AhR Cancer Research Results

AhR, aryl hydrocarbon receptor: Click to Expand ⟱
Source:
Type:
AhR is a ligand-activated transcription factor that plays a crucial role in regulating various cellular processes, including cell growth, differentiation, and immune responses.
AhR is overexpressed in lung cancer cells and is associated with poor prognosis.
-Cell proliferation: AhR activation promotes cell growth and proliferation.
-Apoptosis: AhR activation inhibits apoptosis (programmed cell death), allowing cancer cells to survive.
-Angiogenesis: AhR activation promotes the formation of new blood vessels, which is essential for tumor growth.
-Immune suppression: AhR activation inhibits the immune response, allowing cancer cells to evade immune detection.
AhR regulates expression of CYP1A1, CYP1B1, and COX-2
AhR is often overexpressed in various types of cancer, including breast, lung, liver, and skin cancer. AhR expression is often higher in tumor cells compared to normal cells.
Scientific Papers found: Click to Expand⟱
232- AL,    A Single Meal Containing Raw, Crushed Garlic Influences Expression of Immunity- and Cancer-Related Genes in Whole Blood of Humans
- Human, Nor, NA
*AhR↑, x2.6 increase
*ARNT↑, x1.8 increase
*Hif1a↑, x1.6 increase (whole blood)
*Jun↑, x1.7 increase, x12@3-6hrs
*NFAT↑,
*NFAM1↑, 3 fold increase
*REL↑, x1.7 increase
*OSM↑, x1.8 increase
*NFAT↑, x1.4 increase NFATC3
*CXCc↑, x1.3 increase CXCL14
*IL2↑, x1.1
*IL6↑, x1.3
*LIF↑, x1.4

7441- CYN,    Cynaropicrin attenuates UVB-induced oxidative stress via the AhR-Nrf2-Nqo1 pathway
- in-vitro, Nor, NA
*ROS↓, Cyn actively inhibited generation of reactive oxygen species from keratinocytes irradiated with ultraviolet B (UVB) in a Nrf2-dependent manner.
*NRF2↑,
*Inflam↓, Cyn also inhibited the production of proinflammatory cytokines such as interleukin 6 and tumor necrosis factor-α from UVB-treated keratinocytes.
*IL6↓,
*TNF-α↓,
*AhR↑, Our findings demonstrate that Cyn is a potent activator of the AhR-Nrf2-Nqo1 pathway, and could therefore be applied to prevention of UVB-induced photo aging.
*NQO1↑,

7607- I3C,    Indole-3-carbinol induces G1 cell cycle arrest and apoptosis through aryl hydrocarbon receptor in THP-1 monocytic cell line
- in-vitro, AML, THP1
AhR↑, Indole-3-carbinol (I3C) is an AhR agonist and a potential anticancer agent.
TumCP↓, I3C inhibits the proliferation of THP-1 cells in a dose- and time-dependent manner with minimal toxicity over normal monocytes.
selectivity↑,
Bcl-2↓, I3C downregulated BCL2 and upregulated FasR in THP-1 cells (p < .05 to p < .001).
Fas↑,
P21↑, G1-acting cell cycle genes (P21, P27 and P53) were overexpressed (p < .05 to p < .001), while CDK2 was downregulated upon I3C treatment (p < .01 to p < .001).
p27/CDKN1B↑,
P53↓,
CDK2↓,

7587- I3C,    Indole-3-Carbinol, a Phytochemical Aryl Hydrocarbon Receptor-Ligand, Induces the mRNA Overexpression of UBE2L3 and Cell Proliferation Arrest
- in-vitro, Cerv, HeLa
AhR↑, We found that I3C promotes the activation of AhR and decreases cell proliferation, possibly through UBE2L3 mRNA induction, which would result in the ubiquitination of HPV E7
UBE2L3/UBCH7↑,
Dose↝, all concentrations used activated the AhR

7584- I3C,    Functional effect of indole-3 carbinol in the viability and invasive properties of cultured cancer cells
- in-vitro, Cerv, HeLa - in-vitro, CRC, HCT8 - in-vitro, Liver, HepG2
TumCP↓, I3C impairs cell proliferation, induces apoptosis, and affects cancer cell mobility, invasion and mitochondrial function.
Apoptosis↑,
TumCI↓,
*antiOx↑, Indole-3-carbinol (I3C) is a natural antioxidant agent that has been studied as a potential cancer treatment.
AhR↑, I3C is an agonist of the aryl hydrocarbon receptor (AhR), a transcription factor that plays a role in the expression of genes related to development, immunity, circadian rhythm, and cancer.
MMP↓, impaired carcinogenic properties and alterations in mitochondrial membrane potential after treatment with I3C.
Casp3↑, Caspase 3, 4, and 8 were significantly overexpressed in all cell lines when cultured with 10 μM of I3C.
Casp8↑,

7592- I3C,    Indole-3-carbinol as a chemopreventive and anti-cancer agent
- Review, Var, NA
JNK↑, indole-3-carbinol has been shown to activate the stress-induced MAP kinases p38 and c-jun N-terminal kinase (JNK) in prostate cancer cells (66), and to inhibit constitutively active STAT3,
STAT3↓,
TumCCA↑, Indole-3-carbinol and DIM exhibit the ability to cause G1 arrest in breast and prostate cancer cells
P21↑, upregulation of the CDK inhibitors p21WAF1 and p27kip1, and the concurrent downregulation of cyclin D1, cyclin E, and CDKs 2, 4, and 6,
p27/CDKN1B↑,
cycD1/CCND1↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,
CDK6↓,
AhR↑, indole-3-carbinol has been reported to increase AhR expression in MCF-7 cells
ER-α36↓, Indole-3-carbinol is a negative regulator of ERα signaling in human tumor cells
ChemoSen↑, Consequently, indole-3-carbinol could cooperate with tamoxifen to inhibit breast cancer proliferation
ER Stress↑, indole-3-carbinol and DIM induced endoplasmic reticulum stress responses in cancer cells via unfolded protein response pathways,
UPR↑,
BRCA1↑, indole-3-carbinol/DIM-induced endoplasmic reticulum stress and upregulation of the expression of the tumor suppressor genes BRCA1 and BRCA2 in prostate and breast cancer cells
BRCA2↑,
TumCMig↓, Indole-3-carbinol has been reported to inhibit the migration and invasion of breast cancer cells
TumCI↓,
VEGF↓, decreased vascular endothelial growth factor (VEGF), increased interleukin-8 (IL-8) secretion, and decreased activities of MMP-2 and MMP-9
IL8↓,
MMP2↓,
MMP9↓,
RadioS↑, Chemo- and radiosensitizing effects of indole-3-carbinol/DIM
Akt↓, Inhibition of Akt/NF-κB signaling
NF-kB↓,
DR4↑, Induction of death receptor (DR)4 and DR5 expression
DR5↑,

3312- SIL,    Silymarin Alleviates Oxidative Stress and Inflammation Induced by UV and Air Pollution in Human Epidermis and Activates β-Endorphin Release through Cannabinoid Receptor Type 2
- Human, Nor, NA
*antiOx↑, silymarin (SM), an antioxidant and anti-inflammatory complex of flavonoids,
*Inflam↓,
*ROS↓, SM decreased morphological alterations, ROS, and IL-1a in UV+urban-dust-stressed RHE.
*IL1α↓,
*AhR↑, AHR- and Nrf2-related genes were upregulated, which control the antioxidant effector and barrier function.
*NRF2↑,
*IL8↓, Interleukin 8 gene expression was decreased.

2216- SK,    Shikonin upregulates the expression of drug-metabolizing enzymes and drug transporters in primary rat hepatocytes
- in-vivo, Nor, NA
*NRF2↑, Shikonin effectively upregulates the transcription of CYP isozymes, phase II detoxification enzymes, and phase III membrane transporters and this function is at least partially through activation of AhR and Nrf2
*AhR↑,
*CYP1A1↑, shikonin dose-dependently increased the protein expression of CYP1A1, CYP1A2, CYP2C6, CYP2D1, and CYP3A2.
*CYP1A2↑,
*CYP2C6↑,
*CYP2D1↑,
*CYP3A2↑,
*NQO1↑, Compared with the controls, cells treated with 2 uM shikonin had 5.5-, 3.0-, and 2.0-fold higher UGT1A1, NQO1, and PGST protein levels


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:


NA, unassigned(tgid=0) ⓘ

UBE2L3/UBCH7↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Cell Death(tgid=5) ⓘ

AhR↑, 4,   Akt↓, 1,   Apoptosis↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp8↑, 1,   DR4↑, 1,   DR5↑, 1,   Fas↑, 1,   JNK↑, 1,   p27/CDKN1B↑, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,   UPR↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

BRCA1↑, 1,   BRCA2↑, 1,   P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 2,   CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21↑, 2,   TumCCA↑, 1,  

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

STAT3↓, 1,  

Migration(tgid=13) ⓘ

ER-α36↓, 1,   MMP2↓, 1,   MMP9↓, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL8↓, 1,   NF-kB↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   Dose↝, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BRCA1↑, 1,  
Total Targets: 40

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   CYP1A1↑, 1,   NQO1↑, 2,   NRF2↑, 3,   ROS↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

CYP2C6↑, 1,   CYP3A2↑, 1,  

Cell Death(tgid=5) ⓘ

AhR↑, 4,  

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

Jun↑, 1,  

Migration(tgid=13) ⓘ

CYP2D1↑, 1,   NFAM1↑, 1,   NFAT↑, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↑, 1,   REL↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CXCc↑, 1,   IL1α↓, 1,   IL2↑, 1,   IL6↓, 1,   IL6↑, 1,   IL8↓, 1,   Inflam↓, 2,   LIF↑, 1,   OSM↑, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

ARNT↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

CYP1A2↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,   IL6↑, 1,  
Total Targets: 28

Scientific Paper Hit Count for: AhR, aryl hydrocarbon receptor
4 Indole-3-carbinol
1 Allicin (mainly Garlic)
1 Cynaropicrin
1 Silymarin (Milk Thistle) silibinin
1 Shikonin
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

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