IL10 Cancer Research Results

IL10, Interleukin-10: Click to Expand ⟱

Source:

Type:

IL-10 is a multifaceted immune-suppressive cytokine and possesses immune-regulatory and angiogenic functions.
It primarily acts as an anti-inflammatory cytokine, protecting the body from an uncontrolled immune response, mostly through the Jak1/Tyk2 and STAT3 signaling pathway. On the other hand, IL-10 can also have immunostimulating functions under certain conditions.
The role of IL-10 in tumor pathogenesis is currently highly controversial, with some findings showing that IL-10 promotes tumor development and angiogenesis, while others supporting that it inhibits tumor growth and metastasis.

IL-10 is often expressed in various cancers, including breast cancer, colorectal cancer, melanoma, and lymphoma. Its expression can vary significantly depending on the tumor type and the immune context.
Elevated levels of IL-10 are frequently associated with the presence of tumor-infiltrating immune cells, particularly Tregs and M2 macrophages.

Scientific Papers found: Click to Expand⟱

1543-

Api,

Therapeutical properties of apigenin: a review on the experimental evidence and basic mechanisms

Review,

NA,

TNF-α↓,
IL1β↓,
IL6↓,
IL10↓,
COX2↓, blocks the nitric oxide-mediated cyclooxygenase-2 expression
iNOS↓,
Inflam↓,
Dose∅, apigenin contents were reported high in celery and parsley with amounts of 19 and 215 mg per 100 g, respectively
Dose∅, dried parsley contains highest concentration of apigenin (45,035 μg/g). The dried chamomile flowers contain 3,000 to 5,000 μg/g of apigenin.

563-

ART/DHA,

Artesunate down-regulates immunosuppression from colorectal cancer Colon26 and RKO cells in vitro by decreasing transforming growth factor β1 and interleukin-10

in-vitro,

Colon,

colon26

in-vitro,

CRC,

RKO

TGF-β↓,
IL10↓,

1304-

ASA,

Aspirin Inhibits Colorectal Cancer via the TIGIT-BCL2-BAX pathway in T Cells

in-vitro,

CRC,

in-vivo,

NA,

mice

TumCP↓,
Apoptosis↑,
Bcl-2↓,
BAX↑,
IL10↓,
TNF-β↓, transforming growth factor-β1

2712-

BBR,

Suppression of colon cancer growth by berberine mediated by the intestinal microbiota and the suppression of DNA methyltransferases (DNMTs)

in-vitro,

Colon,

HT29

in-vivo,

NA,

TumCG↓, BBR reduced the growth of colon cancer cells to a certain extent in vitro and in vivo,
GutMicro↑, BBR significantly mediated the abundance, composition and metabolic functions of the intestinal microbial flora in mice with colon cancer
other↝, The effect of BBR on inflammatory cytokines, including IL-6, FGF, and PDGF, was not obvious
IL10↓, BBR significantly downregulated IL-10 levels (P < 0.05) and reduced c-Myc, DNMT1, and DNMT3B
cMyc↓,
DNMT1↓,
DNMTs↓,

2725-

BetA,

Betulinic acid protects against renal damage by attenuation of oxidative stress and inflammation via Nrf2 signaling pathway in T-2 toxin-induced mice

in-vivo,

Nor,

*RenoP↑, BA pretreatment alleviated excessive glomerular hemorrhage and inflammatory cell infiltration in kidneys caused by T-2 toxin.
*SOD?, Moreover, pretreatment with BA mitigated T-2 toxin-induced renal oxidative damage by up-regulating the activities of SOD and CAT, and the content of GSH, while down-regulating the accumulation of ROS and MDA
*Catalase↑,
*GSH↑,
*ROS↓,
*MDA↓,
*IL1β↓, decreasing the mRNA expression of IL-1β, TNF-α and IL-10, and increasing IL-6 mRNA expression
*TNF-α↓,
*IL10↓,
*IL6↑,
*NRF2↑, pretreatment with BA could activate Nrf2 signaling pathway.

5705-

Brut,

A flavonoid-rich extract from bergamot juice prevents carcinogenesis in a genetic model of colorectal cancer, the Pirc rat (F344/NTac-Apcam1137)

in-vivo,

CRC,

rats

Risk↓, Rats treated with BJe showed a significant dose-related reduction in the colon preneoplastic lesions mucin-depleted foci (MDF). strategy to prevent CRC in high-risk patients.
TumMeta↓, Colon and small intestinal tumours were also significantly reduced in rats supplemented with 70 mg/kg of BJe.
Apoptosis↑, Moreover, in colon tumours from rats fed with 70 mg/kg BJe, apoptosis was significantly higher than in controls.
COX2↓, significant down-regulation of inflammation-related genes (COX-2, iNOS, IL-1β, IL-6 and IL-10 and Arginase 1).
iNOS↓,
IL1β↓,
IL6↓,
IL10↓,
P53↑, Up-regulation of p53 and down-regulation of survivin and p21 genes was also observed.
P21↓,
survivin↓,
chemoPv↑, These data indicate a strong chemopreventive activity of BJe that, at least in part, is due to its pro-apoptotic and anti-inflammatory actions.
*Inflam↓,

1032-

Buty,

Gut microbiome-derived butyrate inhibits the immunosuppressive factors PD-L1 and IL-10 in tumor-associated macrophages in gastric cancer

in-vivo,

GC,

AGS

human and mice

GutMicro↑, Restoration of the intestinal microbiome and its metabolic functions inhibit tumor growth The abundances of Faecalibacterium and Bifidobacterium in the intestinal flora were lower in GC patients than in healthy individuals.
PD-L1↓, Butyrate, a representative microbiome metabolite, suppressed the expression levels of PD-L1 and IL-10 in immune cells.
IL10↓,
TumCG↓, Butyrate inhibited tumor growth in mice

5988-

Chit,

Chitosan immunomodulation: insights into mechanisms of action on immune cells and signaling pathways

Review,

Var,

DDS↑, various biomedical applications, including drug delivery, cartilage repair, wound healing, and tissue engineering, because of its unique physicochemical properties.
*Cartilage↑,
*Wound Healing↑,
Imm↑, investigation of the immunomodulatory properties of chitosan, since the biopolymer has been shown to modulate the maturation, activation, cytokine production, and polarization of dendritic cells and macrophages
cGAS–STING↑, Several signaling pathways, including the cGAS–STING, STAT-1, and NLRP3 inflammasomes, are involved in chitosan-induced immunomodulation. CS activates the cGAS–STING signaling pathway
STAT1↑, One crucial factor is DDA, as it was observed that 80% DDA CS activated the STAT-1 pathway, whereas 98% DDA did not
NLRP3↑, activation of the NLRP3 inflammasome by CS requires the presence of mitochondrial ROS.
*DCells↑, CS has been studied for its potential impact on DC activation, which is a crucial step in initiating the immune response.
*IL10↓, The use of CS also reduced IL-10 production and increased TGF-β1, TNF-α, and interleukin-1 beta (IL-1β) (p < 0.001) levels.
*TGF-β1↓,
*TNF-α↓,
IL1β↓,
ROS↑, CS internalization in DCs caused mitochondrial stress and led to the production of reactive oxygen species (ROS)

428-

Chit,

docx,

CUR,

Chitosan-based nanoparticle co-delivery of docetaxel and curcumin ameliorates anti-tumor chemoimmunotherapy in lung cancer

vitro+vivo,

Lung,

H460

4, 8, 12, 16, 20, 24 and 28 μg/mL, 24 h; 5 mg/kg, 24 h

vitro+vivo,

Lung,

H1299

vitro+vivo,

Lung,

A549

vitro+vivo,

Lung,

PC9

MDSCs↓,
TregCell↓,
IL10↓,
NK cell↑,

2785-

CHr,

Emerging cellular and molecular mechanisms underlying anticancer indications of chrysin

Review,

Var,

*NF-kB↓, suppressed pro-inflammatory cytokine expression and histamine release, downregulated nuclear factor kappa B (NF-kB), cyclooxygenase 2 (COX-2), and inducible nitric oxide synthase (iNOS)
*COX2↓,
*iNOS↓,
angioG↓, upregulated apoptotic pathways [28], inhibited angiogenesis [29] and metastasis formation
TOP1↓, suppressed DNA topoisomerases [31] and histone deacetylase [32], downregulated tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β)
HDAC↓,
TNF-α↓,
IL1β↓,
cardioP↑, promoted protective signaling pathways in the heart [34], kidney [35] and brain [8], decreased cholesterol level
RenoP↑,
neuroP↑,
LDL↓,
BioAv↑, bioavailability of chrysin in the oral route of administration was appraised to be 0.003–0.02% [55], the maximum plasma concentration—12–64 nM
eff↑, Chrysin alone and potentially in combination with metformin decreased cyclin D1 and hTERT gene expression in the T47D breast cancer cell line
cycD1/CCND1↓,
hTERT/TERT↓,
MMP-10↓, Chrysin pretreatment inhibited MMP-10 and Akt signaling pathways
Akt↓,
STAT3↓, Chrysin declined hypoxic survival, inhibited activation of STAT3, and reduced VEGF expression in hypoxic cancer cells
VEGF↓,
EGFR↓, chrysin to inhibit EGFR was reported in a breast cancer stem cell model [
Snail↓, chrysin downregulated MMP-10, reduced snail, slug, and vimentin expressions increased E-cadherin expression, and inhibited Akt signaling pathway in TNBC cells, proposing that chrysin possessed a reversal activity on EMT
Slug↓,
Vim↓,
E-cadherin↑,
eff↑, Fabrication of chrysin-attached to silver and gold nanoparticles crossbred reduced graphene oxide nanocomposites led to augmentation of the generation of ROS-induced apoptosis in breast cancer
TET1↑, Chrysin induced augmentation in TET1
ROS↑, Pretreatment with chrysin induced ROS formation, and consecutively, inhibited Akt phosphorylation and mTOR.
mTOR↓,
PPARα↓, Chrysin inhibited mRNA expression of PPARα
ER Stress↑, ROS production by chrysin was the critical mediator behind induction of ER stress, leading to JNK phosphorylation, intracellular Ca2+ release, and activation of the mitochondrial apoptosis pathway
Ca+2↑,
ERK↓, reduced protein expression of p-ERK/ERK
MMP↑, Chrysin pretreatment led to an increase in mitochondrial ROS creation, swelling in isolated mitochondria from hepatocytes, collapse in MMP, and release cytochrome c.
Cyt‑c↑,
Casp3↑, Chrysin could elevate caspase-3 activity in the HCC rats group
HK2↓, chrysin declined HK-2 combined with VDAC-1 on mitochondria
NRF2↓, chrysin inhibited the Nrf2 expression and its downstream genes comprising AKR1B10, HO-1, and MRP5 by quenching ERK and PI3K-Akt pathway
HO-1↓,
MMP2↓, Chrysin pretreatment also downregulated MMP2, MMP9, fibronectin, and snail expression
MMP9↓,
Fibronectin↓,
GRP78/BiP↑, chrysin induced GRP78 overexpression, spliced XBP-1, and eIF2-α phosphorylation
XBP-1↓,
p‑eIF2α↑,
*AST↓, Chrysin administration significantly reduced AST, ALT, ALP, LDH and γGT serum activities
ALAT↓,
ALP↓,
LDH↓,
COX2↑, chrysin attenuated COX-2 and NFkB p65 expression, and Bcl-xL and β-arrestin levels
Bcl-xL↓,
IL6↓, Reduction in IL-6 and TNF-α and augmentation in caspases-9 and 3 were observed due to chrysin supplementation.
PGE2↓, Chrysin induced entire suppression NF-kB, COX-2, PG-E2, iNOS as well.
iNOS↓,
DNAdam↑, Chrysin induced apoptosis of cells by causing DNA fragmentation and increasing the proportions of DU145 and PC-3 cells
UPR↑, Also, it induced ER stress via activation of UPR proteins comprising PERK, eIF2α, and GRP78 in DU145 and PC-3 cells.
Hif1a↓, Chrysin increased the ubiquitination and degradation of HIF-1α by increasing its prolyl hydroxylation
EMT↓, chrysin was effective in HeLa cell by inhibiting EMT and CSLC properties, NF-κBp65, and Twist1 expression
Twist↓,
lipid-P↑, Chrysin disrupted intracellular homeostasis by altering MMP, cytosolic Ca (2+) levels, ROS generation, and lipid peroxidation, which plays a role in the death of choriocarcinoma cells.
CLDN1↓, Chrysin decreased CLDN1 and CLDN11 expression in human lung SCC
PDK1↓, Chrysin alleviated p-Akt and inhibited PDK1 and Akt
IL10↓, Chrysin inhibited cytokines release, TNF-α, IL-1β, IL-10, and IL-6 induced by Ni in A549 cells.
TLR4↓, Chrysin suppressed TLR4 and Myd88 mRNA and protein expression.
NOTCH1↑, Chrysin inhibited tumor growth in ATC both in vitro and in vivo through inducing Notch1
PARP↑, Pretreating cells with chrysin increased cleaved PARP, cleaved caspase-3, and declined cyclin D1, Mcl-1, and XIAP.
Mcl-1↓,
XIAP↓,

3723-

Gb,

Can We Use Ginkgo biloba Extract to Treat Alzheimer’s Disease? Lessons from Preclinical and Clinical Studies

Review,

AD,

*memory↑, GBE displayed generally consistent anti-AD effects in animal experiments, and it might improve AD symptoms in early-stage AD patients after high doses and long-term administration.
*antiOx↑, Antioxidant properties
*Casp3↓, ↓caspase-3
*APP↓, ↓APP
*AChE↓, ↓AChE activity
*Aβ↓, ↓Aβ oligomers
*5HT↑, ↑5-HT in the striatum
*SOD↓, ↓SOD ↓MDA ↓NO
*MDA↓,
*NO↓,
*GSH↑, ↓SOD ↑GSH ↓MDA
*Bcl-2↑, ↑Bcl-2 ↓Bax
*BAX↑,
*TNF-α↓, ↓TNF-α, IL-1β, ccl-2, iNOS, and IL-10
*IL1β↑,
*iNOS↓,
*IL10↓,
*p‑tau↓, ↓tau phosphorylation
*ROS↓, ↓ROS
*MAOB↓, ↓MAO-B enzyme activity
*cognitive↑, A total of 819 patients who had been diagnosed with AD, or that had AD-like symptoms, received lower SKT scores after GBE treatment for 12 to 24 weeks
*neuroP↑, Neuroprotective Mechanism Analysis
*Apoptosis↓, GBE Inhibits Cell Apoptosis

4511-

GLA,

Gamma-Linolenic Acid (GLA) Protects against Ionizing Radiation-Induced Damage: An In Vitro and In Vivo Study

vitro+vivo,

Nor,

RAW264.7

*radioP↑, mice exposed to lethal radiation (survival~20%) is significantly enhanced (to ~80%) by GLA treatment
*ROS↓, GLA reduced DNA damage (as evidenced by micronuclei formation) and enhanced metabolic viability, which led to an increase in the number of surviving RAW 264.7 cells in vitro by reducing ROS generation
*DNAdam↓, GLA reduced DNA damage
*IL6↓, by restoring altered levels of duodenal HMGB1, IL-6, TNF-α, and IL-10 concentrations, as well as the expression of NF-kB, IkB, Bcl-2, Bax, delta-6-desaturase, COX-2, and 5-LOX genes, and pro- and anti-oxidant enzymes (SOD, catalase, glutathione), to
*TNF-α↓,
*IL10↓,
*NF-kB↓,
*SOD↑, GLA pre-treated RAW cells (GLA + irradiation) showed improved antioxidant status and a significant (p < 0.01) increase in SOD, catalase, and GPx
*Catalase↑,
*GSH↑,

2514-

H2,

Hydrogen: A Novel Option in Human Disease Treatment

Review,

NA,

*Inflam↓, Anti-Inflammatory Effect of H2
*IL1β↓, decrease the overexpression of early proinflammatory cytokines, such as interleukin- (IL-) 1β, IL-6, IL-8, IL-10, tumor necrosis factor-alpha (TNF-α
*IL6↓,
*IL8↓,
*IL10↓,
*TNF-α↓,
*ROS↓, . H2 can also downregulate ROS directly or as a regulator of a gas-mediated signal.
*HO-1↓, H2 can enhance the expression of the heme oxygenase-1 (HO-1) antioxidant by activating nuclear factor erythroid 2-related factor 2 (Nrf-2), an upstream regulating molecule of HO-1
*NRF2↑,
*ER Stress↓, hydrogen inhalation significantly reduced the ER stress-related protein and alleviated tissue damage in myocardial I/R injury a
H2O2↑, H2-induced ROS production can also be observed in cancer cells.

3772-

H2,

Therapeutic potential of hydrogen-rich water in zebrafish model of Alzheimer’s disease: targeting oxidative stress, inflammation, and the gut-brain axis

in-vivo,

AD,

zebrafish AD model

*cognitive↑, HRW can significantly improve cognitive impairment and depression-like behavior in zebrafish AD model, reduce Aβ deposition
*Aβ↓, A critical finding of this study was the reduction of Aβ deposition in HRW-treated zebrafish,
*Inflam↓, reduce neuroinflammation, and reduce oxidative stress.
*ROS↓,
*GutMicro↑, HRW reduced the number of harmful bacteria linked to AD pathology by restoring the balance of microbiota in the gut.
*TNF-α↓, HRW significantly decreased pro-inflammatory cytokine levels (TNF-α, IL-6, IL-1β) and increased IL-10 levels in zebrafish brains, suggesting that HRW exerts a strong anti-inflammatory effect.
*IL6↓,
*IL1β↓,
*IL10↓,
*Catalase↑, increase in antioxidative enzymes such as CAT and GSH
*GSH↑,

2868-

HNK,

Honokiol: A review of its pharmacological potential and therapeutic insights

Review,

Var,

Review,

Sepsis,

*P-gp↓, reduction in the expression of defective proteins like P-glycoproteins, inhibition of oxidative stress, suppression of pro-inflammatory cytokines (TNF-α, IL-10 and IL-6),
*ROS↓,
*TNF-α↓,
*IL10↓,
*IL6↓,
eIF2α↑, Bcl-2, phosphorylated eIF2Î±, CHOP,GRP78, Bax, cleaved caspase-9 and phosphorylated PERK
CHOP↑,
GRP78/BiP↑,
BAX↑,
cl‑Casp9↑,
p‑PERK↑,
ER Stress↑, endoplasmic reticulum stress and proteins in apoptosis in 95-D and A549 cells
Apoptosis↑,
MMPs↓, decrease in levels of matrix metal-mloproteinases, P-glycoprotein expression, the formation of mammosphere, H3K27 methyltransferase, c-FLIP, level of CXCR4 receptor,pluripotency-factors, Twist-1, class I histone deacetylases, steroid receptor co
cFLIP↓,
CXCR4↓,
Twist↓,
HDAC↓,
BMPs↑, enhancement in Bax protein, and (BMP7), as well as interference with an activator of transcription 3 (STAT3), (mTOR), (EGFR), (NF-kB) and Shh
p‑STAT3↓, secreased the phosphorylation of STAT3
mTOR↓,
EGFR↓,
NF-kB↓,
Shh↓,
VEGF↓, induce apoptosis, and regulate the vascular endothelial growth factor-A expression (VEGF-A)
tumCV↓, human glioma cell lines (U251 and U-87 MG) through inhibition of colony formation, glioma cell viability, cell migration, invasion, suppression of ERK and AKT signalling cascades, apoptosis induction, and reduction of Bcl-2 expression.
TumCMig↓,
TumCI↓,
ERK↓,
Akt↓,
Bcl-2↓,
Nestin↓, increased the Bax expression, lowered the CD133, EGFR, and Nesti
CD133↓,
p‑cMET↑, HKL through the downregulating the phosphorylation of c-Met phosphorylation and stimulation of Ras,
RAS↑,
chemoP↑, Cheng and coworker determined the chemopreventive role of HKL against the proliferation of renal cell carcinoma (RCC) 786â0 cells through multiple mechanism
*NRF2↑, , HKL also effectively activate the Nrf2/ARE pathway and reverse this pancreatic dysfunction in in vivo and in vitro model
*NADPH↓, (HUVECs) such as inhibition of NADPH oxidase activity, suppression of p22 (phox) protein expression, Rac-1 phosphorylation, reactive oxygen species production, inhibition of degradation of Ikappa-B-alpha, and suppression of activity of of NF-kB
*p‑Rac1↓,
*ROS↓,
*IKKα↑,
*NF-kB↓,
*COX2↓, Furthermore, HKL treatment the inhibited cyclooxygenase (COX-2) upregulation, reduces prostaglandin E2 production, enhanced caspase-3 activity reduction
*PGE2↓,
*Casp3↓,
*hepatoP↑, compound also displayed hepatoprotective action against oxidative injury in tert-butyl hydroperoxide (t-BHP)-injured AML12 liver cells in in vitro model
*antiOx↑, compound reduces the level of acetylation on SOD2 to stimulate its antioxidative action, which results in reduced reactive oxygen species aggregation in AML12 cells
*GSH↑, HKL prevents oxidative damage induced by H2O2 via elevating antioxidant enzymes levels which includes glutathione and catalase and promotes translocation and activation transcription factor Nrf2
*Catalase↑,
*RenoP↑, imilarly, the compound protects renal reperfusion/i-schemia injury (IRI) in adult male albino Wistar rats via reducing theactivities of serum alkaline phosphatase (ALP), aspartate aminotrans- ferase (AST) and alanine aminotransferase (ALT)
*ALP↓,
*AST↓,
*ALAT↓,
*neuroP↑, Several reports and works have shown that HKL displays some neuroprotective properties
*cardioP↑, Cardioprotection
*HO-1↑, the expression level of heme oxygenase-1 (HO-1)was remarkably up-regulated and miR-218-5p was significantly down-regulated in septic mice treated with HKL
*Inflam↓, anti-inflammatory action of HKL at dose of 10 mg/kg in the muscle layer of mice

3531-

Lyco,

Lycopene attenuates the inflammation and apoptosis in aristolochic acid nephropathy by targeting the Nrf2 antioxidant system

in-vivo,

Nor,

rats

*NRF2↑, After LYC intervened in the body, it activated Nrf2 nuclear translocation and its downstream HO-1 and NQO1 antioxidant signaling pathways
*HO-1↑, Lycopene activates Nrf2-HO-1 antioxidant pathway to inhibit oxidative stress injury induced by AAI exposure in NRK52E cells
*NQO1↑,
*ROS↓, LYC inhibited ROS production by renal tubular epithelial cells, and alleviated mitochondrial damage.
*mtDam↓,
*Bcl-2↑, LYC was able to up-regulate the expression of Bcl-2, down-regulate Bax expression and inhibit the activation of cleaved forms of Caspase-9 and Caspase-3, which finally attenuated the apoptosis
*BAX↓,
*Casp9↓,
*Casp3↓,
*Apoptosis↓,
*RenoP↑, Interestingly, there was a significant improvement in damaged renal tissue in mice with AAN after lycopene intervention
*lipid-P↓, lycopene significantly decreased the expression of AAI-induced lipid peroxidation product (MDA), and increased the expression of antioxidant enzyme systems (T-AOC, SOD, and GSH-PX)
*SOD↑,
*GPx↑,
*Inflam↓, Lycopene improves inflammatory responses in the kidneys of AAN mice
*TNF-α↓, TNF-α, IL-6, IL-10, was increased and the expression of IL-12 was decreased in the kidneys of model mice compared with the control group. However, LYC intervention reversed the expression of these genes in a dose-dependent manner
*IL6↓,
*IL10↓,

3529-

Lyco,

The antioxidant and anti-inflammatory properties of lycopene in mice lungs exposed to cigarette smoke

in-vivo,

Nor,

mice

*antiOx↑, Lycopene is a carotenoid with known antioxidant and anti-inflammatory properties.
*Inflam↓,
*ROS↓, Lycopene concentrations of 1 μM and 2 μM were able to reduce the production of ROS in 24 h compared with CS.
*TNF-α↓, There was an increase in the levels of tumor necrosis factor-α, interferon-γ and interleukin-10 after exposure to CS, and these effects were suppressed by both doses of lycopene.
*IFN-γ↓,
IL10↓,

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↓,

1672-

PBG,

The Potential Use of Propolis as an Adjunctive Therapy in Breast Cancers

Review,

BC,

ChemoSen↓, 4 human clinical trials that demonstrated the successful use of propolis in alleviating side effects of chemotherapy and radiotherapy while increasing the quality of life of breast cancer patients, with minimal adverse effects.
RadioS↑,
Inflam↓, immunomodulatory, anti-inflammatory, and anti-cancer properties.
AntiCan↑,
Dose∅, Indonesia: IC50 = 4.57 μg/mL and 10.23 μg/mL
mtDam↑, Poland: propolis induced mitochondrial damage and subsequent apoptosis in breast cancer cells.
Apoptosis?,
OCR↓, China: CAPE inhibited mitochondrial oxygen consumption rate (OCR) by reducing basal, maximal, and spare respiration rate and consequently inhibiting ATP production
ATP↓,
ROS↑, Iran: inducing intracellular ROS production, IC50 = 65-96 μg/mL
ROS↑, Propolis induced mitochondrial dysfunction and lactate dehydrogenase release indicating the occurrence of ROS-associated necrosis.
LDH↓,
TP53↓, Interestingly, a reduced expression of apoptosis-related genes such as TP53, CASP3, BAX, and P21)
Casp3↓,
BAX↓,
P21↓,
ROS↑, CAPE: inducing oxidative stress through upregulation of e-NOS and i-NOS levels
eNOS↑,
iNOS↑,
eff↑, The combination of propolis and mangostin significantly reduced the expression of Wnt2, FAK, and HIF-1α, when compared to propolis or mangostin alone
hTERT/TERT↓, downregulation of the mRNA levels of hTERT and cyclin D1
cycD1/CCND1↓,
eff↑, Synergism with bee venom was observed
eff↑, Statistically significant decrease was found in the MCF-7 cell viability 48 h after applying different combinations of cisplatin (3.12 μg/mL) and curcumin (0.31 μg/mL) and propolis (160 μg/mL)
eff↑, Nanoparticles of chrysin had significantly higher cytotoxicity against MCF-7 cells, compared to chrysin
eff↑, Propolis nanoparticles appeared to increase cytotoxicity of propolis against MCF-7 cells
STAT3↓, Chrysin also inhibited the hypoxia-induced STAT3 tyrosine phosphorylation suggesting the mechanism of action was through STAT3 inhibition.
TIMP1↓, Propolis reduced the expression of TIMP-1, IL-4, and IL-10.
IL4↓,
IL10↓,
OS↑, patients supplemented with propolis had significantly longer median disease free survival time (400 mg, 3 times daily for 10 d pre-, during, and post)
Dose∅, 400 mg, 3 times daily for 10 d pre-, during, and post
ER Stress↑, endoplasmic reticulum stress
ROS↑, upregulating the expression of Annexin A7 (ANXA7), reactive oxygen species (ROS) level, and NF-κB p65 level, while simultaneously reducing the mitochondrial membrane potential.
NF-kB↓,
p65↓,
MMP↓,
TumAuto↑, propolis induced autophagy by increasing the expression of LC3-II and reducing the expression of p62 level
LC3II↑,
p62↓,
TLR4↓, propolis downregulates the inflammatory TLR4
mtDam↑, propolis induced mitochondrial dysfunction and lactate dehydrogenase release indicating ROS-associated necrosis in MDA MB-231cancer cells
LDH↓,
ROS↑,
Glycolysis↓, inhibit the proliferation of MDA-MB-231 cells by targeting key enzymes of glycolysis, namely glycolysis-hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase muscle isozyme M2 (PKM2), and lactate dehydrogenase A (LDHA),
HK2↓,
PFK↓,
PKM2↓,
LDH↓,
IL10↓, propolis significantly reduced the relative number of CD4+, CD25+, FoxP3+ regulatory T cells expressing IL-10
HDAC8↓, Chrysin, a propolis bioactive compound, inhibits HDAC8
eff↑, combination of propolis and mangostin significantly reduced the expression of Wnt2, FAK, and HIF-1α, when compared to propolis or mangostin alone.
eff↑, Propolis also upregulated the expression of catalase, HTRA2/Omi, FADD, and TRAIL-associated DR5 and DR4 which significantly enhanced the cytotoxicity of doxorubicin in MCF-7 cells
P21↑, Chrysin, a propolis bioactive compound, inhibits HDAC8 and significantly increases the expression of p21 (waf1/cip1) in breast cancer cells, leading to apoptosis.

3255-

PBG,

Propolis reversed cigarette smoke-induced emphysema through macrophage alternative activation independent of Nrf2

in-vivo,

Nor,

Eight-week-old male C57BL/6 mice

*IGF-1↓, propolis downregulated IGF1 expression
*MMP2↑, Propolis also increased MMP-2 and decreased MMP-12 expression, favoring the process of tissue repair.
*ROS↓, propolis recruited leukocytes, including macrophages, without ROS release.
*Inflam↓, thus increasing the number of arginase-positive cells and IL-10 levels and favoring an anti-inflammatory microenvironment
*IL10↓,
*NRF2∅, Proteins and enzymes related to Nrf2 were not altered,

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.

5624-

ProBio,

Bif,

A randomized double-blind placebo-controlled trial of probiotics in post-surgical colorectal cancer

Trial,

Testi,

Fifty-two patients with colorectal cancer were randomized at four weeks after surgery to receive either a placebo

Dose↝, 07 mg of Lactobacillus acidophilus BCMC® 12,130, Lactobacillus lactis BCMC® 12,451, Lactobacillus casei subsp BCMC® 12,313, Bifidobacterium longum BCMC® 02120, Bifidobacterium bifidum BCMC® 02290 and Bifidobacterium infantis
TNF-α↓, Significant reduction in the level of pro-inflammatory cytokine, TNF-α, IL-6, IL-10, IL-12, IL-17A, IL-17C and IL-22 were observed in CRC patients who received probiotics as compared to pre-treatment level (P < 0.05).
IL6↓,
IL10↓,
IL12↓,
IL22↓,
toxicity↓, We have shown that probiotics containing six viable microorganisms of Lactobacillus and Bifidobacteria strains are safe to be consumed at four weeks after surgery in colorectal cancer patients and have reduced pro-inflammatory cytokines (except for I

910-

QC,

The Anti-Cancer Effect of Quercetin: Molecular Implications in Cancer Metabolism

tumCV↓,
Apoptosis↑,
PI3k/Akt/mTOR↓, QUE induces cell death by inhibiting PI3K/Akt/mTOR and STAT3 pathways in PEL cells
Wnt/(β-catenin)↓, reducing β-catenin
MAPK↝,
ERK↝, ERK1/2
TumCCA↑, cell cycle arrest at the G1 phase
H2O2↑,
ROS↑,
TumAuto↑,
MMPs↓, Consistently, QUE was able to reduce the protein levels of MMP-2, MMP-9, VEGF and mTOR, and p-Akt in breast cancer cell lines
P53↑,
Casp3↑,
Hif1a↓, by inactivating the Akt-mTOR pathway [64,74] and HIF-1α
cFLIP↓,
IL6↓, QUE decreased the release of interleukin-6 (IL-6) and IL-10
IL10↓,
lactateProd↓,
Glycolysis↓, It is suggested that QUE alters glucose metabolism by inhibiting monocarboxylate transporter (MCT) activity
PKM2↓,
GLUT1↓,
COX2↓,
VEGF↓,
OCR↓,
ECAR↓,
STAT3↓,
MMP2↓, Consistently, QUE was able to reduce the protein levels of MMP-2, MMP-9, VEGF and mTOR, and p-Akt in breast cancer cell lines
MMP9:TIMP1↓,
mTOR↓,

916-

QC,

Quercetin and cancer: new insights into its therapeutic effects on ovarian cancer cells

Review,

Ovarian,

COX2↓,
CRP↓,
ER Stress↑, Quercetin can result in stimulate the ER stress pathway that lead to the cause of cell death and apoptosis
Apoptosis↑,
GRP78/BiP↑,
CHOP↑,
p‑STAT3↓, quercetin suppresses STAT3 and PI3K/AKT/mTOR pathways
PI3K↓,
Akt↓,
mTOR↓,
cMyc↓, leading to downregulate the prosurvival cellular proteins expression, including cMyc, cyclin D1, and c-FLIP
cycD1/CCND1↓,
cFLIP↓,
IL6↓, decreased the IL-6 and IL-10 release
IL10↓,

3343-

QC,

Quercetin, a Flavonoid with Great Pharmacological Capacity

Review,

Var,

Review,

AD,

Review,

Arthritis,

*antiOx↑, Quercetin has a potent antioxidant capacity, being able to capture reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive chlorine species (ROC),which act as reducing agents by chelating transition-metal ions.
*ROS↓, Quercetin is a potent scavenger of reactive oxygen species (ROS), protecting the organism against oxidative stress
*angioG↓,
*Inflam↓, anti-inflammatory properties; the ability to protect low-density lipoprotein (LDL) oxidation, and the ability to inhibit angiogenesis;
*BioAv↓, It is known that the bioavailability of quercetin is usually relatively low (0.17–7 μg/mL), less than 10% of what is consumed, due to its poor water solubility (hydrophobicity), chemical stability, and absorption profile.
*Half-Life↑, their slow elimination since their half-life ranges from 11 to 48 h, which could favor their accumulation in plasma after repeated intakes
*GSH↑, Animal and cell studies have demonstrated that quercetin induces the synthesis of GSH
*SOD↑, increase in the expression of superoxide dismutase (SOD), catalase (CAT), and GSH with quercetin pretreatment
*Catalase↑,
*Nrf1↑, quercetin accomplishes this process involves increasing the activity of the nuclear factor erythroid 2-related factor 2 (NRF2), enhancing its binding to the ARE, reducing its degradation
*BP↓, quercetin has been shown to inhibit ACE activity, reducing blood pressure
*cardioP↑, quercetin has positive effects on cardiovascular diseases
*IL10↓, Under the influence of quercetin, the levels of interleukin 10 (IL-10), IL-1β, and TNF-α were reduced.
*TNF-α↓,
*Aβ↓, quercetin’s ability to modulate the enzyme activity in clearing amyloid-beta (Aβ) plaques, a hallmark of AD pathology.
*GSK‐3β↓, quercetin can inhibit the activity of glycogen synthase kinase 3β,
*tau↓, thus reducing tau aggregation and neurofibrillary tangles in the brain
*neuroP↑,
*Pain↓, quercetin reduces pain and inflammation associated with arthritis
*COX2↓, quercetin included the inhibition of oxidative stress, production of cytokines such as cyclooxygenase-2 (COX-2) and proteoglycan degradation, and activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) (Nrf2/HO-1)
*NRF2↑,
*HO-1↑,
*IL1β↓, Mechanisms included decreased levels of TNF-α, IL-1β, IL-17, and monocyte chemoattractant protein-1 (MCP-1)
*IL17↓,
*MCP1↓,
PKCδ↓, studies with human leukemia 60 (HL-60) cells report that concentrations between 20 and 30 µM are sufficient to exert an inhibitory effect on cytosolic PKC activity and membrane tyrosine protein kinase (TPK) activity.
ERK↓, 50 µM resulted in the blockade of the extracellular signal-regulated kinases (ERK1/2) pathway
BAX↓, higher doses (75–100 µM) were used, as these doses reduced the expression of proapoptotic factors such as Bcl-2-associated X protein (Bax) and caspases 3 and 9
cMyc↓, induce apoptosis at concentrations of 80 µM and also causes a downregulation of cellular myelocytomatosis (c-myc) and Kirsten RAt sarcoma (K-ras) oncogenes
KRAS↓,
ROS↓, compound’s antioxidative effect changes entirely to a prooxidant effect at high concentrations, which induces selective cytotoxicity
selectivity↑, On the other hand, when noncancerous cells are exposed to quercetin, it exerts cytoprotective effects;
tumCV↓, decrease cell viability in human glioma cultures of the U-118 MG cell line as well as an increase in death by apoptosis and cell arrest at the G2 checkpoint of the cell cycle.
Apoptosis↑,
TumCCA↑,
eff↑, quercetin combined with doxorubicin can induce multinucleation of invasive tumor cells, downregulate P-glycoprotein (P-gp) expression, increase cell sensitivity to doxorubicin,
P-gp↓,
eff↑, resveratrol, quercetin, and catechin can effectively block the cell cycle and reduce cell proliferation in vivo
eff↑, cotreatment with epigallocatechin gallate (EGCG) inhibited catechol-O-methyltransferase (COMT) activity, decreasing COMT protein content and thereby arresting the cell cycle of PC-3 human prostate cancer cells
eff↑, synergistic treatment of tamoxifen and quercetin was also able to inhibit prostate tumor formation by regulating angiogenesis
eff↑, coadministration of 2.5 μM of EGCG, genistein, and quercetin suppressed the cell proliferation of a prostate cancer cell line (CWR22Rv1) by controlling androgen receptor and NAD (P)H: quinone oxidoreductase 1 (NQO1) expression
CycB/CCNB1↓, It can also downregulate cyclin B1 and cyclin-dependent kinase-1 (CDK-1),
CDK1↓,
CDK4↓, quercetin causes a decrease in cyclins D1/Cdk4 and E/Cdk2 and an increase in p21 in vascular smooth muscle cells
CDK2↓,
TOP2↓, quercetin is known to be a potent inhibitor of topoisomerase II (TopoII), a cell cycle-associated enzyme necessary for DNA replication
Cyt‑c↑, quercetin can induce apoptosis (cell death) through caspase-3 and caspase-9 activation, cytochrome c release, and poly ADP ribose polymerase (PARP) cleavage
cl‑PARP↑,
MMP↓, quercetin induces the loss of mitochondrial membrane potential, leading to the activation of the caspase cascade and cleavage of PARP.
HSP70/HSPA5↓, apoptotic effects of quercetin may result from the inhibition of HSP kinases, followed by the downregulation of HSP-70 and HSP-90 protein expression
HSP90↓,
MDM2↓, (MDM2), an onco-protein that promotes p53 destruction, can be inhibited by quercetin
RAS↓, quercetin can prevent Ras proteins from being expressed. In one study, quercetin was found to inhibit the expression of Harvey rat sarcoma (H-Ras), K-Ras, and neuroblastoma rat sarcoma (N-Ras) in human breast cancer cells,
eff↑, there was a substantial difference in EMT markers such as vimentin, N-cadherin, Snail, Slug, Twist, and E-cadherin protein expression in response to AuNPs-Qu-5, inhibiting the migration and invasion of MCF-7 and MDA-MB cells

3368-

QC,

The potential anti-cancer effects of quercetin on blood, prostate and lung cancers: An update

Review,

Var,

*Inflam↓, quercetin is known for its anti-inflammatory, antioxidant, and anticancer properties.
*antiOx↑,
*AntiCan↑,
Casp3↓, Quercetin increases apoptosis and autophagy in cancer by activating caspase-3, inhibiting the phosphorylation of Akt, mTOR, and ERK, lessening β-catenin, and stabilizing the stabilization of HIF-1α.
p‑Akt↓,
p‑mTOR↓,
p‑ERK↓,
β-catenin/ZEB1↓,
Hif1a↓,
AntiAg↓, Quercetin have revealed an anti-tumor effect by reducing development of blood vessels. I
VEGFR2↓, decrease tumor growth through targeting VEGFR-2-mediated angiogenesis pathway and suppressing the downstream regulatory component AKT in prostate and breast malignancies.
EMT↓, effects of quercetin on inhibition of EMT, angiogenesis, and invasiveness through the epidermal growth factor receptor (EGFR)/VEGFR-2-mediated pathway in breast cancer
EGFR↓,
MMP2↓, MMP2 and MMP9 are two remarkable compounds in metastatic breast cancer (28–30). quercetin on breast cancer cell lines (MDA-MB-231) and showed that after treatment with this flavonoid, the expression of these two proteinases decreased
MMP↓,
TumMeta↓, head and neck (HNSCC), the inhibitory effect of quercetin on the migration of tumor cells has been shown by regulating the expression of MMPs
MMPs↓,
Akt↓, quercetin by inhibiting the Akt activation pathway dependent on Snail, diminishing the expression of N-cadherin, vimentin, and ADAM9 and raising the expression of E-cadherin and proteins
Snail↓,
N-cadherin↓,
Vim↓,
E-cadherin↑,
STAT3↓, inhibiting STAT3 signaling
TGF-β↓, reducing the expression of TGF-β caused by vimentin and N-cadherin, Twist, Snail, and Slug and increasing the expression of E-cadherin in PC-3 cells.
ROS↓, quercetin exerted an anti-proliferative role on HCC cells by lessening intracellular ROS independently of p53 expression
P53↑, increasing the expression of p53 and BAX in hepatocellular carcinoma (HepG2) cell lines through the reduction of PKC, PI3K, and cyclooxygenase (COX-2)
BAX↑,
PKCδ↓,
PI3K↓,
COX2↓,
cFLIP↓, quercetin by inhibiting PI3K/AKT/mTOR and STAT3 pathways, decreasing the expression of cellular proteins such as c-FLIP, cyclin D1, and c-Myc, as well as reducing the production of IL-6 and IL-10 cytokines, leads to the death of PEL cells
cycD1/CCND1↓,
cMyc↓,
IL6↓,
IL10↓,
Cyt‑c↑, In addition, quercetin induced c-cytochrome-dependent apoptosis and caspase-3 almost exclusively in the HSB2 cell line
TumCCA↑, Exposure of K562 cells to quercetin also significantly raised the cells in the G2/M phase, which reached a maximum peak in 24 hours
DNMTs↓, pathway through DNA demethylation activity, histone deacetylase (HDAC) repression, and H3ac and H4ac enrichment
HDAC↓,
ac‑H3↑,
ac‑H4↑,
Diablo↑, SMAC/DIABLO exhibited activation
Casp3↑, enhanced levels of activated caspase 3, cleaved caspase 9, and PARP1
Casp9↑,
PARP1↑,
eff↑, green tea and quercetin as monotherapy caused the reduction of levels of anti-apoptotic proteins, CDK6, CDK2, CYCLIN D/E/A, BCL-2, BCL-XL, and MCL-1 and an increase in expression of BAX.
PTEN↑, Quercetin upregulates the level of PTEN as a tumor suppressor, which inhibits AKT signaling
VEGF↓, Quercetin had anti-inflammatory and anti-angiogenesis effects, decreasing VGEF-A, NO, iNOS, and COX-2 levels
NO↓,
iNOS↓,
ChemoSen↑, quercetin and chemotherapy can potentiate their effect on the malignant cell
eff↑, combination with hyperthermia, Shen et al. Quercetin is a method used in cancer treatment by heating, and it was found to reduce Doxorubicin hydrochloride resistance in leukemia cell line K562
eff↑, treatment with ellagic acid, luteolin, and curcumin alone showed excellent anticancer effects.
eff↑, co-treatment with quercetin and curcumin led to a reduction of mitochondrial membrane integrity, promotion of cytochrome C release, and apoptosis induction in CML cells
uPA↓, A-549 cells were shown to have reduced mRNA expressions of urokinase plasminogen activator (uPA), Upar, protein expression of CXCR-4, CXCL-12, SDF-1 when quercetin was applied at 20 and 40 mM/ml by real-time PCR.
CXCR4↓,
CXCL12↓,
CLDN2↓, A-549 cells, indicated that quercetin could reduce mRNA and protein expression of Claudin-2 in A-549 cell lines without involving Akt and ERK1/2,
CDK6↓, CDK6, which supports the growth and viability of various cancer cells, was hampered by the dose-dependent manner of quercetin (IC50 dose of QR for A-549 cells is 52.35 ± 2.44 μM).
MMP9↓, quercetin up-regulated the rates of G1 phase cell cycle and cellular apoptotic in both examined cell lines compared with the control group, while it declined the expressions of the PI3K, AKT, MMP-2, and MMP-9 proteins
TSP-1↑, quercetin increased TSP-1 mRNA and protein expression to inhibit angiogenesis,
Ki-67↓, significant reductions in Ki67 and PCNA proliferation markers and cell survival markers in response to quercetin and/or resveratrol.
PCNA↓,
ROS↑, Also, quercetin effectively causes intracellular ROS production and ER stress
ER Stress↑,

3369-

QC,

Pharmacological basis and new insights of quercetin action in respect to its anti-cancer effects

Review,

Pca,

FAK↓, Quercetin can inhibit HGF-induced melanoma cell migration by inhibiting the activation of c-Met and its downstream Gabl, FAK and PAK [84]
TumCCA↑, stimulation of cell cycle arrest at the G1 stage
p‑pRB↓, mediated through regulation of p21 CDK inhibitor and suppression of pRb phosphorylation resulting in E2F1 sequestering.
CDK2↑, low dose of quercetin has brought minor DNA injury and Chk2 induction
CycB/CCNB1↓, quercetin has a role in the reduction of cyclin B1 and CDK1 levels,
CDK1↓,
EMT↓, quercetin suppresses epithelial to mesenchymal transition (EMT) and cell proliferation through modulation of Sonic Hedgehog signaling pathway
PI3K↓, quercetin on other pathways such as PI3K, MAPK and WNT pathways have also been validated in cervical cancer
MAPK↓,
Wnt↓,
ROS↑, colorectal cancer, quercetin has been shown to suppress carcinogenesis through various mechanisms including affecting cell proliferation, production of reactive oxygen species and expression of miR-21
miR-21↑,
Akt↓, Figure 1 anti-cancer mechanisms
NF-kB↓,
FasL↑,
Bak↑,
BAX↑,
Bcl-2↓,
Casp3↓,
Casp9↑,
P53↑,
p38↑,
MAPK↑,
Cyt‑c↑,
PARP↓,
CHOP↑,
ROS↓,
LDH↑,
GRP78/BiP↑,
ERK↑,
MDA↓,
SOD↑,
GSH↑,
NRF2↑,
VEGF↓,
PDGF↓,
EGF↓,
FGF↓,
TNF-α↓,
TGF-β↓,
VEGFR2↓,
EGFR↓,
FGFR1↓,
mTOR↓,
cMyc↓,
MMPs↓,
LC3B-II↑,
Beclin-1↑,
IL1β↓,
CRP↓,
IL10↓,
COX2↓,
IL6↓,
TLR4↓,
Shh↓,
HER2/EBBR2↓,
NOTCH↓,
DR5↑, quercetin has enhanced DR5 expression in prostate cancer cells
HSP70/HSPA5↓, Quercetin has also suppressed the upsurge of hsp70 expression in prostate cancer cells following heat treatment and enhanced the quantity of subG1 cells
CSCs↓, Quercetin could also suppress cancer stem cell attributes and metastatic aptitude of isolated prostate cancer cells through modulating JNK signaling pathway
angioG↓, Quercetin inhibits angiogenesis-mediated of human prostate cancer cells through negatively modulating angiogenic factors (TGF-β, VEGF, PDGF, EGF, bFGF, Ang-1, Ang-2, MMP-2, and MMP-9)
MMP2↓,
MMP9↓,
IGFBP3↑, Quercetin via increasing the level of IGFBP-3 could induce apoptosis in PC-3 cells
uPA↓, Quercetin through decreasing uPA and uPAR expression and suppressing cell survival protein and Ras/Raf signaling molecules could decrease prostate cancer progression
uPAR↓,
RAS↓,
Raf↓,
TSP-1↑, Quercetin through TSP-1 enhancement could effectively inhibit angiogenesis

3076-

RES,

Resveratrol for targeting the tumor microenvironment and its interactions with cancer cells

Review,

Var,

IL6↓, A dose-dependent reduction of IL-6 by resveratrol led to attenuation of matrix metalloproteinases (MMPs), including MMP2 and MMP9
MMPs↓,
MMP2↓,
MMP9↓,
BioAv↓, The most important weakness of the usual form of resveratrol is its low absorption in the intestine and its low bioavailability
Half-Life↑, some covers such as liposomes and micelles also can facilitate absorption and increase half-life
BioAv↑, another study showed that carboxymethyl chitosan can increase bioavailability by more than 3.5 times
Dose↝, low concentrations of resveratrol (lower than 50 uM) cause no remarkable toxicity for normal cells, while higher concentrations are associated with increased oxidative injury
angioG↓, It is suggested that inhibition of STAT3, IL-10, and a reduction of vascular endothelial growth factor (VEGF) by resveratrol is involved in the suppression of macrophages and reduction of invasion and angiogenesis
IL10↓,
VEGF↓,
NF-kB↓, Inhibition of NF-kB by resveratrol can attenuate the expression of COX-2.
COX2↓,
SIRT1↑, Activation of Sirt-1 by resveratrol has a role in the suppression of NF-kB
Wnt↓, Resveratrol has also been shown that inhibit the Wnt/C-Myc pathway too
cMyc↓,
STAT3↓, Resveratrol has been shown that attenuate the expression of STAT3 through reduction of IL-6 level
PTEN↑, Downregulation of miR-17, miR-20a and miR-106b by resveratrol can activate PTEN, which leads to suppression of PI3K and induction of apoptosis in cancer cells
ROS↑, Resveratrol can trigger NOX5-induced ROS, leading to the induction of DNA damage and cancer cells senescence
RadioS↑, The combination of radiation and resveratrol has shown that has a synergic effect for stimulation of ROS production and induction of senescence in non-small cell lung carci- noma
Hif1a↓, Resveratrol can inhibit HIF-1Î± and its downstream proteins, including E-cadherin and vimentin
E-cadherin↓,
Vim↓,
angioG↓, Furthermore, resveratrol inhibits angiogenesis markers and tumor growth through the inhibition of HIF-1a

3646-

SIL,

"Silymarin", a promising pharmacological agent for treatment of diseases

Review,

NA,

*P-gp↓, The possible known mechanisms of action of silymarin protection are blockade and adjustment of cell transporters, p-glycoprotein, estrogenic and nuclear receptors.
*Inflam↓, silymarin anti-inflammatory effects through reduction of TNF-α, protective effects on erythrocyte lysis and cisplatin-induced acute nephrotoxicity
*hepatoP↑, first usage of Milk thistle, however, was for its hepatoprotectant and antioxidant activities
*antiOx↑,
*GSH↑, increasing the glutathione concentrations
*BioAv↑, Milk thistle extract is now marketing as silymarin and silybinin capsules and tablets with an improved bioavailability under the trade names like Livergol, Silipide and Legalon
*SOD↑, increases the superoxide dismutase activity within the erythrocytes and lymphocytes (
*IFN-γ↓, enhances the IFN-γ, IL-4 and IL-10 secretion in cultures containing lymphocytes.
*IL4↓,
*IL10↓,
*Half-Life↓, Silymarin has a short half-life and quick conjugation in the liver and principal excretion in bile.
*TNF-α↓, Silybinin inhibits elevated intra-hepatic messenger RNA (mRNA) levels of IL-2, IL-4, IFN-γ, and TNF-α significantly
*ALAT↓, reduces the alanine aminotransferase and aspartate aminotransferase levels and suppressed the apoptosis in hepatocytes
*AST↓,
Akt↓, HepG2 -cells death occurs via inhibition of Akt kinase stimulated by palmitate exposure and silymarin prevents this inhibition as it has hepatoprotective activity different from its antioxidant property
chemoP↑, Silymarin can be applied as a co-treatment with the other chemotherapeutics agents while silybin is mainly useful as a hepatoprotective substance against chemotherapeutics-induced oxidative stress.
β-catenin/ZEB1↓, silymarin inhibits β-catenin increase, which will suppress the proliferation of hepatocellular carcinoma HepG2 cells.
TumCP↓,
MMP↓, mitochondrial membrane potential of HepG2 cells decreases by silymarin that causes disruption of membrane permeability so that cytochrome C transfers from the intermembrane space to the cytoplasm
Cyt‑c↑,
*RenoP↑, Renal protection
*BBB↑, silymarin has antioxidant activities in the central nervous system, which enables it to enter the CNS via the blood–brain barrier (BBB)

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

2415-

SK,

Shikonin induces programmed death of fibroblast synovial cells in rheumatoid arthritis by inhibiting energy pathways

in-vivo,

Arthritis,

 paw swelling in rat arthritic tissues

Apoptosis?, shikonin induced apoptosis and autophagy in RA-FLSs by activating the production of reactive oxygen species (ROS) and inhibiting intracellular ATP levels, glycolysis-related proteins, and the PI3K-AKT-mTOR signaling pathway.
TumAuto↑,
ROS↑,
ATP↓,
Glycolysis↓, shikonin can inhibit RA-glycolysis in FLSs
PI3K↓,
Akt↓,
mTOR↓,
*Apoptosis↓, Shikonin can significantly reduce the expression of apoptosis-related proteins, paw swelling in rat arthritic tissues, and the levels of inflammatory factors in peripheral blood, such as TNF-α, IL-6, IL-8, IL-10, IL-17A, and IL-1β while showing less
*Inflam↓,
*TNF-α↓,
*IL6↓,
*IL8↓,
*IL10↓,
*IL17↓,
*hepatoP↑, while showing less toxicity to the liver and kidney.
*RenoP↑,
PKM2↓, The expression of glycogen proteins PKM2, GLUT1, and HK2 decreased with increasing concentrations of shikonin
GLUT1↓,
HK2↓,

3427-

TQ,

Chemopreventive and Anticancer Effects of Thymoquinone: Cellular and Molecular Targets

ROS⇅, It appears that the cellular and/or physiological context(s) determines whether TQ acts as a pro-oxidant or an anti-ox- idant in vivo
Fas↑, Figure 2, cell death
DR5↑,
TRAIL↑,
Casp3↑,
Casp8↑,
Casp9↑,
P53↑,
mTOR↓,
Bcl-2↓,
BID↓,
CXCR4↓,
JNK↑,
p38↑,
MAPK↑,
LC3II↑,
ATG7↑,
Beclin-1↑,
AMPK↑,
PPARγ↑, cell survival
eIF2α↓,
P70S6K↓,
VEGF↓,
ERK↓,
NF-kB↓,
XIAP↓,
survivin↓,
p65↓,
DLC1↑, epigenetic
FOXO↑,
TET2↑,
CYP1B1↑,
UHRF1↓,
DNMT1↓,
HDAC1↓,
IL2↑, inflammation
IL1↓,
IL6↓,
IL10↓,
IL12↓,
TNF-α↓,
iNOS↓,
COX2↓,
5LO↓,
AP-1↓,
PI3K↓, invastion
Akt↓,
cMET↓,
VEGFR2↓,
CXCL1↓,
ITGA5↓,
Wnt↓,
β-catenin/ZEB1↓,
GSK‐3β↓,
Myc↓,
cycD1/CCND1↓,
N-cadherin↓,
Snail↓,
Slug↓,
Vim↓,
Twist↓,
Zeb1↓,
MMP2↓,
MMP7↓,
MMP9↓,
JAK2↓, cell proliferiation
STAT3↓,
NOTCH↓,
cycA1/CCNA1↓,
CDK2↓,
CDK4↓,
CDK6↓,
CDC2↓,
CDC25↓,
Mcl-1↓,
E2Fs↓,
p16↑,
p27↑,
P21↑,
ChemoSen↑, Such chemo-potentiating effects of TQ in different cancer cells have been observed with 5-fluorouracil in gastric cancer and colorectal cancer models

Showing Research Papers: 1 to 32 of 32

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 32

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 6, Catalase↑, 6, GPx↓, 1, GPx↑, 1, GSH↑, 8, HO-1↓, 1, HO-1↑, 3, lipid-P↓, 1, MDA↓, 3, MPO↓, 1, NQO1↑, 1, Nrf1↑, 1, NRF2↑, 6, NRF2∅, 1, ROS↓, 11, SOD?, 1, SOD↓, 1, SOD↑, 5,

Mitochondria & Bioenergetics ⓘ

mtDam↓, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 3, NADPH↓, 1,

Cell Death ⓘ

Apoptosis↓, 3, BAX↓, 1, BAX↑, 1, Bcl-2↑, 2, Casp3↓, 3, Casp9↓, 1, iNOS↓, 2,

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,

DNA Damage & Repair ⓘ

DNAdam↓, 1,

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1, IGF-1↓, 1,

Migration ⓘ

APP↓, 1, Cartilage↑, 1, MMP2↑, 1, MMP9↓, 1, p‑Rac1↓, 1, TGF-β↓, 1, TGF-β1↓, 1, α-SMA↓, 1,

Angiogenesis & Vasculature ⓘ

angioG↓, 1, NO↓, 1,

Barriers & Transport ⓘ

BBB↑, 1, P-gp↓, 2,

Immune & Inflammatory Signaling ⓘ

COX2↓, 4, DCells↑, 1, IFN-γ↓, 2, IFN-γ↑, 1, IKKα↑, 1, IL10↓, 13, IL17↓, 2, IL1β↓, 5, IL1β↑, 1, IL4↓, 1, IL5↓, 1, IL6↓, 8, IL6↑, 1, IL8↓, 3, Inflam↓, 11, MCP1↓, 1, NF-kB↓, 4, PGE2↓, 2, TLR4↓, 1, TNF-α↓, 13,

Synaptic & Neurotransmission ⓘ

5HT↑, 1, AChE↓, 1, tau↓, 1, p‑tau↓, 1,

Protein Aggregation ⓘ

Aβ↓, 3, MAOB↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 2, BioAv↑, 1, Half-Life↓, 1, Half-Life↑, 1,

Clinical Biomarkers ⓘ

ALAT↓, 3, ALP↓, 1, AST↓, 4, BP↓, 1, GutMicro↑, 1, IL6↓, 8, IL6↑, 1,

Functional Outcomes ⓘ

AntiCan↑, 1, cardioP↑, 2, cognitive↑, 2, hepatoP↑, 3, memory↑, 1, neuroP↑, 3, Pain↓, 1, radioP↑, 1, RenoP↑, 5, Wound Healing↑, 1,

Infection & Microbiome ⓘ

Sepsis↓, 1,
Total Targets: 92

Scientific Paper Hit Count for: IL10, Interleukin-10

5 Quercetin
3 Lycopene
3 Propolis -bee glue
2 chitosan
2 Hydrogen Gas
2 Silymarin (Milk Thistle) silibinin
1 Apigenin (mainly Parsley)
1 Artemisinin
1 Aspirin -acetylsalicylic acid
1 Berberine
1 Betulinic acid
1 Bruteridin(bergamot juice)
1 Butyrate
1 Docetaxel
1 Curcumin
1 Chrysin
1 Ginkgo biloba
1 γ-linolenic acid (Borage Oil)
1 Honokiol
1 immunotherapy
1 probiotics
1 Bifidobacterium
1 Resveratrol
1 Shikonin
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#:562  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

IL10 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Home Page