IL23 Cancer Research Results
IL23, Interleukin 23: Click to Expand ⟱
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A heterodimeric cytokine composed of an IL-12B subunit and an IL-23A subunit. IL-23 is part of the IL-12 family of cytokines.
IL-23 is an inflammatory cytokine. IL-23 is overexpressed in a number of cancer types.
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Scientific Papers found: Click to Expand⟱
*antiOx↑, Curcumin, a natural compound with potent antioxidant and anti-inflammatory properties
*Inflam↓,
*AntiAge↑, Its potential anti-aging properties are due to its power to alter the levels of proteins associated with senescence, such as adenosine 5′-monophosphate-activated protein kinase (AMPK) and sirtuins
*AMPK↑,
*SIRT1↑,
*NF-kB↓, preventing pro-aging proteins, such as nuclear factor-kappa-B (NF-κB) and mammalian target of rapamycin (mTOR)
*mTOR↓,
*NLRP3↓, Moreover, curcumin, by inhibiting the NF-κB pathway, can directly restrain the assembly or even inhibit the activation of the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome
*NADPH↓, by inhibiting nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and elevating the activity of antioxidant enzymes and consequently lowering reactive oxygen species (ROS)
*ROS↓,
*COX2↓, (COX-2), granulocyte colony-stimulating factor (G-CSF), and monocyte chemotactic protein-1 (MCP-1) can be decreased by curcumin
*MCP1↓,
*IL1β↓, by decreasing IL-1β, IL-17, IL-23, TNF-α, and myeloperoxidase, enhancing levels of IL-10, and downregulating activation of NF-κB
*IL17↓,
*IL23↓,
*TNF-α↓,
*MPO↓,
*IL10↑,
*lipid-P↓, curcumin showed a significant decline in lipid peroxidation and increased superoxide dismutase levels, in addition to a reduction in Aβ aggregation and tau hyperphosphorylation through the regulation of GSK3β, Cdk5, p35, and p25
*SOD↑,
*Aβ↓,
*p‑tau↓,
*GSK‐3β↓,
*CDK5↓,
*TXNIP↓, Curcumin also has an inhibitory role on the thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome pathway
*NRF2↑, well as upregulation of Nrf2, NAD(P)H quinine oxidoreductase 1 (NQO1), HO-1, and γ-glutamyl cysteine synthetase (γ-GCS) in brain cells.
*NQO1↑,
*HO-1↑,
*OS↑, significant improvement in OS, and a positive evolution in memory and spatial learning
*memory↑,
*BDNF↑, Besides that, it promoted neurogenesis through increasing brain-derived neurotrophic factor (BDNF) levels
*neuroP↑, Curcumin can promote neuroprotection
*BACE↓, Figure 7
*AChE↓, figure 7
*LDL↓, and reduced total cholesterol and LDL levels.
*antiOx↑, shows potent antioxidant, antimicrobial, and immunoregulatory activities
*OS↑, JUG treatment significantly ameliorated body weight loss and disease activity index and improved the survival probability, colon length, and tissue damage.
*IL6↓, JUG reversed the DSS-induced up-regulation of proinflammatory cytokines, including interleukin (IL)-6, 12, 21, and 23, and tumor necrosis factor-alpha, and anti-inflammatory cytokines, such as IL-10 and transforming growth factor-beta,
*IL12↓,
*IL23↓,
*TNF-α↓,
*Inflam↓,
*NF-kB↓, the activation of mitochondrial uncoupling protein 2 and phospho-Nuclear Factor-kappa B p65 and the inhibition of the kelch-like ECH-associated protein 1 and NF-E2-related factor 2 induced by DSS were also reversed under JUG administration.
*NFE2L2↓,
*ROS↓, JUG could be a promising agent for UC prevention to regulate inflammatory cytokines and oxidative stress.
BMD↑, loss reduced
Cartilage↑, more intact cartilage surfaces and denser proteoglycan
IL17↓,
IL22↓,
IL23↓,
IL28↓,
CD4+↓, tremendously attenuated
CD8+↓, In this investigation, data showed that RMF treatment decreased CD3-expressing proliferative cells via immunostaining and reduced CD4+/CD8+ T-cells via flow cytometry in AS mice
LAMB3↑,
COL4↓,
THBS2↓,
ITGA11↓,
PPARγ↑, mice have decreased expression of peroxisome proliferator-activated receptor γ (PPAR-γ), a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily, which RMF reverses.
ACAA1↓,
PLIN1↓,
FABP4↓,
PCK1↓,
UCP1↓,
TNF-α↓,
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NA |
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AD, |
NA |
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*other↝, Nimbolide is one of the most potent limonoids derived from the flowers and leaves of neem (Azadirachta indica), which is widely used to treat a variety of human diseases.
*Inflam↓, Nimbolide has anti-inflammatory, anti-microbial, and anti-cancer properties, which make it an intriguing compound for research.
AntiCan↑,
*Bacteria↓, pharmacological properties including antimalaria, antibacterial, antiviral, antioxidative, anti-inflammatory, antiinvasive, neuroprotective, hepatoprotective, and pro-apoptotic properties
*AntiViral↑,
*neuroP↑,
*hepatoP↑,
*ROS?, Inhibit oxidative stress, Activate Nrf2/HO-1 signaling
*NRF2↑,
*HO-1↑,
*TLR4↓, Inhibit oxidative stress Anti-inflammatory and antioxidant TLR4/NF-κB signaling pathway
*NF-kB↓,
*AChE↓, down regulation of AChE and Aβ GSK-3β interaction
*Aβ↓,
*GSK‐3β↓,
*LDL↓, Nimbolide reduced intracellular cholesterol, free fatty acids, and triglycerides and enhanced hepatocyte function by inhibiting oxidative DNA damage and lipid peroxidation through its antioxidant effects
*DNAdam↓,
*lipid-P↓,
*antiOx↑, Nimbolide showed immense antioxidant properties.
*SOD1↑, nimbolide treatment increased superoxide dismutase (SOD-1), Nrf-2, GSH, and HO-1 protein expression
*GSH↑,
*IL6↓, Nimbolide treatment resulted in a reduction of the inflammatory cytokines IL-6, IL-1β, and TNF-α, as well as inflammatory cellular signaling molecules IkB-α, STAT3, and NF-kB.
*IL1β↓,
*STAT3↓,
*GPx↑, Glutathione peroxidase, catalase (CAT), concentration were all found to be up, while malondialdehyde and nitric oxide levels were shown to be significantly reduced by nimbolide.
*Catalase↑,
*MDA↓,
*AntiDiabetic↑, Anti-diabetic effect of nimbolide in diabetes
*HDL↓, suppression of the levels of pro-inflammatory mediators, (cholesterol, TG, LDL, and HDL, MCP-1, VEGF, and MMP-9)
*MCP1↓,
*VEGF↓,
*MMP9↓,
*GutMicro↑, nimbolide showed to reduce inflammation, oxidative stress, and to reverse gut microbiota, which protects them from gestational diabetes.
TumCP↓, Nimbolide reported to decrease cell proliferation, EMT, cell cycle progression, and migration, in breast cancer cells via downregulating the NF-κB pathway
TumCCA↑,
TumCMig↓,
NF-kB↓,
ROS↑, nimbolide stimulates the overproduction of ROS, consequently modulating both autophagy and apoptosis in pancreatic cancer cells.
PI3K↓, nimbolide-induced ROS generation hindered cell proliferation by suppressing PI3K/AKT/mTOR and ERK signaling pathways.
Akt↓,
mTOR↓,
ERK↓,
EMT↓, nimbolide-mediated ROS generation reduced EMT, migration, colony forming abilities and invasion, thereby inhibiting metastasis.
TumMeta↓,
ChemoSen↑, use of nimbolide in combination with 5-FU showed a higher inhibitory rate in breast cancer than 5-FU alone
eff↑, nimbolide synergized the effect of TRAIL to induce apoptosis in tumor cell lines, but not normal breast cells
selectivity↑,
CDK4↓, slows tumor growth by inhibiting CDK4/6 activity
CDK6↓,
Wnt↓, nimbolide suppressed the Wnt/β-catenin signaling pathway mediated by NF-κB in HCC and pancreatic cancer cells
β-catenin/ZEB1↓,
STAT3↓, nimbolide can significantly suppress the activation of oncogenic transcription factor STAT3.
MMP2↓, inhibits tumor cell growth and migration by downregulating VEGF-A and MMP-2/9 expression,
Sp1/3/4↓, nimbolide inhibited MMP-9 activity by inhibiting the binding activity of Sp-1, AP-1 and NFk-B motifs, all of which are important transcription factors.
AP-1↓,
P21↑, Nimbolide exhibited dose-dependent inhibitory effects on HeLa cell viability by causing cell cycle arrest at G0/G1 phase with p53-dependent accumulation of p21.
*AntiArt↑, The findings of the study suggest that nimbolide has the ability to reduce the severity of rheumatoid arthritis by suppressing the expression levels of toll-like receptors, IL-23, IL-17, IFN-γ and HSP70.
*IL23↓,
*IL17↓,
*IFN-γ↓,
*HSP70/HSPA5↓,
Dose↝, India: ar-turmerone 16.7–25.7%, α-turmerone 30.1–32.0%, β-turmerone 14.7–18.4%
Casp3↑, Ar-turmerone has been shown to induce apoptosis in human lymphoma and lymphoblast cells through the activation of caspase-3
MMP9↓, ar-turmerone significantly inhibits the TPA-induced upregulation of MMP-9 and COX-2 expression in human breast cancer cells, effectively blocking critical signaling pathways such as NF-kB, PI3K/Akt, and ERK1/2
COX2↓,
NF-kB↓,
PI3K↓,
Akt↓,
ERK↓,
Inflam↓, Ar-turmerone also mitigates skin inflammation by lowering the levels of TNF-α and IL-6 while downregulating the mRNA synthesis of IL-17, IL-22, and IL-23.
TNF-α↓,
IL6↓,
IL17↓,
IL22↓,
IL23↓,
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(tgid=1) ⓘ
ROS↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
UCP1↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ACAA1↓, 1, FABP4↓, 1, PCK1↓, 1, PLIN1↓, 1, PPARγ↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 2, Casp3↑, 1,
Kinase & Signal Transduction(tgid=6) ⓘ
Sp1/3/4↓, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK4↓, 1, P21↑, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
EMT↓, 1, ERK↓, 2, mTOR↓, 1, PI3K↓, 2, STAT3↓, 1, Wnt↓, 1,
Migration(tgid=13) ⓘ
AP-1↓, 1, Cartilage↑, 1, COL4↓, 1, ITGA11↓, 1, LAMB3↑, 1, MMP2↓, 1, MMP9↓, 1, THBS2↓, 1, TumCMig↓, 1, TumCP↓, 1, TumMeta↓, 1, β-catenin/ZEB1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD4+↓, 1, COX2↓, 1, IL17↓, 2, IL22↓, 2, IL23↓, 2, IL28↓, 1, IL6↓, 1, Inflam↓, 1, NF-kB↓, 2, TNF-α↓, 2,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CDK6↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 1, Dose↝, 1, eff↑, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
BMD↑, 1, IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1,
Infection & Microbiome(tgid=24) ⓘ
CD8+↓, 1,
Total Targets: 50
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiArt↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 3, Catalase↑, 1, GPx↑, 1, GSH↑, 1, HDL↓, 1, HO-1↑, 2, lipid-P↓, 2, MDA↓, 1, MPO↓, 1, NFE2L2↓, 1, NQO1↑, 1, NRF2↑, 2, ROS?, 1, ROS↓, 2, SOD↑, 1, SOD1↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
AMPK↑, 1, LDL↓, 2, NADPH↓, 1, SIRT1↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↝, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
HSP70/HSPA5↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
GSK‐3β↓, 2, mTOR↓, 1, STAT3↓, 1,
Migration(tgid=13) ⓘ
CDK5↓, 1, MMP9↓, 1, TXNIP↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
VEGF↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2↓, 1, IFN-γ↓, 1, IL10↑, 1, IL12↓, 1, IL17↓, 2, IL1β↓, 2, IL23↓, 3, IL6↓, 2, Inflam↓, 3, MCP1↓, 2, NF-kB↓, 3, TLR4↓, 1, TNF-α↓, 2,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 2, BDNF↑, 1, p‑tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 2, BACE↓, 1, NLRP3↓, 1,
Clinical Biomarkers(tgid=22) ⓘ
GutMicro↑, 1, IL6↓, 2,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiDiabetic↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 2, OS↑, 2,
Infection & Microbiome(tgid=24) ⓘ
AntiViral↑, 1, Bacteria↓, 1,
Total Targets: 60
Scientific Paper Hit Count for: IL23, Interleukin 23
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#:543 State#:% Dir#:1
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