GRP94 Cancer Research Results

GRP94, Glucose-Regulated Protein 94: Click to Expand ⟱
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GRP94 (Glucose-Regulated Protein 94) is a molecular chaperone that plays a crucial role in protein folding, assembly, and quality control in the endoplasmic reticulum (ER). It is also known as GP96 or HSP90B1.
High GRP94 expression(common) is associated with poor prognosis, increased tumor aggressiveness, and reduced overall survival.
Scientific Papers found: Click to Expand⟱
5175- Ash,    Withaferin A Induces Proteasome Inhibition, Endoplasmic Reticulum Stress, the Heat Shock Response and Acquisition of Thermotolerance
- in-vitro, Cerv, CCL-102
Inflam↓, In the present study, withaferin A (WA), a steroidal lactone with anti-inflammatory and anti-tumor properties, inhibited proteasome activity
AntiTum↑,
Proteasome↓,
ER Stress↑, and induced endoplasmic reticulum (ER) and cytoplasmic HSP accumulation in Xenopus laevis A6 kidney epithelial cells.
HSPs↑,
GRP94↑, WA induced the accumulation of HSPs including ER chaperones, BiP and GRP94, as well as cytoplasmic/nuclear HSPs, HSP70 and HSP30.
Akt↑, WA-induced an increase in the relative levels of the protein kinase, Akt,
eff↑, WA acted synergistically with mild heat shock to enhance HSP70 and HSP30 accumulation to a greater extent than the sum of both stressors individually
HSP70/HSPA5↑, WA Induced Accumulation of BiP, GRP94, HSP70 and HSP30

3512- Bor,    Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake
- in-vitro, Pca, DU145
TumCP↓, Treatment of DU-145 prostate cancer cells with physiological concentrations of BA inhibits cell proliferation without causing apoptosis and activates eukaryotic initiation factor 2 (eIF2α).
eIF2α↑, Phosphorylation of eIF2α occurs following BA treatment of DU-145 and LNCaP prostate cells
ATF4↑, post-treatment increases in eIF2α protein at 30 min and ATF4 and ATF6 proteins at 1 h and 30 min, respectively
ATF6↑,
GADD34↑, The increase in ATF4 was accompanied by an increase in the expression of its downstream genes growth arrest and DNA damage-induced protein 34 (GADD34) and homocysteine-induced ER protein (Herp),
CHOP↓, but a decrease in GADD153/CCAAT/enhancer-binding protein homologous protein (CHOP), a pro-apoptotic gene.
GRP78/BiP↑, The increase in ATF6 was accompanied by an increase in expression of its downstream genes GRP78/BiP, calreticulin, Grp94, and EDEM.
GRP94↑,
Risk↓, Low boron status has been associated with increased cancer risk, low bone mineralization, and retinal degeneration
*BMD↑,
Ca+2↓, LNCaP and DU-145: BA binds to cADPR and inhibits cADPR-activated Ca2+ release from the endoplasmic reticulum (ER) in a dose-dependent manner [15, 16] and lowers ER luminal Ca2+ concentrations
*Half-Life↝, lood levels of BA are dynamic, rising rapidly after a meal with an elimination half-life from 4 to 27.8 h depending on dose
IRE1∅, BA does not activate IRE1
chemoP↑, Dietary boron has been connected to three seemingly unconnected observations, increased bone mass and strength [10, 74, 75], chemoprevention

6010- CGA,    The Biological Activity Mechanism of Chlorogenic Acid and Its Applications in Food Industry: A Review
- Review, Nor, NA
*antiOx↑, mainly shown as anti-oxidant, liver and kidney protection, anti-bacterial, anti-tumor, regulation of glucose metabolism and lipid metabolism, anti-inflammatory, protection of the nervous system,
*hepatoP↑,
*RenoP↑,
AntiTum↑,
*glucose↝,
*Inflam↓,
*neuroP↑,
*ROS↓, ↓Active oxygen (ROS) , ↓Keap1,↑Nrf2, ↑SOD, ↑CAT, ↑Glutathione Peroxidase (GSH-Px), ↑Glutathione (GSH), ↓MDA
*Keap1↓,
*NRF2↑,
*SOD↑,
*Catalase↑,
*GPx↑,
*GSH↑,
*MDA↓,
*p‑ERK↑, ↑ERK1/2 phosphorylation
*GRP78/BiP↑, ↑Glucose regulatory protein 78 (GRP78)
*CHOP↑, ↑C/EBP homologous protein (CHOP)
*GRP94↑, ↑Glucose Regulatory Protein 94 (GRP94)
*Casp3↓, ↓Caspase-9/Caspase-3
*Casp9↓,
*HGF/c-Met↑, ↑Hepatocyte Growth Factor (HGF)
*TNF-α↓, ↓Tumor Necrosis Factor-α (TNF-α)/Interferonγ (IFN-γ)
*TLR4↓, ↓TLR4
*MAPK↓, ↓MAPK signal pathway
*IL1β↓, ↓Interleukin 1β (IL-1β)/Interleukin 6 (IL-6)
*iNOS↓, ↓Inducible Nitric Oxide Synthase (iNOS)
TCA↓, ↓Tricarboxylic acid cycle (TCA) ↓Glycolysis
Glycolysis↓,
Bcl-2↓, ↓Anti-apoptotic gene Bcl-2/Bcl-XL
BAX↑, ↑Pro-apoptotic gene Bax/Bcl-XS/Bad
MAPK↑, ↑p38 mitogen-activated protein kinase (p38 MAPK)
JNK↑, ↑c-Jun N-terminal Kinase (JNK)
CSCs↓, ↓Stem cell marker genes Nanog, POU5F1, Sox2, CD44, Oct4
Nanog↓,
SOX2↓,
CD44↓,
OCT4↓,
P53↑, ↑P53
P21↑, ↑p21
*SOD1↑, ↑CuZnSOD (SOD1)/MnSOD (SOD2)
*AGEs↓, ↓Glycosylation end products (AGEs)
*GLUT2↑, ↑Glucose Transporter 2 (GLUT2)
*HDL↑, ↑High-density lipoprotein (HDL)
*Fas↓, ↓Fatty acid synthase (FAS)
*HMG-CoA↓, ↓β-hydroxy-β-methylglutamyl-CoA (HMG-CoA) reductase
*NF-kB↓, ↑NF-κB signaling pathway
*HO-1↓, ↑Nrf2/HO-1 signaling pathway
*COX2↓, ↓Cyclooxygenase-2 (COX-2)
*TLR4↓, ↓Toll-like receptor 4 (TLR4)
*BioAv↑, One route may be immediate absorption in the stomach or upper gastrointestinal tract, and the other route may be slowly absorbed throughout the small intestine.
*BioAv↝, It indicates that the bioavailability of CGA is closely related to the metabolic capacity of the organism's gut flora
TumCP↓, CGA also inhibits the proliferation, migration, and invasion of cancer cells.
TumCMig↓,
TumCI↓,

3460- EP,    Picosecond pulsed electric fields induce apoptosis in HeLa cells via the endoplasmic reticulum stress and caspase-dependent signaling pathways
- in-vitro, Cerv, HeLa
tumCV↓, psPEF displayed strong growth inhibitory effects on HeLa cells.
Apoptosis↑, psPEF led to marked cell apoptosis and cell cycle arrest at the G2/M phase.
TumCCA↑,
GRP78/BiP↑, psPEF affected the phosphorylation levels of endoplasmic reticulum sensors and upregulated the expression of glucose-regulated protein 78 (GRP78), glucose-regulated protein 94 (GRP94) and CCAAT enhancer-binding protein (C/EBP) homologous protein (CH
GRP94↑,
CEBPA↑,
CHOP↑,
Ca+2↑, These changes were accompanied by the elevation of intracellular Ca2+ concentrations
Casp12↑, activation of caspase-12, -9 and -3, led to the release of cytochrome c, as well as the upregulation of Bax and the downregulation of Bcl-2, as observed in the HeLa cells.
Casp9↑,
Casp3↑,
Cyt‑c↑,
BAX↑,
Bcl-2↓,
ER Stress↑, at least partially, via the endoplasmic reticulum stress and caspase-dependent signaling pathways.
MMP↓, which subsequently leads to mitochon- drial depolarization and initiates a cell death cascade

839- Gra,    Functional proteomic analysis revels that the ethanol extract of Annona muricata L. induces liver cancer cell apoptosis through endoplasmic reticulum stress pathway
- in-vitro, Liver, HepG2
tumCV↓,
Apoptosis↑,
HSP70/HSPA5↑,
GRP94↑,
ER Stress↑, evidenced by the up-regulation of HSP70, GRP94 and PDI-related protein 5
p‑PERK↑,
p‑eIF2α↑,
GRP78/BiP↑,
CHOP↑,

2923- LT,    Luteolin induces apoptosis through endoplasmic reticulum stress and mitochondrial dysfunction in Neuro-2a mouse neuroblastoma cells
- in-vitro, NA, NA
Apoptosis↑, Luteolin induced apoptotic cell death and activation of caspase-12, -9, and -3
TumCD↑,
Casp12↑,
Casp9↑,
Casp3↑,
ER Stress↑, Luteolin also induced expression of endoplasmic reticulum (ER) stress-associated proteins, including C/EBP homologous protein (CHOP) and glucose-regulated proteins (GRP) 94 and 78, cleavage of ATF6α, and phosphorylation of eIF2α
CHOP↑,
GRP78/BiP↑,
GRP94↑,
cl‑ATF6↑,
p‑eIF2α↑,
MMP↓, rapid reduction of mitochondrial membrane potential by luteolin
JNK↓, luteolin induced activation of mitogen-activated protein kinases such as JNK, p38, and ERK
p38↑,
ERK↑,
Cyt‑c↑, cytochrome c release.

3459- MF,    EFFECT OF PULSED ELECTROMAGNETIC FIELDS ON ENDOPLASMIC RETICULUM STRESS
- in-vitro, Cerv, HeLa
GRP78/BiP↑, the expression of BiP, Grp94 and CHOP were increased in HeLa cells upon PEMF exposure.
GRP94↑,
CHOP↑,
ER Stress↓, Our main findings are that PEMF exposure (8 Hz and meant flux density of 0.56 mT) is able to reduce the elevated activity of ER stress markers induced by tunicamycin, in HepG2 cell line.

3065- RES,    Resveratrol-induced cytotoxicity in human Burkitt's lymphoma cells is coupled to the unfolded protein response
- in-vitro, lymphoma, NA
UPR↑, treatment with RES lead to the activation of all 3 branches of the UPR
IRE1↑, with early splicing of XBP-1 indicative of IRE1 activation, phosphorylation of eIF2α consistent with ER resident kinase (PERK) activation, activating transcription factor 6 (ATF6) splicing
p‑eIF2α↑,
PERK↑,
ATF6↑,
GRP78/BiP↑, increase in expression levels of the downstream molecules GRP78/BiP, GRP94 and CHOP/GADD153 in human Burkitt's lymphoma Raji and Daudi cell lines.
GRP94↑,
CHOP↑,
GADD34↑, RES induces a pathway initiated by phosphorylation of eIF2α and followed by the upregulation of GADD34 and ATF4.
ATF4↑,
XBP-1↑, RES increased XBP-1 expression both in Raji and in Daudi cells
Ca+2↑, RES was found to significantly increase cytosolic Ca2+
ER Stress↑, RES was able to induce ER stress and activated all 3 branches of the UPR.


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:


Mitochondria & Bioenergetics ⓘ

MMP↓, 2,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,   TCA↓, 1,  

Cell Death ⓘ

Akt↑, 1,   Apoptosis↑, 3,   BAX↑, 2,   Bcl-2↓, 2,   Casp12↑, 2,   Casp3↑, 2,   Casp9↑, 2,   Cyt‑c↑, 2,   GADD34↑, 2,   JNK↓, 1,   JNK↑, 1,   MAPK↑, 1,   p38↑, 1,   Proteasome↓, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

ATF6↑, 2,   cl‑ATF6↑, 1,   CHOP↓, 1,   CHOP↑, 5,   eIF2α↑, 1,   p‑eIF2α↑, 3,   ER Stress↓, 1,   ER Stress↑, 5,   GRP78/BiP↑, 6,   GRP94↑, 7,   HSP70/HSPA5↑, 2,   HSPs↑, 1,   IRE1↑, 1,   IRE1∅, 1,   PERK↑, 1,   p‑PERK↑, 1,   UPR↑, 1,   XBP-1↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   CEBPA↑, 1,   CSCs↓, 1,   ERK↑, 1,   Nanog↓, 1,   OCT4↓, 1,   SOX2↓, 1,  

Migration ⓘ

Ca+2↓, 1,   Ca+2↑, 2,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 2,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Functional Outcomes ⓘ

AntiTum↑, 2,   chemoP↑, 1,   Risk↓, 1,  
Total Targets: 58

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   HDL↑, 1,   HO-1↓, 1,   Keap1↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,   SOD1↑, 1,  

Core Metabolism/Glycolysis ⓘ

glucose↝, 1,   GLUT2↑, 1,   HMG-CoA↓, 1,  

Cell Death ⓘ

Casp3↓, 1,   Casp9↓, 1,   Fas↓, 1,   HGF/c-Met↑, 1,   iNOS↓, 1,   MAPK↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   GRP78/BiP↑, 1,   GRP94↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL1β↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   TLR4↓, 2,   TNF-α↓, 1,  

Protein Aggregation ⓘ

AGEs↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

BMD↑, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,   neuroP↑, 1,   RenoP↑, 1,  
Total Targets: 39

Scientific Paper Hit Count for: GRP94, Glucose-Regulated Protein 94
1 Ashwagandha(Withaferin A)
1 Boron
1 Chlorogenic acid
1 Electrical Pulses
1 Graviola
1 Luteolin
1 Magnetic Fields
1 Resveratrol
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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