Imm Cancer Research Results
Imm, immunostimulatory: Click to Expand ⟱
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Enhance the immune response in patients.
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Scientific Papers found: Click to Expand⟱
TumCP↓, mechanism of action of celastrol in terms of inhibition of cell proliferation and regulation of the cell cycle, regulation of apoptosis and autophagy, inhibition of cell invasion and metastasis, anti-inflammation, regulation of immunotherapy, and an
TumCCA↑,
Apoptosis↑,
TumAuto↑,
TumCI↓,
TumMeta↓,
Imm↝,
angioG↓,
Cyt‑c↑, release of cytochrome c (CytC)
ROS↑, increasing ROS levels, and activating the mitochondrial apoptosis pathway
BAX↑, upregulating the expression of CytC and the pro-apoptotic protein Bax, activating caspase-3 and caspase-9, and leading to the cleavage of PARP
Casp3↑,
Casp9↑,
cl‑PARP↑,
PrxII↓, binds to peroxiredoxin-2 (Prdx2) and inhibits its enzyme activity,
ER Stress↑, resulting in ROS-dependent endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and apoptosis in gastric cancer cells
mtDam↑,
CHOP/DDIT3↑, celastrol upregulates the expression of CHOP, Bip, XBP1s, and IRE1 proteins,
Inflam↓, Anti-inflammatory properties of celastrol
NF-kB↓, Celastrol additionally obstructed NF-κB and its downstream gene products, such as CXCR4 and MMP9, and reduced serum IL-6 and TNF-α levels to inhibit cell invasion and migration in vivo
CXCR4↓,
MMP9↓,
IL6↓,
TNF-α↓,
HSP90↓, accumulation may be due to the inhibition of HSP90 and the stress response
neuroP↑, Our mass spectrometry research also showed that celastrol directly binds to HSP90 and HSP70, exerting antitumor and neuroprotective effects
STAT3↓, Celastrol exerts anti-tumor activity by inhibiting STAT3
Prx↓, celastrol binds directly to Prdx1, Prdx2, Prdx4, and Prdx6 via active cysteine sites, inhibiting their antioxidant activity without affecting protein expression
HO-1↑, Celastrol also targeted heme oxygenase-1 (HO-1), increasing its expression in activated hematopoietic stem cells
eff↑, Research has indicated that celastrol, combined with 17-N-Allylamino-17-demethoxygeldanamycin (17-AAG), inhibits the toxic stress response of HSP90-targeted proteins, reduces the sensitization of human glioblastomas to celastrol treatment, an
eff↑, celastrol, when combined with EGFR tyrosine kinase inhibitors (EGFR-TKIs), effectively inhibits the growth and invasion of T790M mutant human lung cancer H1975
BioAv↑, nano-delivery systems present a novel pathway for the development and clinical application of celastrol, potentially overcoming existing limitations and maximizing its therapeutic potential.
toxicity↑, several significant challenges, including its pronounced hepatic and renal toxicity and potential for causing immunosuppression
CardioT↑, celastrol, which includes hepatotoxicity, cardiotoxicity, infertility toxicity, hematopoietic system toxicity and nephrotoxicity.
hepatoP↓,
*Inflam↓, Fucoidan, a sulfated polysaccharide derived from brown seaweeds, exhibits notable anti-inflammatory, antioxidant, and anticancer properties.
*antiOx↑,
AntiCan↑,
BioAv↑, Researchers have explored fucoidan-based nanoparticles to improve its solubility, enhance tumor-targeting efficiency, and expand its therapeutic potential.
Apoptosis↑, fucoidan induces cancer cell apoptosis, suppresses angiogenesis, and modulates immune responses.
angioG↓,
Imm↝,
ChemoSen↑, When combined with chemotherapeutics, siRNA, or immunomodulators, fucoidan nanoparticles exhibit synergistic anticancer effects while minimizing systemic toxicity.
chemoP↑,
antiOx↑, anti-oxidant, antiviral, immunoregulatory, anti-coagulant, anti-thrombotic, anti-lipidemic, anti-diabetic, anti-tumor, anti-metastatic, and anti-angiogenic properties
AntiViral↑,
Imm↝,
*AntiThr↑,
*AntiDiabetic↑,
AntiTum↑,
TumMeta↑,
angioG↓,
Hif1a↓, ↓ HIF-1α and VEGF in hypoxic-like conditions
VEGF↓,
MMPs↓, ↓ MMPs
EMT↓, ↓ EMT (↓ N-cadherin; ↑ E-cadherin)
N-cadherin↓,
E-cadherin↑,
TIMP1↑, ↑ TIMP
PI3K↓, ↓ PI3K/Akt/mTOR
Akt↓,
mTOR↓,
MMP2↓, ↓ MMP-2, 9
ChemoSen↑, available findings indicate that oral intake of fucoidan as dietary supplement in combination with conventional adjuvant chemotherapy can prolong survival time, decrease some adverse effects (e.g., fatigue)
OS↑,
fatigue↓,
CD31/PECAM-1↓, fig 2
angioG↓, HNE exerted anti-angiogenetic effects in HUVEC and anti-proliferative effects in five cancer cell lines
TumCP↓,
*Inflam↓, a broad pharmacological spectrum is ascribed to Christmas rose: anti-bacterial, anti-inflammatory, cholesterol- and blood glucose-lowering, neuroprotective, hepatoprotective and immune-modulating effects.
*Bacteria↓,
*glucose↓,
*neuroP↓,
*hepatoP↓,
*Imm↝,
ChemoSen↑, It enhances the efficacy of chemotherapies, such as cisplatin and paclitaxel, RTK inhibitors, such as cabozantinib and erlotinib, and mAbs, such as cetuximab.
Imm↝, honokiol aids in post-transplant cancer prevention by modulating immune responses, reducing tumor progression, and lowering the required dose of immunosuppressants, such as cyclosporine A and rapamycin.
*hepatoP↑, figure1
*cardioP↑,
*neuroP↑,
*AntiCan↑,
*Inflam↓,
*antiOx↑,
eff↑, By lowering systemic glucose levels, metformin limits the energy supply available to cancer cells, thereby inhibiting their growth and proliferation. Studies have shown that combining metformin with honokiol yields promising synergistic effects.
*TNF-α↓, potent anti-inflammatory properties, contributing to its anti-cancer effects. It inhibits the production of key pro-inflammatory cytokines, including tumor necrosis factor-alpha, IL-1 beta, and IL-6,
*IL1?,
*IL6?,
*BioAv↓, pharmacokinetic studies indicate that following oral administration, only a small portion of isovitexin is directly absorbed, while the majority is transferred to the intestine and metabolized by gut microbiota.
*Imm↝, Isovitexin demonstrates diverse biological activities, including immunomodulatory, antioxidant properties, anticancer activity, neuroprotection, regulation of bone homeostasis, and hepatoprotective effects.
*antiOx↑,
*AntiCan↑,
*neuroP↑,
*hepatoP↑,
*Inflam↓, These activities are mediated through multiple mechanisms, including anti-inflammatory effects through inhibition of the Nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase pathways,
*NF-kB↓,
*MAPK↓,
*MPO↓, antioxidant effects by suppression of myeloperoxidase activity and the scavenging of reactive oxygen species (ROS), and anticancer activity by promoting autophagy and apoptosis.
*ROS↓,
TumAuto↑,
Apoptosis↑,
Apoptosis↑, 20 Hz; 3 mT, 60mins/day PEMFs increased apoptosis in MCF7 cells but had no effect on MCF10 cells
selectivity↑,
ROS↑, 50 Hz, 0.1–1.0 mT) for 30 min, and long‐term PEMF: undifferentiated PC12 cells increased ROS levels and decreased catalase activity
Catalase↓,
TumVol↓, 1 Hz, 100 mT, Mice exposed for 60 and 180 min daily showed a 30% and 70% tumor reduction
angioG↓, PEMFs inhibit angiogenesis in tumor tissues, suppressing tumor vascularization and reducing tumor growth, as shown by in vivo studies
Ca+2↝, During immediate PEMF exposure in undifferentiated PC12 cells, no change in intracellular Ca2+ concentration was observed, while it increased after long‐term exposure.
eff↝, undifferentiated PC12 cells were more sensitive to PEMFs exposure, while the differentiated PC12 cells were more stable and resistant to stress, probably due to the action of the cell surface NGF receptors such as p75NR
angioG↓, PEMFs inhibit angiogenesis in tumor tissues, suppressing tumor vascularization and reducing tumor growth, as shown by in vivo studies 95, 96, 97, 98, 99, 104.
Imm↝, PEMFs have also an immunomodulatory effect, as supported by in vivo evidence showing an increase in tumor necrosis factor alpha levels that induce an anti‐tumoral response
TNF-α↑,
Casp8↑, leading to the activation of a proapoptotic pathway induced by caspase‐8 interaction with Fas‐associated death domain,
Showing Research Papers: 1 to 7 of 7
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, Catalase↓, 1, HO-1↑, 1, Prx↓, 1, PrxII↓, 1, ROS↑, 2,
Mitochondria & Bioenergetics(tgid=3) ⓘ
mtDam↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Apoptosis↑, 4, BAX↑, 1, Casp3↑, 1, Casp8↑, 1, Casp9↑, 1, Cyt‑c↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↑, 1, ER Stress↑, 1, HSP90↓, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
TumAuto↑, 2,
DNA Damage & Repair(tgid=10) ⓘ
cl‑PARP↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
TumCCA↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
EMT↓, 1, mTOR↓, 1, PI3K↓, 1, STAT3↓, 1,
Migration(tgid=13) ⓘ
Ca+2↝, 1, CD31/PECAM-1↓, 1, E-cadherin↑, 1, MMP2↓, 1, MMP9↓, 1, MMPs↓, 1, N-cadherin↓, 1, TIMP1↑, 1, TumCI↓, 1, TumCP↓, 2, TumMeta↓, 1, TumMeta↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 6, Hif1a↓, 1, VEGF↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CXCR4↓, 1, IL6↓, 1, Imm↝, 5, Inflam↓, 1, NF-kB↓, 1, TNF-α↓, 1, TNF-α↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 2, ChemoSen↑, 3, eff↑, 3, eff↝, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, AntiTum↑, 1, CardioT↑, 1, chemoP↑, 1, fatigue↓, 1, hepatoP↓, 1, neuroP↑, 1, OS↑, 1, toxicity↑, 1, TumVol↓, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiViral↑, 1,
Total Targets: 63
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 3, MPO↓, 1, ROS↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
glucose↓, 1,
Cell Death(tgid=5) ⓘ
MAPK↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
AntiThr↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IL1?, 1, IL6?, 1, Imm↝, 2, Inflam↓, 4, NF-kB↓, 1, TNF-α↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1,
Clinical Biomarkers(tgid=22) ⓘ
IL6?, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 2, AntiDiabetic↑, 1, cardioP↑, 1, hepatoP↓, 1, hepatoP↑, 2, neuroP↓, 1, neuroP↑, 2,
Infection & Microbiome(tgid=24) ⓘ
Bacteria↓, 1,
Total Targets: 22
Scientific Paper Hit Count for: Imm, immunostimulatory
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#:1332 State#:% Dir#:4
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