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⟱
2794- CHr,    An updated review on the versatile role of chrysin in neurological diseases: Chemistry, pharmacology, and drug delivery approaches
- Review, Park, NA - Review, Stroke, NA
*neuroP↑, chrysin has protective effects against neurological conditions by modulating oxidative stress, inflammation, and apoptosis in animal models.
*ROS↓,
*Inflam↓,
*Apoptosis↓,
*IL1β↓, attenuated IL-1β and TNF-α, COX-2, iNOS, and NF-kB expression, activated JNK
*TNF-α↓,
*COX2↓,
*iNOS↓,
*NF-kB↓,
*JNK↓,
*HDAC↓, alleviated histone deacetylase (HDCA) activity, GSK-3β levels, IFNγ, IL-17,
*GSK‐3β↓,
*IFN-γ↓,
*IL17↓,
*GSH↑, increased GSH levels
*NRF2↑, Park's: Increased Nrf2, modulated HO-1, SOD, CAT, decreased MDA, inhibited NF-κB and iNOS
*HO-1↑, upregulated expression of hallmark antioxidant enzymes, including HO-1, SOD, and CAT; and decreased levels of MDA
*SOD↑,
*MDA↓,
*NO↓, Attenuated NO, increased GPx
*GPx↑,
*TBARS↓, decreased levels of TBARS, AChE, restored activities of GR, GSH, SOD, CAT and Vitamin C
*AChE↓,
*GR↑,
*Catalase↑,
*VitC↑,
*memory↑, attenuated memory impairment
*lipid-P↓, attenuated lipid peroxidation
*ROS↓, attenuated ROS

3222- EGCG,    Epigallocatechin gallate and mitochondria—A story of life and death
- Review, Nor, NA
*lipid-P↓, ↓Lipid peroxidation ↑SOD, CAT, GPx, GR, and GST, ↑GSH
*SOD↑,
*Catalase↑,
GPx↑,
*GR↑,
*GSTs↑,
*GSH↑,
*SIRT1↑, EGCG upregulated the levels of NAD+ -dependent protein deacetylase sirtuin-1 (SIRT1), peroxi- some proliferator-activated receptor  co-activator-1 (PGC-1), glutathione peroxidase (GPx), and SOD in MPP + -treated PC12 cells.
*PGC1A↑,
*other↑, EGCG (2 mg/kg day-1 administered through oral gavage for 30 days) upregulated the activities of brain mitochondrial antioxidant enzymes (SOD, CAT, and GPx) in aged, but not in young rats.

1708- Lyco,    The Anti-Cancer Activity of Lycopene: A Systematic Review of Human and Animal Studies
- Review, Var, NA
OS↑, reduced prostate cancer-specific mortality in men at high risk for prostate cancer
ChemoSen↑, improved the response to docetaxel chemotherapy in advanced castrate-resistant prostate cancer
QoL↑, lycopene improved the quality of life, and provided relief from bone pain and control of lower urinary tract symptoms
PSA∅, PSA stabilisation in prostate cancer
eff↑, Lycopene co-supplementation with vitamin E also showed an improvement in the results of prostate cancer treatment
AntiCan↑, lycopene intake showed a strong protective effect against stomach cancer, regardless of H. pylori status
AntiCan↑, A lycopene-rich diet was shown to reduce the incidence of pancreatic cancer in humans by 31%
angioG↓,
VEGF↓,
Hif1a↓,
SOD↑,
Catalase↑,
GPx↑,
GSH↑,
GPx↑,
GR↑,
MDA↓,
NRF2↑,
HO-1↑,
COX2↓,
PGE2↓,
NF-kB↓,
IL4↑,
IL10↑,
IL6↓,
TNF-α↓,
PPARγ↑,
TumCCA↑, G(0)/G(1) phase
FOXO3↓,
Casp3↑,
IGF-1↓, breast cancer,crc
p27↑,
STAT3↓,
CDK2↓,
CDK4↓,
P21↑,
PCNA↓,
MMP7↓,
MMP9↓,

4488- Se,  Chit,  PEG,    Anticancer effect of selenium/chitosan/polyethylene glycol/allyl isothiocyanate nanocomposites against diethylnitrosamine-induced liver cancer in rats
- in-vivo, Liver, HepG2 - in-vivo, Nor, HL7702
tumCV↓, The SCPg-AI-NCs effectively decreased the cell viability and induced apoptosis in the HepG2 cells.
Apoptosis↑,
*GSH↑, The SCPg-AI-NCs treatment effectively decreased the TBARS and improved the GSH, vitamin-C & -E contents in the DEN-induced rats
*VitC↑,
*VitE↑,
*SOD↑, The activities of SOD, GPx, and GR were also improved by the SCPg-AI-NCs treatment in the DEN-induced rats.
*GPx↑,
*GR↑,
ALAT↓, The activities of ALT, ALP, AST, LDH, and GGT was remarkably decreased by the SCPg-AI-NCs treatment in the DEN-provoked liver cancer rats.
ALP↓,
AST↓,
LDH↓,
selectivity↑, same doses of SCPg-AI-NCs did not showed the cytotoxicity to the normal liver HL7702 cells
eff↑, The utilization of nanocomposites as drug delivery systems has a efficacy to solve the several side effects triggered by chemotherapeutic drugs to normal cells

2106- TQ,    Cancer: Thymoquinone antioxidant/pro-oxidant effect as potential anticancer remedy
- Review, Var, NA
Apoptosis↑, The anticancer power of TQ is accomplished by several aspects; including promotion of apoptosis, arrest of cell cycle and ROS generation.
TumCCA↑,
ROS↑,
*Catalase↑, activation of antioxidant cytoprotective enzymes including, CAT, SOD, glutathione reductase (GR) [80], glutathione-S-transferase (GST) [81] and glutathione peroxidase (GPx) - scavenging H2O2 and superoxide radicals and preventing lipid peroxidation
*SOD↑,
*GR↑,
*GSTA1↓,
*GPx↑,
*H2O2↓,
*ROS↓,
*lipid-P↓,
*HO-1↑, application of TQ to HaCaT (normal) cells promoted the expression of HO-1 in a concentration and time-dependent pattern
p‑Akt↓, TQ could induce ROS which provoked phosphorylation and activation of Akt and AMPK-α
AMPKα↑,
NK cell↑, TQ was outlined to enhance natural killer (NK) cells activity
selectivity↑, Many researchers have noticed that the growth inhibitory potential of TQ is particular to cancer cells
Dose↝, Moreover, TQ has a dual effect in which it can acts as both pro-oxidant and antioxidant in a dose-dependent manner; it acts as an antioxidant at low concentration whereas, at higher concentrations it possess pro-oxidant property
eff↑, Pro-oxidant property of TQ occurs in the presence of metal ions including copper and iron which induce conversion of TQ into semiquinone. This leads to generation of reactive oxygen species (ROS) causing DNA damage and induction of cellular apoptosis
GSH↓, TQ for one hour resulted in three-fold increase of ROS while reduced GSH level by 60%
eff↓, pre-treatment of cells with N-acetylcysteine, counteracted TQ-induced ROS production and alleviated growth inhibition
P53↑, TQ provokes apoptosis in MCF-7 cancer cells by up regulating the expression of P53 by time-dependent manner.
p‑STAT3↓, TQ inhibited the phosphorylation of STAT3
PI3K↑, via up regulation of PI3K and MPAK signalling pathway
MAPK↑,
GSK‐3β↑, TQ produced apoptosis in cancer cells and modulated Wnt signaling by activating GSK-3β, translocating β-catenin
ChemoSen↑, Co-administration of TQ and chemotherapeutic agents possess greater cytotoxic influence on cancer cells.
RadioS↑, Treatment of cells with both TQ and IR enhanced the antiproliferative power of TQ as observed by shifting the IC50 values for MCF7 and T47D cells from ∼104 and 37 μM to 72 and 18 μM, respectively.
BioAv↓, TQ cannot be used as the primary therapeutic agent because of its poor bioavailability [177,178] and lower efficacy
NRF2↑, TQ to HaCaT cells promoted the expression of HO-1 in a concentration and time-dependent pattern. This was achieved via increasing stabilization of Nrf2


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   GPx↑, 3,   GSH↓, 1,   GSH↑, 1,   HO-1↑, 1,   MDA↓, 1,   NRF2↑, 2,   ROS↑, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   LDH↓, 1,   PPARγ↑, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 2,   Casp3↑, 1,   MAPK↑, 1,   p27↑, 1,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   P21↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

FOXO3↓, 1,   GSK‐3β↑, 1,   IGF-1↓, 1,   PI3K↑, 1,   STAT3↓, 1,   p‑STAT3↓, 1,  

Migration ⓘ

MMP7↓, 1,   MMP9↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL10↑, 1,   IL4↑, 1,   IL6↓, 1,   NF-kB↓, 1,   NK cell↑, 1,   PGE2↓, 1,   PSA∅, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

GR↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 2,   Dose↝, 1,   eff↓, 1,   eff↑, 3,   RadioS↑, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   IL6↓, 1,   LDH↓, 1,   PSA∅, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   OS↑, 1,   QoL↑, 1,  
Total Targets: 62

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 3,   GPx↑, 3,   GSH↑, 3,   GSTA1↓, 1,   GSTs↑, 1,   H2O2↓, 1,   HO-1↑, 2,   lipid-P↓, 3,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 3,   SOD↑, 4,   TBARS↓, 1,   VitC↑, 2,   VitE↑, 1,  

Core Metabolism/Glycolysis ⓘ

PGC1A↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   iNOS↓, 1,   JNK↓, 1,  

Transcription & Epigenetics ⓘ

other↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1,   HDAC↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IFN-γ↓, 1,   IL17↓, 1,   IL1β↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,  

Hormonal & Nuclear Receptors ⓘ

GR↑, 4,  

Functional Outcomes ⓘ

memory↑, 1,   neuroP↑, 1,  
Total Targets: 35

Scientific Paper Hit Count for: GR, glucocorticoid receptors
1 Chrysin
1 EGCG (Epigallocatechin Gallate)
1 Lycopene
1 Selenium
1 chitosan
1 polyethylene glycol
1 Thymoquinone
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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