IRE1 Cancer Research Results

IRE1, Inositol-Requiring Enzyme 1: Click to Expand ⟱
Source:
Type:
A protein that plays a crucial role in the unfolded protein response (UPR), a cellular stress response mechanism that helps maintain endoplasmic reticulum (ER) homeostasis.
IRE1 is activated in response to ER stress, which occurs when the ER is overwhelmed with misfolded or unfolded proteins.
IRE1 is overexpressed in various types of cancer, including breast, lung, colon, and pancreatic cancer. This overexpression is often associated with poor prognosis and reduced overall survival.
Scientific Papers found: Click to Expand⟱
3206- EGCG,    Insights on the involvement of (-)-epigallocatechin gallate in ER stress-mediated apoptosis in age-related macular degeneration
- Review, AMD, NA
*Ca+2↓, EGCG restores [Ca2+]i homeostasis by decreasing ROS production through inhibition of prohibitin1 which regulate ER-mitochondrial tether site and inhibit apoptosis.
*ROS↓,
*Apoptosis↓,
*GRP78/BiP↓, EGCG downregulated GRP78, CHOP, PERK, ERO1α, IRE1α, cleaved PARP, cleaved caspase 3, caspase 12 and upregulated expression of calnexinin MRPE cells
*CHOP↓,
*PERK↓,
*IRE1↓,
*p‑PARP↓,
*Casp3↓,
*Casp12↓,
*ER Stress↓,
*UPR↓, EGCG mitigates ER stress; maintain calcium homeostasis and inhibition of UPR to control the progression of AMD.

2076- PB,    Sodium Butyrate Induces Endoplasmic Reticulum Stress and Autophagy in Colorectal Cells: Implications for Apoptosis
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT29
TumCP↓, Sodium butyrate suppressed colorectal cancer cell proliferation, induced autophagy, and resulted in apoptotic cell death
TumAuto↑,
Apoptosis↑,
ER Stress↑, sodium butyrate treatment markedly enhanced the expression of endoplasmic reticulum stress-associated proteins, including BIP, CHOP, PDI, and IRE-1a.
BID↑,
CHOP↑,
PDI↑,
IRE1↓,
LC3‑Ⅱ/LC3‑Ⅰ↑, A marked conversion of free LC3-I to heavier lipid bound LC3-II was detected after exposing HCT-116 (Fig 3A) and HT-29 (Fig 3B) cells to 2mM sodium butyrate for 24 h
LC3B↑, mRNA levels of Beclin 1 and LC3B, but not ATG3, significantly increased with increasing doses of NaBu
Beclin-1↑,
other↝, These results strongly suggested that NaB induced autophagy was mediated by ER stress in CRC cells.
other↝, Inhibition of autophagy enhanced NaB-induced apoptotic cell death

4297- QC,    Quercetin attenuates tau hyperphosphorylation and improves cognitive disorder via suppression of ER stress in a manner dependent on AMPK pathway
- in-vitro, AD, SH-SY5Y
*AMPK↑, administration of quercetin enhanced AMPK activity, inhibited IRE1α and PERK phosphorylation, NLRP3 expression and tau phosphorylation
*IRE1↓,
*p‑PERK↓,
*p‑tau↓,
*cognitive↑, and improved cognitive disorder in mice exposed to high fat diets
*antiOx↑, exert anti-oxidative, anti-ER stress, anti-inflammatory activities and regulating glucose homeostasis, which can prevent neurodegenerative disorders, diabetes, and obesity
*ER Stress↓,
*Inflam↓,
*neuroP↑,
*TXNIP↓, Quercetin and quercetin-3-O-glucuronide suppressed ER stress with decreased phosphorylation of IRE1α and PERK, thereby inhibited TXNIP and NLRP3 inflammasome activation,
*NLRP3↓, effectively protected neuronal cells from inflammatory insult by blocking ER stress/NLRP3 inflammasome activation.

3337- QC,    Endoplasmic Reticulum Stress-Relieving Effect of Quercetin in Thapsigargin-Treated Hepatocytes
- in-vitro, NA, HepG2
*Inflam↓, quercetin exerts anti-inflammatory and anti–insulin resistance actions by suppressing UPR in cells experiencing ER stress
*UPR↓,
*GRP58↓, (GRP78) and the downstream proteins such as X-box binding protein 1 (XBP1). The increased expression was significantly inhibited by quercetin, indicating that this compound can relieve ER stress
*XBP-1↓,
*ER Stress↓, previous reports as well as our results, we suggest that quercetin can inhibit ER stress in hepatocytes
*antiOx↑, Quercetin, a well-known antioxidant, is one of the most abundant flavonols in vegetables and fruits and has been shown to have many pharmacological actions
TNF-α↓, Quercetin suppressed the increased expression of TNF-α significantly and dose-dependently
p‑eIF2α↓, quercetin treatment suppressed the phosphorylation of eIF2α, IRE1α and JNK and the mRNA expression of XBP-1, GRP78 and CHOP
p‑IRE1↓,
p‑JNK↓,
CHOP↓,

3365- QC,    Quercetin attenuates sepsis-induced acute lung injury via suppressing oxidative stress-mediated ER stress through activation of SIRT1/AMPK pathways
- in-vivo, Sepsis, NA
*ER Stress↓, quercetin could inhibit the level of ER stress as evidenced by decreased mRNA expression of PDI, CHOP, GRP78, ATF6, PERK, IRE1α
*PDI↓,
*CHOP↓,
*GRP78/BiP↓,
*ATF6↓,
*PERK↓,
*IRE1↓,
*MMP↑, and improve mitochondrial function, as presented by increased MMP, SOD level and reduced production of ROS, MDA.
*SOD↑,
*ROS↓,
*MDA↓,
*SIRT1↑, quercetin upregulated SIRT1/AMPK mRNA expression.
*AMPK↑,
*Sepsis↓, quercetin could protect against sepsis-induced ALI by suppressing oxidative stress-mediated ER stress and mitochondrial dysfunction via induction of the SIRT1/AMPK pathways.

3021- RosA,    Rosmarinic acid ameliorates septic-associated mortality and lung injury in mice via GRP78/IRE1α/JNK pathway
- in-vivo, Sepsis, NA
*eff↑, RA (40 mg/kg) significantly decreased mortality and alleviated septic-associated lung injury.
*SOD↑, RA significantly reversed LPS induced decrease in serum T-aoc level and superoxide dismutase (SOD) activity, and increase in malondialdehyde (MDA) activity.
*MDA↓,
*GRP78/BiP↓, LPS induced activation of GRP78/IRE1α/JNK pathway was suppressed by RA pretreatment.
*IRE1↓,
*JNK↓,
*Sepsis↓,

3023- RosA,    Rosmarinic acid alleviates septic acute respiratory distress syndrome in mice by suppressing the bronchial epithelial RAS-mediated ferroptosis
- in-vivo, Sepsis, NA
*GPx4↑, RA notably inhibited the infiltration into the lungs of neutrophils and monocytes with increased amounts of GPX4 and ACE2 proteins, lung function improvement,
*Inflam↓, decreased inflammatory cytokines levels and ER stress in LPS-induced ARDS in mice.
*ER Stress↓,
*Ferroptosis↓, the anti-ferroptosis effect of RA in LPS-induced septic
*Sepsis↓,
*GRP78/BiP↓, Previously, we reported that RA markedly ameliorated septic-associated mortality and lung injury via inhibiting GRP78/IRE1α/JNK pathway-mediated ERS
*IRE1↓,
JNK↓,

3025- RosA,    Rosmarinic acid alleviates intestinal inflammatory damage and inhibits endoplasmic reticulum stress and smooth muscle contraction abnormalities in intestinal tissues by regulating gut microbiota
- in-vivo, IBD, NA
*GutMicro↑, RA upregulated the abundance of Lactobacillus johnsonii and Candidatus Arthromitus sp SFB-mouse-NL and downregulated the abundance of Bifidobacterium pseudolongum, Escherichia coli, and Romboutsia ilealis.
*ROCK1↓, RA downregulated the expressions of ROCK, RhoA, CaM, MLC, MLCK, ZEB1, ZO-1, ZO-2, occludin, E-cadherin, IL-1β, IL-6, TNF-α, GRP78, PERK, IRE1, ATF6, CHOP, Caspase12, Caspase9, Caspase3, Bax, Cytc, RIPK1, RIPK3, MLKL
*Rho↓,
*CaMKII ↓,
*Zeb1↓,
*ZO-1↓,
*E-cadherin↓,
*IL1β↓,
*IL6↓,
*TNF-α↓,
*GRP78/BiP↓,
*PERK↓,
*IRE1↓,
*ATF6↓,
*CHOP↓,
*Casp12↓,
*Casp9↓,
*BAX↓,
*Casp3↓,
*Cyt‑c↓,
*RIP1↓,
*MLKL↓,
*IL10↑, upregulated the expression of IL-10 and Bcl-2.
*Bcl-2↑,
*ER Stress↓, RA inhibited the inflammation, which is caused by tight junction damage, by repairing intestinal flora dysbiosis, relieved endoplasmic reticulum stress, inhibited cell death


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:


Cell Death ⓘ

Apoptosis↑, 1,   BID↑, 1,   JNK↓, 1,   p‑JNK↓, 1,  

Transcription & Epigenetics ⓘ

other↝, 2,  

Protein Folding & ER Stress ⓘ

CHOP↓, 1,   CHOP↑, 1,   p‑eIF2α↓, 1,   ER Stress↑, 1,   IRE1↓, 1,   p‑IRE1↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   LC3B↑, 1,   TumAuto↑, 1,  

Migration ⓘ

TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

PDI↑, 1,  

Immune & Inflammatory Signaling ⓘ

TNF-α↓, 1,  
Total Targets: 18

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Ferroptosis↓, 1,   GPx4↑, 1,   MDA↓, 2,   ROS↓, 2,   SOD↑, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2,   SIRT1↑, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   BAX↓, 1,   Bcl-2↑, 1,   Casp12↓, 2,   Casp3↓, 2,   Casp9↓, 1,   Cyt‑c↓, 1,   Ferroptosis↓, 1,   GRP58↓, 1,   JNK↓, 1,   MLKL↓, 1,   RIP1↓, 1,  

Kinase & Signal Transduction ⓘ

CaMKII ↓, 1,  

Protein Folding & ER Stress ⓘ

ATF6↓, 2,   CHOP↓, 3,   ER Stress↓, 6,   GRP78/BiP↓, 5,   IRE1↓, 6,   PERK↓, 3,   p‑PERK↓, 1,   UPR↓, 2,   XBP-1↓, 1,  

DNA Damage & Repair ⓘ

p‑PARP↓, 1,  

Migration ⓘ

Ca+2↓, 1,   E-cadherin↓, 1,   Rho↓, 1,   ROCK1↓, 1,   TXNIP↓, 1,   Zeb1↓, 1,   ZO-1↓, 1,  

Angiogenesis & Vasculature ⓘ

PDI↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL10↑, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 3,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

p‑tau↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

cognitive↑, 1,   neuroP↑, 1,  

Infection & Microbiome ⓘ

Sepsis↓, 3,  
Total Targets: 53

Scientific Paper Hit Count for: IRE1, Inositol-Requiring Enzyme 1
3 Quercetin
3 Rosmarinic acid
1 EGCG (Epigallocatechin Gallate)
1 Phenylbutyrate
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#:618  State#:%  Dir#:1
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