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.


Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


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↓, *antiOx↑, *neuroP↑, *BioAv↑, *Half-Life↝, *toxicity↓, *PGE2↓, *TNF-α↓, *IL1β↓, *NO↓, *NF-kB↓, *PPARγ↓, COX2↓, *ROS↓, *SOD↑, *Catalase↑, *TAC↑, *MDA↓, *lipid-P↓, *NRF2↑, *HO-1↑, *NADPH↑, *GPx↑, *AntiBio↑, *eff↑, *AntiFungal↑, *AntiViral↑, *TRPA1↑, eff↑, TumCCA↑, ROS↑, MAPK↝, mTOR↝, Apoptosis↑, survivin↓, Akt↓, p38↑, cl‑PARP↑, cl‑Casp3⇅, P53↑, BAX↑, Cyt‑c↑, Casp9↑, Dose↝, *Aβ↓, *tau↓, *GSK‐3β↓, *BACE↓, *cardioP↑, MFN2↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned

MFN2↑, 1,  

Redox & Oxidative Stress

ROS↑, 1,  

Cell Death

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

DNA Damage & Repair

P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State

mTOR↝, 1,  

Immune & Inflammatory Signaling

COX2↓, 1,  

Drug Metabolism & Resistance

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

Pathway results for Effect on Normal Cells:


NA, unassigned

AntiBio↑, 1,   TRPA1↑, 1,  

Redox & Oxidative Stress

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

NADPH↑, 1,   PPARγ↓, 1,  

Proliferation, Differentiation & Cell State

GSK‐3β↓, 1,  

Angiogenesis & Vasculature

NO↓, 1,  

Immune & Inflammatory Signaling

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

Synaptic & Neurotransmission

tau↓, 1,  

Protein Aggregation

Aβ↓, 1,   BACE↓, 1,  

Drug Metabolism & Resistance

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

Functional Outcomes

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

Infection & Microbiome

AntiFungal↑, 1,   AntiViral↑, 1,  
Total Targets: 32

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:26  Cells:%  prod#:%  Target#:1485  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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