IRF3 Cancer Research Results
IRF3, Interferon Regulatory Factor 3: Click to Expand ⟱
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Interferon Regulatory Factor 3 (IRF3) is a transcription factor that plays a crucial role in the regulation of immune responses, particularly in the context of viral infections and cancer. IRF3 is a key component of the innate immune system, which is the first line of defense against pathogens.
IRF3 has been shown to have both tumor-suppressive and tumor-promoting functions, depending on the type of cancer and the specific cellular context.
Generally, there is lower expression of IRF3 in cancer and is associated with worse prognosis in many cancers, indicating its potential role as a tumor suppressor.
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Scientific Papers found: Click to Expand⟱
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in-vitro, |
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MCF-7 |
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in-vitro, |
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MDA-MB-231 |
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TLR4↓,
IRF3↓,
IFN-γ↓,
TRIF↓,
*Inflam↓, reported by several previous studies for its potent anti-inflammatory effec
*memory↑, TQ in improving learning and memory, using a rat model of AD induced by a combination of aluminum chloride (AlCl3) and d-galactose (d-Gal).
*cognitive↑, TQ improved AD rat cognitive decline, decreased Aβ formation and accumulation, significantly decreased TNF-α and IL-1β at all levels of doses
*Aβ↓,
*TNF-α↓, Fourteen consecutive days of TQ treatment at all levels of doses caused a significant decrease in the rats brain content of TNF-α compared to AD group reaching 39.85, 18.22, and 30.37 versus 65.30, respectively
*IL1β↓, TQ at all levels of doses significantly reduced the brain content of IL-1β compared to AD group reaching 36.55, 14.32, and 27.27 versus 53.65
*TLR2↓, TQ middle dose (20 mg/kg) significantly downregulated the expression of TLR-2 by 82.74% and 77.94% and the expression of TLR-4 by 84.35% and 63.30%,
*NF-kB↓, and significantly downregulated the expression of TLRs pathway components as well as their downstream effectors NF-κB and IRF-3 mRNAs at all levels of doses
*IRF3↓, expression of IRF-3 by 18.19% and 77.96%,
TLR4↓,
MyD88↓, expression of MyD88 by 79.65% and 68.36%
TRIF↓, expression of TRIF by 25.90% and 76.75%
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Review, |
AD, |
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*antiOx↑, promising potential in the prevention and treatment of AD due to its significant antioxidative, anti-inflammatory,
*Inflam↓, anti-inflammatory activity of TQ is mediated through the Toll-like receptors (TLRs)
*AChE↓, In addition, it shows anticholinesterase activity and prevents α-synuclein induced synaptic damage.
AntiCan↑, NS plant, has been proven to have a wide range of pharmacological interventions, including antidiabetic, anticancer, cardioprotective, retinoprotective, renoprotective, neuroprotective, hepatoprotective and antihypertensive effects
*cardioP↑,
*RenoP↑,
*neuroP↑,
*hepatoP↑,
TumCG↓, potential ability to inhibit tumor growth by stimulating apoptosis as well as by suppression of the P13K/Akt pathways, cell cycle arrest and by inhibition of angiogenesis
Apoptosis↑,
PI3K↓,
Akt↑,
TumCCA↑,
angioG↓,
*NF-kB↓, TQ inhibits nuclear translocation of NF-kB which subsequently blocks the production of NF-kB mediated neuroinflammatory cytokines
*TLR2↓, TQ administration at different doses (10, 20, 40 mg/kg) significantly down-regulated the mRNA expression of TLR-2, TLR-4, MyD88, TRIF and their downstream effectors Interferon regulatory factor 3 (IRF-3)
*TLR4↓,
*MyD88↓,
*TRIF↓,
*IRF3↓,
*IL1β↓, TQ also inhibits LPS induced pro-inflammatory cytokine release like IL-1B, IL-6 and IL-12 p40/70 via its interaction with NF-kB
*IL6↓,
*IL12↓,
*NRF2↑, Nuclear erythroid-2 related factor/antioxidant response element (Nrf 2/ARE) being an upstream signaling pathway of NF-kB signaling pathway, its activation by TQ
*COX2↓, TQ also inhibits the expression of all genes regulated by NF-kB, i.e., COX-2, VEGF, MMP-9, c-Myc, and cyclin D1 which distinctively lowers NF-kB activation making it a potentially effective inhibitor of inflammation, proliferation and invasion
*VEGF↓,
*MMP9↓,
*cMyc↓,
*cycD1/CCND1↓,
*TumCP↓,
*TumCI↓,
*MDA↓, it prevents the rise of malondialdehyde (MDA), transforming growth factor beta (TGF-β), c-reactive protein, IL1-β, caspase-3 and concomitantly upregulates glutathione (GSH), cytochrome c oxidase, and IL-10 levels [92].
*TGF-β↓,
*CRP↓,
*Casp3↓,
*GSH↑,
*IL10↑,
*iNOS↑, decline of inducible nitric oxide synthase (iNOS) protein expression
*lipid-P↓, TQ prominently mitigated hippocampal lipid peroxidation and improved SOD activity
*SOD↑,
*H2O2↓, TQ is a strong hydrogen peroxide, hydroxyl scavenger and lipid peroxidation inhibitor
*ROS↓, TQ (0.1 and 1 μM) ensured the inhibition of free radical generation, lowering of the release of lactate dehydrogenase (LDH)
*LDH↓,
*Catalase↑, upsurge the levels of GSH, SOD, catalase (CAT) and glutathione peroxidase (GPX)
*GPx↑,
*AChE↓, TQ exhibited the highest AChEI activity of 53.7 g/mL in which NS extract overall exhibited 84.7 g/mL, which suggests a significant AChE inhibition.
*cognitive↑, Most prominently, TQ has been found to regulate neurite maintenance for cognitive benefits by phosphorylating and thereby activating the MAPK protein, particularly the JNK proteins for embryogenesis and also lower the expression levels of BAX
*MAPK↑,
*JNK↑,
*BAX↓,
*memory↑, TQ portrays its potential of spatial memory enhancement by reversing the conditions as observed by MWM task
*Aβ↓, TQ thus, has been shown to ameliorate the Aβ accumulation
*MMP↑, improving the cellular activity, inhibiting mitochondrial membrane depolarization and suppressing ROS
*Inflam↓, (TQ), the main active constituent of Nigella sativa oil, has been reported by several previous studies for its potent anti-inflammatory effect.
*Aβ↓, TQ improved AD rat cognitive decline, decreased Aβ formation and accumulation, significantly decreased TNF-α and IL-1β at all levels of doses
*TNF-α↓, TQ treatment at all levels of doses caused a significant decrease in the rats brain content of TNF-a compared to AD group reach-
ing 39.85, 18.22, and 30.37 versus 65.30, r
*IL1β↓,
*TLR2↓, and significantly downregulated the expression of TLRs pathway components as well as their downstream effectors NF-κB and IRF-3 mRNAs at all levels of doses ( p < 0.05).
*IRF3↓,
*TLR4↓, TQ inhibits TLR-2 and TLR-4 and their downstream signaling molecule in a dose independent manner
*memory↑, TQ improves learning and memory ability in AD rat model
*NF-kB↓, TQ at all levels of doses for
14 consecutive days caused a significant decrease in
NF-B expression
*MyD88↓, TQ middle dose (20 mg/kg) significantly downregulated the expression of TLR-2 by 82.74% and 77.94% and the expression of TLR-4
by 84.35% and 63.30%, the expression of MyD88
by 79.65% and 68.36%, the expression of TRIF by
25.90% and 76.75%,
*TRIF↓,
*BBB↑, t crosses the blood
brain barrier and exerts diverse therapeutic effects
with respect to neuroinflammation.
*cognitive↑, Thus, we can hypothesize that TQ could improve cognition and the brain morphological changes by attenuating the detrimental inflammatory effect of the pro-inflammatory cytokines release
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Review, |
Stroke, |
NA |
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*BioAv↓, TQ has poor bioavailability and is hydrophobic, prohibiting clinical trials with TQ alone.
*BioAv↑, TQ nanoparticle formulation shows better bioavailability than free TQ,
*Inflam↓, anti-inflammatory effects of TQ involve multiple complex signaling pathways as well as molecular mechanisms
*antiOx↑, antioxidant activity from the inhibition of oxidative stress
*ROS↓,
*GSH↑, GSH prevented ROS-mediated oxidative stress damage
*GSTs↑, TQ was found to exhibit antioxidant properties by increasing the levels of GSH and glutathione-S-transferase enzyme alpha-3 (GSTA3)
*MPO↓, TQ significantly reduced the disease activity index (DAI) and myeloperoxidase (MPO) activity, protecting the internal microenvironment of the colon.
*NF-kB↓, TQ reduced NF-κB signaling gene expression while alleviating the increase of COX-2 in skin cells induced by 12-O-tetradecanoylphorbol-13-acetate
*COX2↓,
*IL1β↓, reduced the expression of inflammatory factors such as IL-1β, TNF-α, IFN-γ, and IL-6
*TNF-α↓,
*IFN-γ↓,
*IL6↓,
*cardioP↑, TQ may exhibit substantial effects in the control of inflammation in CVD
*lipid-P↓, TQ reduces lipid accumulation and enhances antioxidant capacity and renal function.
*TAC↑,
*RenoP↑,
Apoptosis↑, Breast cancer TQ induces apoptosis and cell cycle arrest; reduces cancer cell proliferation, colony formation, and migration;
TumCCA↑,
TumCP↓,
TumCMig↓,
angioG↓, Colorectal Cancer (CRC) TQ inhibits the angiogenesis
TNF-α↓, Lung cancer TQ inhibits tumor cell proliferation by causing lung cancer cell apoptosis to significantly arrest the S phase cell cycle and significantly reduce the activity of TNF-a and NF-κB
NF-kB↓,
ROS↑, Pancreatic cancer TQ significantly increases the level of ROS production in human pancreatic cancer cells
EMT↓, TQ initiates the miR-877-5p and PD-L1 signaling pathways, inhibiting the migration and EMT of bladder cancer cells.
*Aβ↓, TQ significantly reduced the expression of Aβ, phosphorylated-tau, and BACE-1 proteins.
*p‑tau↓,
*BACE↓,
*TLR2↓, Parkinson’s disease (PD) TQ inhibits activation of the NF-κB pathway.
TQ reduces the expression of TLR-2, TLR-4, MyD88, TNF-α, IL-1β, IFN-β, IRF-3, and NF-κB.
*TLR4↓,
*MyD88↓,
*IRF3↓,
*eff↑, TQ pretreatment produced a dose-dependent reduction in the MI area and significantly reduced the elevation of serum cardiac markers caused by ISO.
eff↑, Curcumin and TQ induced apoptosis and cell cycle arrest and reduced cancer cell proliferation, colony formation, and migration in breast cancer cells
DNAdam↑, nanomedicine with TQ that induced DNA damage and apoptosis, inhibited cell proliferation, and prevented cell cycle progression
*iNOS↓, TQ significantly reduced the expression of COX-2 and inducible nitric oxide synthase (iNOS)
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 ⓘ
ROS↑, 1,
Cell Death ⓘ
Akt↑, 1, Apoptosis↑, 2,
DNA Damage & Repair ⓘ
DNAdam↑, 1,
Cell Cycle & Senescence ⓘ
TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, PI3K↓, 1, TumCG↓, 1,
Migration ⓘ
TumCMig↓, 1, TumCP↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 2,
Immune & Inflammatory Signaling ⓘ
IFN-γ↓, 1, MyD88↓, 1, NF-kB↓, 1, TLR4↓, 2, TNF-α↓, 1, TRIF↓, 2,
Drug Metabolism & Resistance ⓘ
eff↑, 1,
Functional Outcomes ⓘ
AntiCan↑, 1,
Infection & Microbiome ⓘ
IRF3↓, 1,
Total Targets: 20
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 2, Catalase↑, 1, GPx↑, 1, GSH↑, 2, GSTs↑, 1, H2O2↓, 1, lipid-P↓, 2, MDA↓, 1, MPO↓, 1, NRF2↑, 1, ROS↓, 2, SOD↑, 1, TAC↑, 1,
Mitochondria & Bioenergetics ⓘ
MMP↑, 1,
Core Metabolism/Glycolysis ⓘ
cMyc↓, 1, LDH↓, 1,
Cell Death ⓘ
BAX↓, 1, Casp3↓, 1, iNOS↓, 1, iNOS↑, 1, JNK↑, 1, MAPK↑, 1,
Cell Cycle & Senescence ⓘ
cycD1/CCND1↓, 1,
Migration ⓘ
MMP9↓, 1, TGF-β↓, 1, TumCI↓, 1, TumCP↓, 1,
Angiogenesis & Vasculature ⓘ
VEGF↓, 1,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, CRP↓, 1, IFN-γ↓, 1, IL10↑, 1, IL12↓, 1, IL1β↓, 4, IL6↓, 2, Inflam↓, 4, MyD88↓, 3, NF-kB↓, 4, TLR2↓, 4, TLR4↓, 3, TNF-α↓, 3, TRIF↓, 2,
Synaptic & Neurotransmission ⓘ
AChE↓, 2, p‑tau↓, 1,
Protein Aggregation ⓘ
Aβ↓, 4, BACE↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 1, eff↑, 1,
Clinical Biomarkers ⓘ
CRP↓, 1, IL6↓, 2, LDH↓, 1,
Functional Outcomes ⓘ
cardioP↑, 2, cognitive↑, 3, hepatoP↑, 1, memory↑, 3, neuroP↑, 1, RenoP↑, 2,
Infection & Microbiome ⓘ
IRF3↓, 4,
Total Targets: 60
Scientific Paper Hit Count for: IRF3, Interferon Regulatory Factor 3
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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