CB2 / CNR2 Cancer Research Results

CB2 / CNR2, Cannabinoid receptor type 2: Click to Expand ⟱
Source:
Type:

CB2 / CNR2 : Druggable immune-enriched cannabinoid receptor involved in microglia, inflammation, immune-cell signaling, pain, neuroprotection, and tumor-immune regulation.

-when a product binds selectively to the CB2 receptors(modulates up) and not the CB1 receptor, it non-psychoactive and therapeutically appealing.
-activation of the CB2 receptor can suppress pro-inflammatory cytokines production, helping to create an anti-tumor immune environment

Field Suggested Entry
Target CB2 / CNR2
Full Name Cannabinoid receptor type 2
Target Class G-protein-coupled receptor; Gi/o-coupled cannabinoid receptor
Primary Biology Immune modulation, microglial activation, inflammatory signaling, cytokine regulation, leukocyte behavior, pain/inflammation signaling
Cancer Relevance Medium and context-dependent: may suppress inflammation or tumorigenesis in some settings, but may also support immune suppression or tumor progression depending on tumor type and immune context
AD Relevance Medium-high: microglial CB2 activation is a promising neuroinflammation strategy, with encouraging preclinical evidence in AD models but limited clinical validation
Therapeutic Direction Usually selective CB2 agonism/modulation for neuroinflammation and inflammatory disease; cancer direction is tumor-context-dependent
Key Product Links β-caryophyllene, PEA, CBD/cannabinoid-system modulators, endocannabinoids, omega-3-derived lipid mediators


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⟱
6503- BCP,    The Potential Therapeutic Role of Beta-Caryophyllene as a Chemosensitizer and an Inhibitor of Angiogenesis in Cancer
- Review, Var, NA
ChemoSen↑, angioG↓, TumCI↓, TumMeta↓, ROS↑, *ROS↓, chemoP↑, CB2 / CNR2↑, Inflam↓, AntiTum↑, *BioAv↑, *BBB↑, Apoptosis↑, TumCP↑, TumCCA↑, RadioS↑, DNArepair↓, ROS↑, STAT3↓, *BioEnh↑, Pain↓, AntiBio↓, ROS↑, Dose↝, NF-kB↓, MAPK↓, TNF-α↓, IL1β↓, IL6↓, cl‑PARP↑, Casp↑, BAX↑, Bcl-2↓, VEGF↓, VEGFR2↓, MMP2↓, p‑p38↓, p‑ERK↓, EPR↑, P-gp↓, MRP1/ABCC1↓, *NRF2↑, *antiOx↑,

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

AntiBio↓, 1,   CB2 / CNR2↑, 1,  

Redox & Oxidative Stress

ROS↑, 3,  

Cell Death

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   MAPK↓, 1,   p‑p38↓, 1,  

DNA Damage & Repair

DNArepair↓, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State

p‑ERK↓, 1,   STAT3↓, 1,  

Migration

MMP2↓, 1,   TumCI↓, 1,   TumCP↑, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature

angioG↓, 1,   EPR↑, 1,   VEGF↓, 1,   VEGFR2↓, 1,  

Barriers & Transport

P-gp↓, 1,  

Immune & Inflammatory Signaling

IL1β↓, 1,   IL6↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 1,   Dose↝, 1,   MRP1/ABCC1↓, 1,   RadioS↑, 1,  

Clinical Biomarkers

IL6↓, 1,  

Functional Outcomes

AntiTum↑, 1,   chemoP↑, 1,   Pain↓, 1,  
Total Targets: 36

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 1,   NRF2↑, 1,   ROS↓, 1,  

Barriers & Transport

BBB↑, 1,  

Drug Metabolism & Resistance

BioAv↑, 1,   BioEnh↑, 1,  
Total Targets: 6

Scientific Paper Hit Count for: CB2 / CNR2, Cannabinoid receptor type 2
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#:1500  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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