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⟱
3061- RES,    The Anticancer Effects of Resveratrol: Modulation of Transcription Factors
- Review, Var, NA
AhR↓, Several reports demonstrate the inhibitory effects of resveratrol on AhR-mediated activation of phase I enzymes.
NRF2↑, Bishayee et al. (18) demonstrated that attenuation of DENA (diethyl nitrosamine)-induced liver carcinogenesis by resveratrol was mediated by increased Nrf2 expression.
*NQO1↑, Induction of Nrf2 signaling by resveratrol resulted in increased expression of NQO1, heme-oxygenase 1 (HO-1), and glutamate cysteine ligase catalytic subunit in cigarette smoke extract-treated bronchial epithelial cells
*HO-1↑,
*GSH↑, observed restored glutathione levels in cigarette smoke extract-treated A549 lung alveolar epithelial cancer cells by resveratrol;
P53↑, we highlight reported resveratrol-induced, p53-mediated anticancer mechanisms.
Cyt‑c↑, release of mitochondria proteins (e.g. cytochrome c, Smac/DIABLO, etc.) to the cytosol, thus triggering suppression of inhibitors of apoptosis proteins (e.g. Bcl2, Bcl-XL, survivin, XIAP, etc.) and caspase activation in several cancers
Diablo↑,
Bcl-2↓,
Bcl-xL↓,
survivin↓,
XIAP↓,
FOXO↑, activation of FoxO transcription factors is implicated in the observed anticancer activities of resveratrol.
p‑PI3K↓, resveratrol's ability to inhibit the phosphorylation of PI3K/Akt (
p‑Akt↓,
BIM↑, Bim/TRAIL/DR4/DR5/p27KIP1 induction and cyclin D1 inhibition) of resveratrol on prostate cancer cells
DR4↑,
DR5↑,
p27↑,
cycD1/CCND1↓,
SIRT1↑, resveratrol is considered a SIRT1 agonist
NF-kB↓, resveratrol not only curbs expression of NF-κB, but also impedes the phosphorylation of IκBα thereby keeping the constitutive NF-κB subunit in an inactive state, resulting in suppression of the inflammatory
ATF3↑, Furthermore, increased ATF3 expression by resveratrol facilitated induction of apoptosis


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:


Redox & Oxidative Stress ⓘ

ATF3↑, 1,   NRF2↑, 1,  

Mitochondria & Bioenergetics ⓘ

XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

SIRT1↑, 1,  

Cell Death ⓘ

AhR↓, 1,   p‑Akt↓, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   BIM↑, 1,   Cyt‑c↑, 1,   Diablo↑, 1,   DR4↑, 1,   DR5↑, 1,   p27↑, 1,   survivin↓, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

FOXO↑, 1,   p‑PI3K↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  
Total Targets: 20

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↑, 1,   HO-1↑, 1,   NQO1↑, 1,  
Total Targets: 3

Scientific Paper Hit Count for: AhR, aryl hydrocarbon receptor
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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