IL1α Cancer Research Results
IL1α, interleukin-1 alpha: Click to Expand ⟱
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The term "IL-1" is often used as an umbrella term for the interleukin-1 family, which includes multiple cytokines. The two best-known members are IL-1α and IL-1β.
L-1α: Often expressed as a precursor that is biologically active even before processing; it can be active in its intracellular form and when expressed on the cell surface.
IL-1α is typically associated with cell damage and tends to act more locally.
High IL-1α levels have been detected in a number of tumor cells and have been associated with enhanced tumor invasion and metastasis in several settings.
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Scientific Papers found: Click to Expand⟱
IL1α↓, berry extracts in silver nanoparticles instead to obtain a particle size ranging from 20 to 80 nm and a significantly reduced production of IL-1 α compared to the control cells
other↝, hyperproliferation of keratinocytes as the psoriatic skin cell lifetime is more than six times shorter than that of normal skin cells, this is thought to be due to hyperactivity of growth factors
TNF-α↓, Apigenin downregulates the TNFα
IL6↓,
IL1α↓,
P53↑,
Bcl-xL↓,
Bcl-2↓,
BAX↑,
Hif1a↓, Apigenin inhibited HIF-1alpha and vascular endothelial growth factor expression
VEGF↓,
TumCCA↑, Apigenin exposure induces G2/M phase cell cycle arrest, DNA damage, apoptosis and p53 accumulation
DNAdam↑,
Apoptosis↑,
CycB/CCNB1↓,
cycA1/CCNA1↓,
CDK1↓,
PI3K↓,
Akt↓,
mTOR↓,
IKKα↓, , decreases IKKα kinase activity,
ERK↓,
p‑Akt↓,
p‑P70S6K↓,
p‑S6↓,
p‑ERK↓, decreased
the expression of phosphorylated (p)-ERK1/2 proteins, p-AKT and p-mTOR
p‑P90RSK↑,
STAT3↓,
MMP2↓, Apigenin down-regulated Signal transducer and activator of transcription 3target genes MMP-2, MMP-9 and vascular endothelial growth factor
MMP9↓,
TumCP↓, Apigenin significantly suppressed colorectal cancer cell proliferation, migration, invasion and organoid growth through inhibiting the Wnt/β-catenin signaling
TumCMig↓,
TumCI↓,
Wnt/(β-catenin)↓,
*Inflam↓, profound application as a traditional remedy for various ailments, especially inflammatory diseases including asthma, arthritis, cerebral edema, chronic pain syndrome, chronic bowel diseases, cancer
AntiCan↑,
*MAPK↑, 11-keto-BAs can stimulate Mitogen-activated protein kinases (MAPK) and mobilize the intracellular Ca(2+) that are important for the activation of human polymorphonuclear leucocytes (PMNL)
*Ca+2↝,
p‑ERK↓, AKBA prohibited the phosphorylation of extracellular signal-regulated kinase-1 and -2 (Erk-1/2) and impaired the motility of meningioma cells stimulated with platelet-derived growth factor BB
TumCI↓,
cycD1/CCND1↓, In the case of colon cancer, BA treatment on HCT-116 cells led to a decrease in cyclin D, cyclin E, and Cyclin-dependent kinases such as CDK2 and CDK4, along with significant reduction in phosphorylated Rb (pRb)
cycE/CCNE↓,
CDK2↓,
CDK4↓,
p‑RB1↓,
*NF-kB↓, convey inhibition of NF-kappaB and subsequent down-regulation of TNF-alpha expression in activated human monocytes
*TNF-α↓,
NF-kB↓, PC-3 prostate cancer cells in vitro and in vivo by inhibiting constitutively activated NF-kappaB signaling by intercepting the activity of IkappaB kinase (IKK
IKKα↓,
MCP1↓, LPS-challenged ApoE-/- mice via inhibition of NF-κB and down regulation of MCP-1, MCP-3, IL-1alpha, MIP-2, VEGF, and TF
IL1α↓,
MIP2↓,
VEGF↓,
Tf↓,
COX2↓, pancreatic cancer cell lines, AKBA inhibited the constitutive expression of NF-kB and caused suppression of NF-kB regulated genes such as COX-2, MMP-9, CXCR4, and VEGF
MMP9↓,
CXCR4↓,
VEGF↓,
eff↑, AKBA and aspirin revealed that AKBA has higher potential via modulation of the Wnt/β-catenin pathway, and NF-kB/COX-2 pathway in adenomatous polyps
PPARα↓, AKBA is also responsible for down-regulation of PPAR-alpha and C/EBP-alpha in a dose and temporal dependent manner in mature adipocytes, ultimately leading to pparlipolysis
lipid-P?,
STAT3↓, activation of STAT-3 in human MM cells could be inhibited by AKBA
TOP1↓, (PKBA; a semisynthetic analogue of 11-keto-β-boswellic acid), had been reported to influence the activity of topoisomerase I & II,
TOP2↑,
5HT↓, (5-LO), responsible for catalyzing the synthesis of leukotrienes from arachidonic acid and human leucocyte elastase (HLE), and serine proteases involved in several inflammatory processes, is considered to be a potent molecular target of BA derivative
p‑PDGFR-BB↓, BA up-regulates SHP-1 with subsequent dephosphorylation of PDGFR-β and downregulation of PDGF-dependent signaling after PDGF stimulation, thereby exerting an anti-proliferative effect on HSCs hepatic stellate cells
PDGF↓,
AR↓, AKBA targets different receptors that include androgen receptor (AR), death receptor 5 (DR5), and vascular endothelial growth factor receptor 2 (VEGFR2), and leads to the inhibition of proliferation of prostate cancer cells
DR5↑, induced expression of DR4 and DR5.
angioG↓, via apoptosis induction and suppression of angiogenesis
DR4↑,
Casp3↑, AKBA resulted in activation of caspase-3 and caspase-8, and initiation of poly (ADP) ribose polymerase (PARP) cleavage.
Casp8↑,
cl‑PARP↑,
eff↑, AKBA was preincubated with LY294002 or wortmannin (inhibitors of PI3K), it caused a significant enhancement of apoptosis in HT-29 cells
chemoPv↑, chemopreventive response of AKBA was estimated against intestinal adenomatous polyposis through the inhibition of the Wnt/β-catenin and NF-κB/cyclooxygenase-2 signaling pathway
Wnt↓,
β-catenin/ZEB1↓,
ascitic↓, AKBA by the suppression of ascites,
Let-7↑, AKBA could up-regulate the expression of let-7 and miR-200
miR-200b↑,
eff↑, anti-tumorigenic effects of curcumin and AKBA on the regulation of specific cancer-related miRNAs in colorectal cancer cells, and confirmed their protective action
MMP1↓, . It can inhibit the expression of MMP-1, MMP-2, and MMP-9 mRNAs along with secretions of TNF-α and IL-1β in THP-1 cells.
MMP2↓,
eff↑, combined administration of metformin, an anti-diabetic drug, and boswellic acid nanoparticles exhibited significant synergism through the inhibition of MiaPaCa-2
pancreatic cancer cell proliferation
BioAv↓, BA as a therapeutic drug is its poor bioavailability
BioAv↑, administration of BSE-018 concomitantly with a high-fat meal led to several-fold increased areas under the plasma
concentration-time curves as well as peak concentrations of beta-boswellic acid (betaBA)
Half-Life↓, drug needs to be given orally at the interval of six hours due to its calculated half- life, which was around 6 hrs.
toxicity↓, BSE has been found to be a safe drug without any adverse side reactions, and is well tolerated on oral administration.
Dose↑, Boswellia serrata extract to the maximum amount of 4200 mg/day is not toxic and it is safe to use though it shows poor bioavailability
BioAv↑, Approaches like lecithin delivery form (Phytosome®), nanoparticle delivery systems like liposomes, emulsions, solid lipid nanoparticles, nanostructured lipid carriers, micelles and poly (lactic-co-glycolic acid) nanoparticles
ChemoSen↑, Like any other natural products BA can also be effective as chemosensitizer
*antiOx↑, silymarin (SM), an antioxidant and anti-inflammatory complex of flavonoids,
*Inflam↓,
*ROS↓, SM decreased morphological alterations, ROS, and IL-1a in UV+urban-dust-stressed RHE.
*IL1α↓,
*AhR↑, AHR- and Nrf2-related genes were upregulated, which control the antioxidant effector and barrier function.
*NRF2↑,
*IL8↓, Interleukin 8 gene expression was decreased.
*memory↑, Long‐term UA treatment significantly improved learning, memory, and olfactory function in different AD transgenic mice.
*Aβ↓, UA also reduced amyloid beta (Aβ) and tau pathologies and enhanced long‐term potentiation
*toxicity↓, A phase I clinical study confirmed that UA was safe in healthy, sedentary older adults, and that activation of mitochondrial biomarkers in muscle and plasma was observed
*BBB↑, may play a therapeutic role in the brain as it crosses the blood–brain barrier.
*p‑tau↓, UA decreased Aβ accumulation and tau phosphorylation in AD mice
*eff↓, and that the effects disappeared if UA treatment was suspended for 1 month.
*IL1α↓, several proinflammatory cytokines were increased in AD mice and decreased after UA treatment, including Interleukin 1 alpha (IL‐1α), monocyte chemoattractant protein‐1 (MCP‐1)
*MCP1↓,
*MIP‑1α↓, macrophage inflammatory protein‐1 alpha (MIP‐1α), tumor necrosis factor (TNFα), Interleukin 2 (IL‐2)
*TNF-α↓,
*IL2↓,
*SIRT1↓, UA induced sirtuin expression, mitophagy, and decreased DNA damage
*DNAdam↓,
*Dose↝, UA at doses from 250 to 2000 mg in humans 25 and 1–450 mg/kg in mice 80 has been reported to be safe.
*Strength↑, UA increased muscle strength and physical performance in a 6‐min walk test in elderly humans after 4 months of supplementation.
*motorD↑, Other studies reported that UA improved motor activity in the rotarod test and increased total distance traveled and average speed in the open field test in young C57BL/6J mice 82 and 3xTg AD mice
*CTSZ↓, Ctsz was highly expressed in multiple AD transgenic mouse models, and its expression was normalized by UA treatment
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 ⓘ
lipid-P?, 1,
Metal & Cofactor Biology ⓘ
Tf↓, 1,
Core Metabolism/Glycolysis ⓘ
PPARα↓, 1, p‑S6↓, 1,
Cell Death ⓘ
Akt↓, 1, p‑Akt↓, 1, Apoptosis↑, 1, BAX↑, 1, Bcl-2↓, 1, Bcl-xL↓, 1, Casp3↑, 1, Casp8↑, 1, DR4↑, 1, DR5↑, 1,
Transcription & Epigenetics ⓘ
other↝, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 1, P53↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 1, CDK2↓, 1, CDK4↓, 1, cycA1/CCNA1↓, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 1, cycE/CCNE↓, 1, p‑RB1↓, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↓, 1, p‑ERK↓, 2, Let-7↑, 1, mTOR↓, 1, p‑P70S6K↓, 1, p‑P90RSK↑, 1, PI3K↓, 1, STAT3↓, 2, TOP1↓, 1, TOP2↑, 1, Wnt↓, 1, Wnt/(β-catenin)↓, 1,
Migration ⓘ
miR-200b↑, 1, MMP1↓, 1, MMP2↓, 2, MMP9↓, 2, PDGF↓, 1, TumCI↓, 2, TumCMig↓, 1, TumCP↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, Hif1a↓, 1, p‑PDGFR-BB↓, 1, VEGF↓, 3,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, CXCR4↓, 1, IKKα↓, 2, IL1α↓, 3, IL6↓, 1, MCP1↓, 1, MIP2↓, 1, NF-kB↓, 1, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
5HT↓, 1,
Hormonal & Nuclear Receptors ⓘ
AR↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 2, ChemoSen↑, 1, Dose↑, 1, eff↑, 4, Half-Life↓, 1,
Clinical Biomarkers ⓘ
AR↓, 1, ascitic↓, 1, IL6↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, chemoPv↑, 1, toxicity↓, 1,
Total Targets: 75
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, NRF2↑, 1, ROS↓, 1,
Core Metabolism/Glycolysis ⓘ
SIRT1↓, 1,
Cell Death ⓘ
AhR↑, 1, MAPK↑, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1,
Migration ⓘ
Ca+2↝, 1,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
CTSZ↓, 1, IL1α↓, 2, IL2↓, 1, IL8↓, 1, Inflam↓, 2, MCP1↓, 1, MIP‑1α↓, 1, NF-kB↓, 1, TNF-α↓, 2,
Synaptic & Neurotransmission ⓘ
p‑tau↓, 1,
Protein Aggregation ⓘ
Aβ↓, 1,
Drug Metabolism & Resistance ⓘ
Dose↝, 1, eff↓, 1,
Functional Outcomes ⓘ
memory↑, 1, motorD↑, 1, Strength↑, 1, toxicity↓, 1,
Total Targets: 26
Scientific Paper Hit Count for: IL1α, interleukin-1 alpha
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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