GADD34 Cancer Research Results

GADD34, Growth Arrest and DNA Damage-inducible protein 34: Click to Expand ⟱
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GADD34 (Growth Arrest and DNA Damage-inducible protein 34) is a protein that plays a crucial role in the regulation of cell growth, apoptosis, and DNA damage response.
GADD34 has been shown to promote tumor growth, invasion, and metastasis by facilitating cell proliferation, survival, and angiogenesis.
GADD34 has been found to be highly expressed in cancer stem cells, which are thought to be responsible for cancer initiation, progression, and recurrence.
Scientific Papers found: Click to Expand⟱
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

737- Bor,    Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Statu
- in-vitro, Pca, DU145
Risk↓, intake is associated with reduced risk of cancer and DNA damage and increased antioxidant status.
p‑eIF2α↑,
ATF4↑,
GADD34↑,

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.

4501- SeNPs,    Mechanisms of the Cytotoxic Effect of Selenium Nanoparticles in Different Human Cancer Cell Lines
- in-vitro, GBM, A172 - in-vitro, Colon, Caco-2 - in-vitro, Pca, DU145 - in-vitro, BC, MCF-7 - in-vitro, Nor, L929
*BioAv↑, In recent decades, studies on the functional features of Se nanoparticles (SeNP) have gained great popularity due to their high biocompatibility, stability, and pronounced selectivity
selectivity↑,
AntiCan↑, A large number of works prove the anticarcinogenic effect of SeNP
Apoptosis↑, SeNP concentration-dependently caused cancer cell apoptosis, but not necrosis
CHOP↑, significant increase in the expression of CHOP, GADD34, BIM, and PUMA
GADD34↑,
BIM↑,
PUMA↑,
Ca+2↝, SeNP Triggered Ca2+ Signals in All Investigated Cancer Cell Lines


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death ⓘ

Apoptosis↑, 1,   BIM↑, 1,   GADD34↑, 4,   PUMA↑, 1,  

Protein Folding & ER Stress ⓘ

ATF6↑, 2,   CHOP↓, 1,   CHOP↑, 2,   eIF2α↑, 1,   p‑eIF2α↑, 2,   ER Stress↑, 1,   GRP78/BiP↑, 2,   GRP94↑, 2,   IRE1↑, 1,   IRE1∅, 1,   PERK↑, 1,   UPR↑, 1,   XBP-1↑, 1,  

Migration ⓘ

Ca+2↓, 1,   Ca+2↑, 1,   Ca+2↝, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 3,  

Drug Metabolism & Resistance ⓘ

selectivity↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoP↑, 1,   Risk↓, 2,  
Total Targets: 26

Pathway results for Effect on Normal Cells:


Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

BMD↑, 1,  
Total Targets: 3

Scientific Paper Hit Count for: GADD34, Growth Arrest and DNA Damage-inducible protein 34
2 Boron
1 Resveratrol
1 Selenium NanoParticles
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#:865  State#:%  Dir#:2
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