GR Cancer Research Results

GR, glucocorticoid receptors: Click to Expand ⟱
Source:
Type:
Glucocorticoid receptors (GR), also known as NR3C1 (nuclear receptor subfamily 3, group C, member 1), are a type of steroid hormone receptor that mediates the effects of glucocorticoids, which are steroid hormones involved in various physiological processes, including metabolism, immune response, and stress response.
In certain cancer subtypes such as gynaecological cancers (endometrial and ovarian) and early stage, untreated triple negative breast cancers, high GR expression is linked with cancer progression and therefore a poorer patient prognosis.

Glucocorticoid receptors play a significant role in various cancers, and their expression can have complex prognostic implications. In some cancer types, high GR expression is associated with better outcomes, while in others, it may correlate with aggressive disease and treatment resistance. The relationship between glucocorticoid receptor expression and cancer prognosis can vary depending on the specific cancer type, stage, and other molecular factors.
Scientific Papers found: Click to Expand⟱
2796- CHr,    Chemopreventive effect of chrysin, a dietary flavone against benzo(a)pyrene induced lung carcinogenesis in Swiss albino mice
- in-vivo, Lung, NA
PCNA↓, PCNA, COX-2 and NF-κB, where chrysin supplementation downregulated the expression of these proteins and maintained cellular homeostasis.
COX2↓,
NF-kB↓,
chemoPv↑, chemopreventive potential of chrysin against B(a)P induced lung cancer in Swiss albino mice
*SOD↑, SOD, CAT, GR and GPx. Chrysin treatment significantly restored all above enzymatic anti-oxidants.
*Catalase↓,
*GR↓,
*GPx↓,
*lipid-P↓, chrysin inhibits LPO thereby preventing the formation of lipid peroxides which are engaged in carcinogenesis
*COX2↓, Chrysin supplementation significantly downregulated the protein expressions of COX-2 and NF-kB,
*NF-kB↓,
*ROS↓, chrysin is capable of protecting the lungs against oxidative damage.

5032- PTS,    Pterostilbene Decreases the Antioxidant Defenses of Aggressive Cancer Cells In Vivo: A Physiological Glucocorticoids- and Nrf2-Dependent Mechanism
- in-vivo, Melanoma, NA
TumCG↓, Intravenous administration of Pter decreased human melanoma growth in vivo
NRF2↓, and thereby downregulated the glucocorticoid receptor- and nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-dependent antioxidant defense system in growing melanomas.
GR↓,
BBB↑, Pter can cross the blood–brain barrier
ACTH↓, Pter inhibits ACTH production in AtT-20 cells
eff↑, combined Pter and GSH depletion treatment chemosensitizes melanoma cells and facilitates their complete elimination.


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

NRF2↓, 1,  

DNA Damage & Repair ⓘ

PCNA↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,  

Hormonal & Nuclear Receptors ⓘ

ACTH↓, 1,   GR↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,  
Total Targets: 10

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   GPx↓, 1,   lipid-P↓, 1,   ROS↓, 1,   SOD↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,  

Hormonal & Nuclear Receptors ⓘ

GR↓, 1,  
Total Targets: 8

Scientific Paper Hit Count for: GR, glucocorticoid receptors
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#:390  State#:%  Dir#:1
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