IFN-γ Cancer Research Results

IFN-γ, Interferon-γ: Click to Expand ⟱

Source:

Type:

Plays a key role in activation of cellular immunity and subsequently, stimulation of antitumor immune-response. Based on its cytostatic, pro-apoptotic and antiproliferative functions, IFN-γ is considered potentially useful for adjuvant immunotherapy for different types of cancer.
Moreover, it IFN-γ may inhibit angiogenesis in tumor tissue, induce regulatory T-cell apoptosis, and/or stimulate the activity of M1 proinflammatory macrophages to overcome tumor progression.
However, the current understanding of the roles of IFN-γ in the tumor microenvironment (TME) may be misleading in terms of its clinical application.

IFN-γ is often expressed in the tumor microenvironment, particularly in response to immune cell infiltration. Its expression can be influenced by the presence of tumor-infiltrating lymphocytes (TILs) and other immune cells.
High levels of IFN-γ are typically associated with a Th1 immune response, which is generally considered beneficial for anti-tumor immunity.

Tumor Suppression:
In many cases, IFN-γ has tumor-suppressive effects, as it can inhibit tumor cell proliferation and induce apoptosis in certain cancer types.

Scientific Papers found: Click to Expand⟱

1000-

AG,

5-FU,

Characterization and anti-tumor bioactivity of astragalus polysaccharides by immunomodulation

vitro+vivo,

BC,

4T1

TumCG↓,
TumCCA↑, cell cycle arrest (G2 phase)
Apoptosis↑,
*IL2↑, in peripheral blood
*TNF-α↑, in peripheral blood
*IFN-γ↑, in peripheral blood

874-

B-Gluc,

Potential promising anticancer applications of β-glucans: a review

Review,

NA,

AntiCan↑,
TumCG↓, reduced the tumor progression in S180 tumor-bearing mice
BAX↑, β-(1-3)-glucan has increased the Bax expression and decreased the Bcl-2 expression, which leads to apoptosis in S180 tumor-bearing mice.
Bcl-2↓,
IFN-γ↑, soluble β-glucan of low molecular weight enhanced IFN-γ production more efficiently than particle β-glucan of high molecular weight
PI3K/Akt↑, The binding of β-glucans to dectin-1 activates several signaling pathways such as PI3K/Akt, MAPK, NFAT, and NF-κB that result in ROS production, phagocytosis, and cytokine secretion
MAPK↑,
NFAT↑,
NF-kB↑,
ROS↑,
NK cell↑, β-glucans specifically activate and enhance the function of NK cells
TumCCA↑, Some β-glucans significantly induce the cell cycle arrest in the G1-phase due to the restriction of ERK1/2 or the ERK5 pathway, while others induce a gradual dose-dependent accumulation of cells at the G2/M phase along with a decrease in the populat
ERK↓, restricting the activity of the ERK1/2 pathway
Telomerase↓, β-glucans can also induce apoptosis by inhibiting the telomerase activity

2713-

BBR,

Berberine improved the microbiota in lung tissue of colon cancer and reversed the bronchial epithelial cell changes caused by cancer cells

in-vitro,

Nor,

BEAS-2B

Thirty-six BALB/c nude mice

*GutMicro↑, Berberine or probiotics significantly increased the alpha diversity of the lung microbiota
*IL6↑, Berberine increased IL-6 and IL-10 and decreased IL-17 and IFN-γ expression in lung tissue
*IL10↑,
*IL17↑,
*IFN-γ↑,
PDGF↓, In addition, HT29 and RKO CM had no significant effect on the expression of PDGF-β in BEAS-2B cells, while berberine significantly reduced its expression.
*RAD51↓, berberine protects lung cells against this stress by enhancing RAD51 expression.

5622-

Bif,

Bifidobacterium bifidum strains synergize with immune checkpoint inhibitors to reduce tumour burden in mice

in-vivo,

Var,

eff↑, Bifidobacterium bifidum was abundant in patients responsive to therapy.
Imm↑, only specific B. bifidum strains reduced tumour burden synergistically with PD-1 blockade or oxaliplatin treatment by eliciting an antitumour host immune response.
IFN-γ↑, In mice, these strains induced tuning of the immunological background by potentiating the production of interferon-γ, probably through the enhanced biosynthesis of immune-stimulating molecules and metabolites.

1205-

Caff,

immuno,

Caffeine-enhanced anti-tumor activity of anti-PD1 monoclonal antibody

in-vivo,

Melanoma,

B16-F10

OS↑,
CD4+↑, increase in infiltration of CD4+ and CD8+ T lymphocytes into the B16F10 melanoma tumors.
CD8+↑,
AntiTum↑,
TNF-α↑, increased intra-tumoral TNF-α and IFN-γ levels
IFN-γ↑, increased intra-tumoral TNF-α and IFN-γ levels

5986-

Chit,

The natural product chitosan enhances the anti-tumor activity of natural killer cells by activating dendritic cells

Study,

Var,

NK cell↑, In this study, we discovered that chitosan enhanced the anti-tumor activity of natural killer (NK) cells by activating dendritic cells (DCs).
IFN-γ↑, In the presence of DCs, chitosan augmented IFN-γ production by human NK cells.
IL12↑, Mechanistically, chitosan activated DCs to express pro-inflammatory cytokines such as interleukin (IL)-12 and IL-15, which in turn activated the STAT4 and NF-κB signaling pathways, respectively, in NK cells.
IL15↑,
STAT4↑,
NF-kB↑, in NK cells
DCells↑, Collectively, our results demonstrate that chitosan activates DCs leading to enhanced capacity for immune surveillance by NK cells.

5987-

Chit,

Chitin, Chitosan, and Glycated Chitosan Regulate Immune Responses: The Novel Adjuvants for Cancer Vaccine

Review,

Var,

other↝, A common method for the synthesis of chitosan is the deacetylation of chitin using sodium hydroxide in excess as a reagent and water as a solvent
other↝, molecular weight of chitosan is between 3800 and 20,000 Daltons. The degree of deacetylation (%DD) ranges from 60% to 100%.
*Weight↝, chitosan and fat is not very well understood and has not been proved clinically yet, chitosan has been used as an effective complement to help lose weight during diet period or to stabilise one's weight
*toxicity↓, Since they are biocompatible, biodegradable, mucoadhesive, and nontoxic, with antimicrobial, antiviral, and adjuvant properties, chitin and chitosan have been widely applied in medicine and pharmacy
*Bacteria↓,
*BioAv↑,
DDS↑, Combined with drugs such as doxorubicin, paclitaxel, docetaxel, and norcantharidin, chitin and chitosan are used as drug carriers.
*Wound Healing↑, Moreover, chitin has some unusual properties that accelerate healing of wounds in humans
*other↝, Because of its mucoadhesive properties, chitin and chitosan are widely applied for mucosal routes of administration, that is, oral, nasal, and ocular mucosa, which are noninvasive routes.
*Imm↑, hypothesized that a viscous chitosan solution, when administered subcutaneously, would not only provide immune stimulation as previously
eff↑, With the development of nanotechnology, chitosan have shown its unique advantages when combined with nanoparticles.
*BioAv↝, Chitosan is soluble in diluted acids but is relatively insoluble in water [66, 67]. The poor solubility of chitosan poses limitations for its biomedical applications.
*BioAv↑, By attaching galactose molecules to the chitosan molecules, a new water-soluble compound, glycated chitosan (GC), was formed
eff↑, Chitosan nanoparticles (CNPs) can be administrated through noninvasive routes such as oral, nasal, pulmonary, and ocular routes
NK cell↑, CNP remarkably increased the killing activities of NK cells activity
IL2↑, CNP also significantly promoted the production of Th1 (IL-2 and IFN-γ) and Th2 (IL-10) cytokines
IFN-γ↑,
IL10↑,

1601-

Cu,

The copper (II) complex of salicylate phenanthroline induces immunogenic cell death of colorectal cancer cells through inducing endoplasmic reticulum stress

in-vitro,

CRC,

i-CRT↓, Cu(sal)phen induced the release of calreticulin (CRT), adenosine triphosphate (ATP) and high mobility group box 1 (HMGB1), the main molecular markers of ICD (immunogenic cell death)
ICD↑,
i-ATP↓,
i-HMGB1↓,
ER Stress↑, accumulation of ROS and inducing ERS
ROS↑,
DCells↑, promoted the maturation of dendritic cells (DCs)
CD8+↑, and activation of CD8+T cells
IL12↑, secretion of interleukin-12 (IL-12) and interferon-γ (IFN-γ)
IFN-γ↑,
TGF-β↓, while downregulating transforming growth factor-β (TGF-β) levels

451-

CUR,

The effect of Curcumin on multi-level immune checkpoint blockade and T cell dysfunction in head and neck cancer

vitro+vivo,

HNSCC,

SCC15

1, 2, 5, 10, 20, 40 and 80 µM, 1, 3, 6, 12 and 24 h; 50 mg/kg, 6 weeks

vitro+vivo,

HNSCC,

SNU1076

vitro+vivo,

HNSCC,

SNU1041

TumCMig↓,
TumCG↓,
PD-L1↓,
PD-L2↓,
Galectin-9↓,
EMT↓,
T-Cell↑,
TILs↑,
PD-1↓,
TIM-3↓,
CD4+↓,
CD25+↓,
FoxP3+↓,
E-cadherin↑,
CD8+↑,
IFN-γ↑,

1841-

dietFMD,

Fasting-Mimicking Diet Is Safe and Reshapes Metabolism and Antitumor Immunity in Patients with Cancer

Trial,

Var,

BG↓, In 101 patients, the FMD was safe, feasible, and resulted in a consistent decrease of blood glucose and growth factor concentration
AntiCan↑, mediate fasting/FMD anticancer effects in preclinical experiments
IFN-γ↑, enrichment of IFNγ
eff↑, Cyclic FMD Is Safe in Combination with Standard Anticancer Treatments
Dose↝, five-day FMD followed by 16 to 23 days of refeeding
CD14↓, end of five-day FMD, we found a significant decrease of total monocytes (CD14+)
IGF-1↓, Preclinical evidence in tumor-bearing mice suggests that fasting/FMD-induced reduction of blood glucose and insulin/IGF1 concentration
IGFR↓, induced reduction of serum IGF1 levels is associated with the downregulation of total and activated IGF1R at the tumor level
CD8+↑, where five-day fasting/FMD in patients with breast cancer increased total and activated intratumor CD8+ T cells, aDCs, NK cells, and Tem cells,
NK cell↑,

1283-

GA,

immuno,

Gallic acid induces T-helper-1-like Treg cells and strengthens immune checkpoint blockade efficacy

vitro+vivo,

CRC,

p‑STAT3↓,
Treg lymp↓,
FOXP3↓,
CD8+↑,
IFN-γ↑,

1041-

Lyco,

immuno,

Lycopene improves the efficiency of anti-PD-1 therapy via activating IFN signaling of lung cancer cells

in-vivo,

Lung,

mice

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↓,

5602-

NaHCO3,

immuno,

Immunotherapy Enhancement by Targeting Extracellular Tumor pH in Triple-Negative Breast Cancer Mouse Model

in-vivo,

BC,

4T1

mouse

eff↑, n this study, oral administration of either sodium bicarbonate or sodium bicarbonate plus anti-PD-L1 combination enhanced responses to anti-tumor immunity by tumor growth inhibition and improving survival time in TNBC.
TumCG↓,
OS↑,
e-pH↑, Here, we show that NaHCO3 increased extracellular pH (pHe) in tumor tissues in vivo
IFN-γ↑, an effect that was accompanied by an increase in T cell infiltration, T cell activation and IFN-γ, IL2 and IL12p40 mRNA expression in tumor tissues
IL2↑, The expression of IFN-γ, IL-2 and IL-12 mRNA was significantly increased in response to NaHCO3 alone
IL12↑,
Dose↝, The mice in group number three were given drinking water with 200 mM NaHCO3 to increase the pHe > 7.2 via bicarbonate-induced metabolic alkalosis
PD-L1↓, Sodium Bicarbonate Therapy Decreases Tumor PD-L1 Expression In Vivo

3257-

PBG,

The Potential Use of Propolis as a Primary or an Adjunctive Therapy in Respiratory Tract-Related Diseases and Disorders: A Systematic Scoping Review

Review,

Var,

CDK4↓, CAPE also induces G1 phase cell arrest by lowering the expression of CDK4, CDK6, Rb, and p-Rb. M
CDK6↓,
pRB↓,
ROS↓, Artepillin C, a bioactive component of Brazilian green propolis, reduces oxidative damage markers, namely 4-HNE-modified proteins, 8-OHdG, malonaldehyde, and thiobarbituric acid reactive substances in lung tissues with pulmonary adenocarcinoma
TumCCA↑, Propolin, a novel component of prenylflavanones in Taiwanese propolis, was demonstrated to have anti-cancer properties. Propolin H induces cell arrest at G1 phase and upregulates the expression of p21
P21↑,
PI3K↓, Propolin C also inhibits PI3K/Akt and ERK-mediated epithelial-to-mesenchymal transition by upregulating E-cadherin (epithelial cell marker) and downregulating vimentin
Akt↓,
EMT↓,
E-cadherin↑,
Vim↓,
*COX2↓, bioactive compounds such as CAPE, galangin significantly reduce the activity of lung cyclooxygenase (COX) and myeloperoxidase (MPO), and malonaldehyde (MDA), TNF-α, and IL-6 levels, while increasing the activity of catalase (CAT) and SOD
*MPO↓,
*MDA↓,
*TNF-α↓,
*IL6↓,
*Catalase↑,
*SOD↑,
*AST↓, Chrysin also reduces the expression of oxidative and inflammatory markers such as aspartate transaminase (AST), alanine aminotransferase (ALT), IL-1β, IL-10, TNF-α, and MDA levels and increases the antioxidant parameters such as SOD, CAT, and GPx
*ALAT↓,
*IL1β↓,
*IL10↓,
*GPx↓,
*TLR4↓, propolis also inhibits the expression of Toll-like receptor 4 (TLR4), macrophage infiltration, MPO activity, and apoptosis of lung tissues in septic animals
*Sepsis↓,
*IFN-γ↑, CAPE also significantly increases IFN-γ
*GSH↑, propolis significantly increased the level of GSH and the histological appearances of propolis-treated bleomycin-induced pulmonary fibrosis rats.
*NRF2↑, CAPE significantly increases the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2)
*α-SMA↓, propolis significantly inhibits the expression of α- SMA, collagen fibers, and TGF-1β.
*TGF-β↓,
*IL5↓, Propolis also inhibits the expression of inflammatory cytokines and chemokines such as TNF-α, IL-5, IL-6, IL-8, IL-10, NF-kB, IFN-γ, PGF2a, and PGE2.
*IL6↓,
*IL8↓,
*PGE2↓,
*NF-kB↓,
*MMP9↓, downregulating the expression of TGF-1β, ICAM-1, α-SMA, MMP-9, IgE, and IgG1.

3347-

QC,

Recent Advances in Potential Health Benefits of Quercetin

Review,

Var,

Review,

AD,

*antiOx↑, Its strong antioxidant properties enable it to scavenge free radicals, reduce oxidative stress, and protect against cellular damage.
*ROS↓,
*Inflam↓, Quercetin’s anti-inflammatory properties involve inhibiting the production of inflammatory cytokines and enzymes,
TumCP↓, exhibits anticancer effects by inhibiting cancer cell proliferation and inducing apoptosis.
Apoptosis↑,
*cardioP↑, cardiovascular benefits such as lowering blood pressure, reducing cholesterol levels, and improving endothelial function
*BP↓, Quercetin‘s ability to reduce blood pressure was also supported by a different investigation
TumMeta↓, The most important impact of quercetin is its ability to inhibit the spread of certain cancers including those of the breast, cervical, lung, colon, prostate, and liver
MDR1↓, quercetin decreased the expression of genes multidrug resistance protein 1 and NAD(P)H quinone oxidoreductase 1 and sensitized MCF-7 cells to the chemotherapy medication doxorubicin
NADPH↓,
ChemoSen↑,
MMPs↓, Inhibiting CT26 cells’ migration and invasion abilities by inhibiting their expression of tissue inhibitors of metalloproteinases (TIMPs) inhibits their invasion and migration abilities
TIMP2↑,
*NLRP3↓, inhibited NLRP3 by acting on this inflammasome
*IFN-γ↑, quercetin significantly upregulates the gene expression and production of interferon-γ (IFN-γ), which is obtained from T helper cell 1 (Th1), and downregulates IL-4, which is obtained from Th2.
*COX2↓, quercetin is known to decrease the production of inflammatory molecules COX-2, nuclear factor-kappa B (NF-κB), activator protein 1 (AP-1), mitogen-activated protein kinase (MAPK), reactive nitric oxide synthase (NOS), and reactive C-protein (CRP)
*NF-kB↓,
*MAPK↓,
*CRP↓,
*IL6↓, Quercetin suppressed the production of inflammatory cytokines such as IL-6, TNF-α, and IL-1β via upregulating TLR4.
*TNF-α↓,
*IL1β↓,
*TLR4↑,
*PKCδ↓, Quercetin employed suppression on the phosphorylation of PKCδ to control the PKCδ–JNK1/2–c-Jun pathway.
*AP-1↓, This pathway arrested the accumulation of AP-1 transcription factor in the target genes, thereby resulting in reduced ICAM-1 and inflammatory inhabitation
*ICAM-1↓,
*NRF2↑, Quercetin overexpressed Nrf2 and targeted its downstream gene, contributing to increased HO-1 levels responsible for the down-regulation of TNF-α, iNOS, and IL-6
*HO-1↑,
*lipid-P↓, Quercetin acts as a potent antioxidant by scavenging ROS, inhibiting lipid peroxidation, and enhancing the activity of antioxidant enzymes
*neuroP↑, This helps to counteract oxidative stress and protect against neurodegenerative processes that contribute to AD
*eff↑, rats treated with chronic rotenone or 3-nitropropionic acid showed enhanced neuroprotection when quercetin and fish oil were taken orally
*memory↑, Both memory and learning abilities in the test animals increased
*cognitive↑,
*AChE↓, The increase in AChE activity brought on by diabetes was prevented in the cerebral cortex and hippocampus by quercetin at a level of 50 mg/kg body weight.
*BioAv↑, consumption of fried onions compared to black tea, suggesting that the form of quercetin present in onions is better absorbed than that in tea
*BioAv↑, This suggests that dietary fat can increase the absorption of quercetin [180]
*BioAv↑, potential of liposomes to enhance the bioactivity and bioavailability of quercetin has been the subject of several investigations
*BioAv↑, several emulsion types that may be employed to encapsulate quercetin, but oil-in-water (O/W) emulsions are the most widely utilized.
*BioAv↑, the kind of oil (triglyceride oils made up of either long-chain or medium-chain fatty acids) affected the bioaccessibility of quercetin and gastrointestinal stability, emphasizing the significance of picking a suitable oil phase

1508-

SFN,

Nrf2 targeting by sulforaphane: A potential therapy for cancer treatment

Review,

Var,

*BioAv↑, RAW: higher amounts were detected when broccoli were eaten raw (bioavailability equal to 37%), compared to the cooked broccoli (bioavailability 3.4%)
HDAC↓, Sulforaphane is able to down-regulate HDAC activity and induce histone hyper-acetylation in tumor cell
TumCCA↓, Sulforaphane induces cell cycle arrest in G1, S and G2/M phases,
eff↓, in leukemia stem cells, sulforaphane potentiates imatinib effect through inhibition of the Wnt/β-catenin functions
Wnt↓,
β-catenin/ZEB1↓,
Casp12?, inducing caspases activation
Bcl-2↓,
cl‑PARP↑,
Bax:Bcl2↑, unbalancing the ratio Bax/Bcl-2
IAP1↓, down-regulating IAP family proteins
Casp3↑,
Casp9↑,
Telomerase↓, In Hep3B cells, sulforaphane reduces telomerase activity
hTERT/TERT↓, inhibition of hTERT expression;
ROS?, increment of ROS, induced by this compound, is essential for the downregulation of transcription and of post-translational modification of hTERT in suppression of telomerase activity
DNMTs↓, (2.5 - 10 μM) represses hTERT by impacting epigenetic pathways, in particular through decreased DNA methyltransferases activity (DNMTs)
angioG↓, inhibit tumor development through regulation of angiogenesis
VEGF↓,
Hif1a↓,
cMYB↓,
MMP1↓, inhibition of migration and invasion activities induced by sulforaphane in oral carcinoma cell lines has been associated to the inhibition of MMP-1 and MMP-2
MMP2↓,
MMP9↓,
ERK↑, inhibits invasion by activating ERK1/2, with consequent upregulation of E-cadherin (an invasion inhibitor)
E-cadherin↑,
CD44↓, downregulation of CD44v6 and MMP-2 (invasion promoters)
MMP2↓,
eff↑, ombination of sulforaphane and quercetin synergistically reduces the proliferation and migration of melanoma (B16F10) cells
IL2↑, induces upregulation of IL-2 and IFN-γ
IFN-γ↑,
IL1β↓, downregulation of IL-1beta, IL-6, TNF-α, and GM-CSF
IL6↓,
TNF-α↓,
NF-kB↓, sulforaphane inhibits the phorbol ester induction of NF-κB, inhibiting two pathways, ERK1/2 and NF-κB
ERK↓,
NRF2↑, At molecular level, sulforaphane modulates cellular homeostasis via the activation of the transcription factor Nrf2.
RadioS↑, sulforaphane could be used as a radio-sensitizing agent in prostate cancer if clinical trials will confirm the pre-clinical results.
ChemoSideEff↓, chemopreventive effects of sulforaphane

3288-

SIL,

Silymarin in cancer therapy: Mechanisms of action, protective roles in chemotherapy-induced toxicity, and nanoformulations

Review,

Var,

Inflam↓, Silymarin, a milk thistle extract, has anti-inflammatory, immunomodulatory, anti-lipid peroxidative, anti-fibrotic, anti-oxidative, and anti-proliferative properties.
lipid-P↓,
TumMeta↓, Silymarin exhibits not only anti-cancer functions through modulating various hallmarks of cancer, including cell cycle, metastasis, angiogenesis, apoptosis, and autophagy, by targeting a plethora of molecules
angioG↓,
chemoP↑, but also plays protective roles against chemotherapy-induced toxicity, such as nephrotoxicity,
EMT↓, Figure 2, Metastasis
HDAC↓,
HATs↑,
MMPs↓,
uPA↓,
PI3K↓,
Akt↓,
VEGF↓, Angiogenesis
CD31↓,
Hif1a↓,
VEGFR2↓,
Raf↓,
MEK↓,
ERK↓,
BIM↓, apoptosis
BAX↑,
Bcl-2↓,
Bcl-xL↓,
Casp↑,
MAPK↓,
P53↑,
LC3II↑, Autophagy
mTOR↓,
YAP/TEAD↓,
*BioAv↓, Additionally, the oral bioavailability of silymarin in rats is only 0.73 %
MMP↓, silymarin treatment reduced mitochondrial transmembrane potential, leading to an increase in cytosolic cytochrome c (Cyt c), downregulating proliferation-associated proteins (PCNA, c-Myc, cyclin D1, and β-catenin)
Cyt‑c↑,
PCNA↓,
cMyc↓,
cycD1/CCND1↓,
β-catenin/ZEB1↓,
survivin↓, and anti-apoptotic proteins (survivin and Bcl-2), and upregulating pro-apoptotic proteins (caspase-3, Bax, APAF-1, and p53)
APAF1↑,
Casp3↑,
MDSCs↓, ↓MDSCs, ↓IL-10, ↑IL-2 and IFN-γ
IL10↓,
IL2↑,
IFN-γ↑,
hepatoP↑, Moreover, in a randomized clinical trial, silymarin attenuated hepatoxicity in non-metastatic breast cancer patients undergoing a doxorubicin/cyclophosphamide-paclitaxel regimen
cardioP↑, For example, Rašković et al. studied the hepatoprotective and cardioprotective effects of silymarin (60 mg/kg orally) in rats following DOX
GSH↑, silymarin could protect the kidney and heart from ADR toxicity by protecting against glutathione (GSH) depletion and inhibiting lipid peroxidation
neuroP↑, silymarin attenuated the neurotoxicity of docetaxel by reducing apoptosis, inflammation, and oxidative stress

1195-

SM,

Salvia miltiorrhiza polysaccharide activates T Lymphocytes of cancer patients through activation of TLRs mediated -MAPK and -NF-κB signaling pathways

in-vitro,

Lung,

A549

in-vitro,

Liver,

HepG2

in-vitro,

CRC,

HCT116

T-Cell↑,
TumCP∅, SMP showed no effect on the proliferation of the tumor cells
IL4↑,
IL6↑,
IFN-γ↑,
TLR4↑,
TLR1↑,
TLR2↑,
p‑JNK↑,
p‑ERK↑,
IKKα↑,

3563-

TQ,

Thymoquinone (TQ) demonstrates its neuroprotective effect via an anti-inflammatory action on the Aβ(1–42)-infused rat model of Alzheimer's disease

in-vivo,

AD,

A rat model of AD was established in 6 month-old rats

*memory↑, TQ treatment ameliorated both impaired memory performance and IFN-γ levels
*IFN-γ↑,
*neuroP↑, TQ might be a strong candidate for preventing or delaying the symptoms of AD by reducing neurotoxicity via its anti-inflammatory activity
*Inflam↓,
*cognitive↑, recovery role of TQ in cognitive functions was also demonstrated in distinct models of neurodegeneration

Showing Research Papers: 1 to 19 of 19

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 19

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

CD8+↑, 5,
Total Targets: 151

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, Catalase↑, 1, GPx↓, 1, GSH↑, 1, HO-1↑, 1, lipid-P↓, 1, MDA↓, 1, MPO↓, 1, NRF2↑, 2, ROS↓, 1, SOD↑, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,

Cell Death ⓘ

MAPK↓, 1,

Transcription & Epigenetics ⓘ

other↝, 1,

DNA Damage & Repair ⓘ

RAD51↓, 1,

Migration ⓘ

AP-1↓, 1, MMP9↓, 1, PKCδ↓, 1, TGF-β↓, 1, α-SMA↓, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 2, CRP↓, 1, ICAM-1↓, 1, IFN-γ↑, 5, IL10↓, 1, IL10↑, 1, IL17↑, 1, IL1β↓, 2, IL2↑, 1, IL5↓, 1, IL6↓, 3, IL6↑, 1, IL8↓, 1, Imm↑, 1, Inflam↓, 2, NF-kB↓, 2, PGE2↓, 1, TLR4↓, 1, TLR4↑, 1, TNF-α↓, 2, TNF-α↑, 1,

Synaptic & Neurotransmission ⓘ

AChE↓, 1,

Protein Aggregation ⓘ

NLRP3↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↑, 8, BioAv↝, 1, eff↑, 1,

Clinical Biomarkers ⓘ

ALAT↓, 1, AST↓, 1, BP↓, 1, CRP↓, 1, GutMicro↑, 1, IL6↓, 3, IL6↑, 1,

Functional Outcomes ⓘ

cardioP↑, 1, cognitive↑, 2, memory↑, 2, neuroP↑, 2, toxicity↓, 1, Weight↝, 1, Wound Healing↑, 1,

Infection & Microbiome ⓘ

Bacteria↓, 1, Sepsis↓, 1,
Total Targets: 63

Scientific Paper Hit Count for: IFN-γ, Interferon-γ

4 immunotherapy
2 chitosan
1 Astragalus
1 5-fluorouracil
1 beta-glucans
1 Berberine
1 Bifidobacterium
1 Caffeine
1 Copper and Cu NanoParticles
1 Curcumin
1 diet FMD Fasting Mimicking Diet
1 Gallic acid
1 Lycopene
1 Bicarbonate(Sodium)
1 Propolis -bee glue
1 Quercetin
1 Sulforaphane (mainly Broccoli)
1 Silymarin (Milk Thistle) silibinin
1 Salvia miltiorrhiza
1 Thymoquinone

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#:442  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

IFN-γ Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

DNA Damage & Repair ⓘ

Migration ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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