IL1 Cancer Research Results

IL1, Interleukin-1: Click to Expand ⟱
Source:
Type:
Interleukin-1 (IL-1) has long been known to be a key mediator of immunity and inflammation. Its dysregulation has been implicated in recent years in tumorigenesis and tumor progression, and its upregulation is thought to be associated with many tumors.

Interleukin-1 (IL-1) is a pro-inflammatory cytokine that plays a crucial role in the immune response and inflammation. It exists in two main forms: IL-1α and IL-1β, both of which are produced by various cell types, including macrophages, monocytes, and dendritic cells. IL-1 is involved in a wide range of biological processes, including cell proliferation, differentiation, and apoptosis.

IL-1 is often overexpressed in various cancers, including breast cancer, colorectal cancer, lung cancer, and melanoma. Its expression can be influenced by the tumor microenvironment and the presence of inflammatory cells.
Elevated levels of IL-1 are frequently associated with tumor progression and metastasis.

IL-1 is considered a pro-tumorigenic cytokine in many contexts. It can promote tumor growth by enhancing cell proliferation, survival, and angiogenesis. IL-1β, in particular, has been shown to stimulate the proliferation of cancer cells and promote the formation of new blood vessels (angiogenesis).
Scientific Papers found: Click to Expand⟱
306- AgNPs,    Cancer Therapy by Silver Nanoparticles: Fiction or Reality?
- Analysis, NA, NA
EPR↝, takes advantage of EPR
ROS↑, silver ions drive the formation of ROS, which triggers massive oxidative stress, thereby activating the cellular pathways leading to cell death
IL1↑, IL-1b
IL8↑, IL-8 mRNA levels
ER Stress↑,
MMP9↑, it has been shown that 20 nm AgNPs increase the MMP-9 secretion
MMP↓, loss of mitochondrial membrane potential and mitochondrial structural disorganization, were reported to accompany the AgNP-induced stres
Cyt‑c↑, cytochrome c release from the mitochondria into the cytoplasm and finally to apoptosis
Apoptosis↑,
Hif1a↑, AgNPs were shown to induce HiF-1α activation, thereby ultimately activating autophagy through the AMPK-mTOR pathway in PC-3 prostate cancer cells [89
BBB↑, AgNPs can affect the integrity of the blood–brain barrier and can cross this barrier in vitro through transcytosis
GutMicro↝, AgNP treatments might influence the composition of the gut microbiota,
eff↑, AgNPs are promising tools for targeted delivery
eff↑, the joint application of the nanoparticles and the HDAC inhibitor caused significantly increased ROS levels,
RadioS↑, idea to use AgNPs as radiosensitizers came along with the phenomenon that metals with high atomic numbers are capable of enhancing the effects of radiation

1574- Citrate,    Citrate Suppresses Tumor Growth in Multiple Models through Inhibition of Glycolysis, the Tricarboxylic Acid Cycle and the IGF-1R Pathway
- in-vitro, Lung, A549 - in-vitro, Melanoma, WM983B - in-vivo, NA, NA
TumCG↓,
eff↑, additional benefit accrued in combination with cisplatin
T-Cell↑, significantly higher infiltrating T-cells
p‑IGF-1R↓, citrate inhibited IGF-1R phosphorylation
p‑Akt↓, inhibited AKT phosphorylation
PTEN↑, activated PTEN
p‑eIF2α↑, increased expression of p-eIF2a p-eIF2a was decreased when PTEN was depleted
OCR↓, citrate treatment of A549 cells dramatically reduced oxygen consumption
ROS↓, observed a decrease in ROS in A549
ECAR∅, acidification rate (ECAR) and found it to be unchanged
IL1↑, s (e.g. interleukin-1, tumor necrosis factor-alpha, etc) and anti-inflammatory cytokines (e.g. interleukin-10 and interleukin 1 receptor antagonist) are activated
TNF-α↑,
IL10↑,
IGF-1R↓, Citrate Inhibits IGF-1R Activation And Its Downstream Pathway
eIF2α↑, eIF2α activity was increased in A549 cells after citrate treatment
PTEN↑, PTEN was activated
TCA↓,
Glycolysis↓, citrate may inhibit tumor growth via inhibiting glycolysis and the TCA cycle and that this effect appears to be selective to tumor tissue.
selectivity↑, citrate may inhibit tumor growth via inhibiting glycolysis and the TCA cycle and that this effect appears to be selective to tumor tissue.
*toxicity∅, Chronic citrate treatment was non-toxic as evidenced by gross pathology in numerous organs (liver, lung, spleen and kidney)
Dose∅, corresponding to approximately 56 g of citrate in a 70 kg person

3277- Lyco,    Recent trends and advances in the epidemiology, synergism, and delivery system of lycopene as an anti-cancer agent
- Review, Var, NA
antiOx↑, lycopene provides a strong antioxidant activity that is 100 times more effective than α-tocopherol and more than double effective that of β-carotene
TumCP↓, In vivo and in vitro experiments have demonstrated that lycopene at near physiological levels (0.5−2 μM) could inhibit cancer cell proliferation [[22], [23], [24]], induce apoptosis [[25], [26], [27]], and suppress metastasis [
Apoptosis↑,
TumMeta↑,
ChemoSen↑, lycopene can increase the effect of anti-cancer drugs (including adriamycin, cisplatin, docetaxel and paclitaxel) on cancer cell growth and reduce tumour size
BioAv↓, low water solubility and bioavailability of lycopene
Dose↝, The concentration of lycopene in plasma (daily intake of 10 mg lycopene) is approximately 0.52−0.6 μM
BioAv↓, significant decrease in lycopene bioavailability in the elderly
BioAv↑, oils and fats favours the bioavailability of lycopene [80], while large molecules such as pectin can hinder the absorption of lycopene in the small intestine due to their action on lipids and bile salt molecules
SOD↑, GC: 50−150 mg/kg BW/day ↑SOD, CAT, GPx ↑IL-2, IL-4, IL-10, TNF-α ↑IgA, IgG, IgM ↓IL-6
Catalase↑,
GPx↑,
IL2↑, lycopene treatment significantly enhanced blood IL-2, IL-4, IL-10, TNF-α levels and reduced IL-6 level in a dose-dependent manner.
IL4↑,
IL1↑,
TNF-α↑,
GSH↑, GC: ↑GSH, GPx, GST, GR
GPx↑,
GSTA1↑,
GSR↑,
PPARγ↑, ↑GPx, SOD, MDA ↑PPARγ, caspase-3 ↓NF-κB, COX-2
Casp3↑,
NF-kB↓,
COX2↓,
Bcl-2↑, AGS cells Lycopene 5 μM ↑Bcl-2 ↓Bax, Bax/Bcl-2, p53 ↓Chk1, Chk2, γ-H2AX, DNA damage ↓ROS Phase arrest
BAX↓,
P53↓,
CHK1↓,
Chk2↓,
γH2AX↓,
DNAdam↓,
ROS↓,
P21↑, CRC: ↑p21 ↓PCNA, β-catenin ↓COX-2, PGE2, ERK1/2 phosphorylated
PCNA↓,
β-catenin/ZEB1↓,
PGE2↓,
ERK↓,
cMyc↓, AGS cells: ↓Wnt-1, c-Myc, cyclin E ↓Jak1/Stat3, Wnt/β-catenin alteration ↓ROS
cycE/CCNE↓,
JAK1↓,
STAT3↓,
SIRT1↑, Huh7: ↑SIRT1 ↓Cells growth ↑PARP cleavage ↓Cyclin D1, TNFα, IL-6, NF-κB, p65, STAT3, Akt activation ↓Tumour multiplicity, volume
cl‑PARP↑,
cycD1/CCND1↓,
TNF-α↓,
IL6↓,
p65↓,
MMP2↓, SK-Hep1 human hepatoma cells Lycopene 5, 10 μM ↓MMP-2, MMP-9 ↓
MMP9↓,
Wnt↓, AGS cells Lycopene 0.5 μM, 1 μM ↓Wnt-1, c-Myc, cyclin E ↓Jak1/Stat3, Wnt/β-catenin alteration ↓ROS

1041- Lyco,  immuno,    Lycopene improves the efficiency of anti-PD-1 therapy via activating IFN signaling of lung cancer cells
- in-vivo, Lung, NA
TumVol↓, combined lycopene and anti-PD-1 reduced the tumor volume and weight compared to control treatment.
TumW↓,
eff↑, lycopene could assist anti-PD-1 to elevate the levels of interleukin (IL)-1 and interferon (IFN) γ while reduce the levels of IL-4 and IL-10
IL1↑,
IFN-γ↑,
IL4↓,
IL10↓,

3480- MF,    Cellular and Molecular Effects of Magnetic Fields
- Review, NA, NA
ROS↑, 50 Hz, 1 mT for 24/48/72 h SH-SY5Y (neuroblastoma Significantly increased ROS levels
*Ca+2↑, There is experimental proof that extremely low-frequency (ELF-MF) magnetic fields interact with Ca2+ channels, leading to increased Ca2+ efflux
*Inflam↓, PEMF stimulates the anti-inflammatory response of mesenchymal stem cells.
*Akt↓, nasopharyngeal carcinoma cell line. Potentially, these alterations were caused by inhibition of the Akt/mTOR signaling pathway
*mTOR↓,
selectivity↑, Ashdown and colleagues observed disruptions in the human lung cancer cell line after PMF (20 mT) exposure; in comparison, normal cells were insensitive to PMF
*memory↑, Ahmed and colleagues proved that PMF has an impact on the hippocampus, the brain region responsible for spatial orientation and memory acquisition.
*MMPs↑, In wound closure, epithelial cells, connective tissue cells, and immune cells, which promote collagen production, matrix metalloproteinase activity, growth factor release (e.g., VEGF, FGF, PDGF, TNF, HGF, and IL-1), and inflammatory environment pro
*VEGF↑,
*FGF↑,
*PDGF↑,
*TNF-α↑,
*HGF/c-Met↑,
*IL1↑,

220- MFrot,  MF,    Effect of low frequency magnetic fields on melanoma: tumor inhibition and immune modulation
- in-vitro, Melanoma, B16-F10
OS↑, prolonged the mouse survival rate
DCells↑,
T-Cell↑,
Apoptosis↑,
IL1↑,
IFN-γ↓, most of cytokines were decreased
IL10↑,
TumCG↓, grow slowed
ROS↑, Phagocyte activity, ROS release and interleukin-1β (IL-1β) production were significantly promoted after continuous exposure to 50 Hz LF-MF (1mT)
TumCP↓, LF-MF inhibits the proliferation of B16-F10 cells
TumCCA↑, the S-phase rate was significantly decreased from 40.76% to 37.24% and the G2/M-phase rate was significantly increased from 8.9% to 11.6%
ChrMod↑, Compared with control cells, the treated cells were characterized by the breaking down of chromatin (white arrow) and black granule accumulation (black arrow).
CXCL9↓, in tumor-bearing mice groups, most of cytokines were decreased after LF-MF exposure, including KC, CCL1, IFN-γ, CXCL9, CXCL12, TREM-1, CCL12, IL-1rα and IL-16.
CXCL12↓,
CD4+↑, After LF-MF exposure, the proportions of CD3+, CD3 + CD4+ and CD3 + CD8+ T cells in tumor-bearing mice were increased to 24.0%, 13.28% and 7.46%, respectively
CD8+↑,


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 2,   GSH↑, 1,   GSR↑, 1,   GSTA1↑, 1,   ROS↓, 2,   ROS↑, 3,   SOD↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   OCR↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   ECAR∅, 1,   Glycolysis↓, 1,   PPARγ↑, 1,   SIRT1↑, 1,   TCA↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 3,   BAX↓, 1,   Bcl-2↑, 1,   Casp3↑, 1,   Chk2↓, 1,   Cyt‑c↑, 1,  

Transcription & Epigenetics ⓘ

ChrMod↑, 1,  

Protein Folding & ER Stress ⓘ

eIF2α↑, 1,   p‑eIF2α↑, 1,   ER Stress↑, 1,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   DNAdam↓, 1,   P53↓, 1,   cl‑PARP↑, 1,   PCNA↓, 1,   γH2AX↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   IGF-1R↓, 1,   p‑IGF-1R↓, 1,   PTEN↑, 2,   STAT3↓, 1,   TumCG↓, 2,   Wnt↓, 1,  

Migration ⓘ

CXCL12↓, 1,   MMP2↓, 1,   MMP9↓, 1,   MMP9↑, 1,   TumCP↓, 2,   TumMeta↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

EPR↝, 1,   Hif1a↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   COX2↓, 1,   CXCL9↓, 1,   DCells↑, 1,   IFN-γ↓, 1,   IFN-γ↑, 1,   IL1↑, 5,   IL10↓, 1,   IL10↑, 2,   IL2↑, 1,   IL4↓, 1,   IL4↑, 1,   IL6↓, 1,   IL8↑, 1,   JAK1↓, 1,   NF-kB↓, 1,   p65↓, 1,   PGE2↓, 1,   T-Cell↑, 2,   TNF-α↓, 1,   TNF-α↑, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 1,   ChemoSen↑, 1,   Dose↝, 1,   Dose∅, 1,   eff↑, 4,   RadioS↑, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

GutMicro↝, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

OS↑, 1,   TumVol↓, 1,   TumW↓, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 90

Pathway results for Effect on Normal Cells:


Cell Death ⓘ

Akt↓, 1,   HGF/c-Met↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

FGF↑, 1,   mTOR↓, 1,  

Migration ⓘ

Ca+2↑, 1,   MMPs↑, 1,   PDGF↑, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL1↑, 1,   Inflam↓, 1,   TNF-α↑, 1,  

Functional Outcomes ⓘ

memory↑, 1,   toxicity∅, 1,  
Total Targets: 13

Scientific Paper Hit Count for: IL1, Interleukin-1
2 Lycopene
2 Magnetic Fields
1 Silver-NanoParticles
1 Citric Acid
1 immunotherapy
1 Magnetic Field Rotating
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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