Catalase↑,
*TAC↑,
*MDA↓,
*lipid-P↓, 1,8-cineole has demonstrated the ability to inhibit LP
*NRF2↑, The antioxidant activity of 1,8-cineole is mediated, in part, by activating the Nrf2/Keap1 system
*HO-1↑, increased expression of phase II detoxifying enzymes and antioxidant proteins, such as heme oxygenase-1 and NAD(P)H: quinone oxidoreductase 1 (NOQ1)
*NADPH↑,
*GPx↑, 1,8-cineole treatment has been shown to enhance the activities of antioxidant enzymes, such as SOD, GPx, and CAT,
*AntiBio↑, Antibacterial properties: activity, synergy with antibiotics, and impact on biofilm formation and cell morphology
*eff↑, Although 1,8-cineole exhibited weaker bactericidal activity than commonly used antibiotics such as gentamicin and amoxicillin (AMX)/clavulanic acid, it significantly reduced the minimum inhibitory concentration of antibiotics when used in combination
*AntiFungal↑, Antifungal properties: inhibition of fungal growth and disruption of biofilm formation
*AntiViral↑, Antiviral properties: inhibition of viral replication and enhancement of antiviral responses
*TRPA1↑, 1,8-cineole could activate TRPA1 channels in the dorsal root ganglia (DRG),
eff↑, when combined with simvastatin, increased G0/G1 cell cycle arrest and sensitized cells to apoptosis
TumCCA↑, 1,8-cineole induced G0/G1 arrest and senescence in HepG2 cells through oxidative stress and various signaling pathways such as MAPK, AMPK, and Akt/mTOR
ROS↑,
MAPK↝,
mTOR↝,
Apoptosis↑, HCT116 and RKO human colon cancer cell lines, 1,8-cineole selectively promoted apoptosis rather than necrosis
survivin↓, This process was linked to survivin and Akt inactivation, along with p38 activation.
Akt↓,
p38↑,
cl‑PARP↑, triggered subsequent cleavage of PARP and caspase-3, resulting in apoptosis.
cl‑Casp3⇅,
P53↑, increasing p53 expression, as well as the expression of apoptotic proteins (Bax/Bcl-2, Cyt-c, caspase-9, and caspase-3)
BAX↑,
Cyt‑c↑,
Casp9↑,
Dose↝, efficacious concentrations of 1,8-cineole reported for inhibiting in vitro cancer cell proliferation range from micromolar [135], [136] to millimolar (mM)
*Aβ↓, 1,8-cineole in rat PC12 cells (pheochromocytoma cells) demonstrated effective mitigation of the Aβ induced cytotoxicity and oxidative stress
*tau↓, 1,8-cineole has shown the ability to modulate tau phosphorylation by suppressing GSK-3β activity and to reduce Aβ production by inhibiting beta-site amyloid precursor protein cleaving enzyme-1 (BACE-1), both in vitro and in vivo
*GSK‐3β↓,
*BACE↓,
*cardioP↑, 1,8-cineole enhanced cell viability, inhibited cardiac hypertrophy, attenuated cardiac remodeling, improved cardiac function, and decreased the concentrations of atrial natriuretic peptide and brain natriuretic peptide in rat hearts
MFN2↑, 1,8-cineole was also found to inhibit the activation of dynamin-related protein 1 and promote mitochondrial fusion by increasing MFN2.

6402- ANE,  FEO,    trans-Anethole of Fennel Oil is a Selective and Nonelectrophilic Agonist of the TRPA1 Ion Channel
- in-vitro, Nor, HEK293
*TRPA1↑, We conclude that trans-anethole is a selective, nonelectrophilic, and seemingly less-irritating agonist of TRPA1.
*Dose↝, Anethole, an aromatic compound, is a major component not only of fennel oil but also of star anise oil
*Bacteria↓, Anethole has been shown to have antibacterial and antifungal properties in vitro, as well as anti-inflammatory and analgesic activity in vivo
*Inflam↓,


Showing Research Papers: 1 to 2 of 2

* 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(tgid=1) ⓘ

MFN2↑, 1,   ROS↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   cl‑Casp3⇅, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   MAPK↝, 1,   p38↑, 1,   survivin↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

mTOR↝, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,   eff↑, 1,  
Total Targets: 18

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1,   TRPA1↑, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,   TAC↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

NADPH↑, 1,   PPARγ↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

GSK‐3β↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   Inflam↓, 2,   NF-kB↓, 1,   PGE2↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   BACE↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   Dose↝, 1,   eff↑, 1,   Half-Life↝, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   neuroP↑, 1,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   AntiViral↑, 1,   Bacteria↓, 1,  
Total Targets: 34

Scientific Paper Hit Count for: TRPA1, Transient Receptor Potential Ankyrin 1
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#:1485  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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