TRPV2 Cancer Research Results

TRPV2, transient receptor potential vanilloid 2: Click to Expand ⟱
Source:
Type:
TRPV2 (transient receptor potential vanilloid 2) tends to be pro-tumor in many epithelial and metastatic contexts, but potentially anti-stemness / pro-differentiation in some brain tumor contexts. In prostate cancer, TRPV2 has been associated with migration, invasion markers, androgen-resistance progression, and metastatic disease. In gastric and esophageal cancers, higher TRPV2 has been linked to worse prognosis, and gastric studies suggest it can support PD-L1-related immune evasion. More recent breast cancer work also supports an oncogenic role, with TRPV2 promoting proliferation, migration, and invasion.

Scientific Papers found: Click to Expand⟱
5815- CBD,    Triggering of the TRPV2 channel by cannabidiol sensitizes glioblastoma cells to cytotoxic chemotherapeutic agents
- in-vitro, GBM, NA
TRPV2↑, We found that CBD increases TRPV2 expression and activity.
selectivity↑, CBD by triggering TRPV2-dependent Ca(2+) influx increases drug uptake and synergizes with cytotoxic agents to induce apoptosis of glioma cells, whereas no effects were observed in normal human astrocytes
ChemoSen↑, Overall, we demonstrated that co-administration of cytotoxic agents together with the TRPV2 agonist CBD increases drug uptake and parallelly potentiates cytotoxic activity in human glioma cells.

5816- CBD,    Cannabidiol inhibits human glioma by induction of lethal mitophagy through activating TRPV4
- in-vitro, GBM, NA
TRPV2↑, Mechanistically, calcium flux induced by CBD through TRPV4 (transient receptor potential cation channel subfamily V member 4) activation played a key role in mitophagy initiation
Ca+2↑,
MitoP↑,
eff↑, Lastly, CBD and temozolomide combination therapy in patient-derived neurosphere cultures and mouse orthotopic models showed significant synergistic effect

5819- CBD,    The potential role of cannabidiol (CBD) in lung cancer therapy: a systematic review of preclinical and clinical evidence
- Review, Lung, NA
Apoptosis↑, Mechanistically, CBD induced apoptosis through pathways such as PPAR-γ activation, mitochondrial dysfunction, and oxidative stress.
PPARγ↓,
mtDam↑,
ROS↑, Induced cell death via apoptosis and increased ROS levels.
EMT↓, It inhibited epithelial-to-mesenchymal transition (EMT), downregulated invasive markers, and modulated the tumor microenvironment by enhancing CD8 + T cell and NK cell activity.
CD8+↑,
NK cell↑,
ChemoSen↑, CBD showed synergistic effects with conventional therapies (e.g., cisplatin, radiotherapy) by increasing drug uptake and overcoming resistance.
ATP↓, CBD decreases intracellular ATP and glucose levels
glucose↓,
Ca+2↑, CBD enhances calcium influx (mediated by TRPV2) and elevates p-ERK expression in CIK cells
TRPV2↑,


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

ROS↑, 1,  

Mitochondria & Bioenergetics

ATP↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis

glucose↓, 1,   PPARγ↓, 1,  

Cell Death

Apoptosis↑, 1,  

Kinase & Signal Transduction

TRPV2↑, 3,  

Autophagy & Lysosomes

MitoP↑, 1,  

Proliferation, Differentiation & Cell State

EMT↓, 1,  

Migration

Ca+2↑, 2,  

Immune & Inflammatory Signaling

NK cell↑, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 2,   eff↑, 1,   selectivity↑, 1,  

Infection & Microbiome

CD8+↑, 1,  
Total Targets: 15

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TRPV2, transient receptor potential vanilloid 2
3 Cannabidiol
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#:1458  State#:%  Dir#:2
wNotes=on sortOrder:rid,rpid

 

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