NK cell Cancer Research Results
NK cell, NK cell activity: Click to Expand ⟱
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Natural Killer (NK) cells are a type of lymphocyte in the immune system that play a crucial role in the body's defense against tumors and virally infected cells.
NK cells can directly kill cancer cells through the release of cytotoxic granules containing perforin and granzymes. Perforin forms pores in the target cell membrane, allowing granzymes to enter and induce apoptosis (programmed cell death).
NK cells produce various cytokines, such as interferon-gamma (IFN-γ), which can enhance the immune response and promote the activation of other immune cells, including macrophages and T cells.
-Monoclonal Antibodies: Using antibodies that engage NK cells to target and kill cancer cells.
-Cytokine Therapy: Administering cytokines like IL-2 or IL-15 to boost NK cell activity.
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Scientific Papers found: Click to Expand⟱
toxicity↑, 3-Bromopyruvate (3BP), a small alkylating
agent, acts as an anti-metabolite to vital substrates in cancer metabolism and exhibits antitumor activity
across various cancer types, but the unformulated 3BP can cause high toxicity
eff↝, This study explores the efficacy of the 3BP clinical derivative KAT/3BP, currently in phase 1 for patients with hepatocellular carcinoma, in lymphoma models.
eff↑, AT/3BP exhibited synergistic activity when combined with lymphoma therapies, including bendamustine and R-CHOP.
Glycolysis↓, At acidic extracellular pH, 3BP enters cancer cells via monocarboxylic acid-1 (MCT-1) and inhibits glycolysis
through hexokinase II (HK-2) covalent modification
HK2↓, with HK-2 inhibition and dissociation from mitochondria, apoptosis-inducing factor (AIF) release, and apoptosis induction (9).
AIF↑,
Apoptosis↑,
NK cell↑, In the latter, tumor growth was in vivo reversed, with an increase in the number of circulating CD4+, CD8+, and NK-
cells
toxicity↑, unformulated 3BP administrations are associated with severe toxicities, including deaths (22,23)
toxicity↓, However, improvements have been made in developing novel 3BP formulations based on
liposomes, polyethylene glycol (PEG), PEGylated liposomes (stealth liposomes), perillyl alcohol
formulations, and others (12,22,24
Dose↝, KAT-101 and KAT-201 are two clinical 3BP derivatives formulated for oral or intratumoral (IT) administration, respectively (National Cancer Institute Thesaurus Codes C193479 and
C193479), now entering the early clinical evaluation of patients with h
AntiTum↑, KAT/3BP has in vivo antitumor activity in a syngeneic mouse model.
Glycolysis↓, Under acidic extracellular pH, 3BP is transported into cancer cells via monocarboxylate transporter 1 (MCT1), inhibiting glycolysis by covalently modifying hexokinase II (HK2).
HK2↓, HK2 dissociation from mitochondria, release of apoptosis-inducing factor (AIF), and induction of apoptosis
AIF↓,
Apoptosis↑,
NK cell↑, In the latter, tumor regression was accompanied by increased circulating CD4+, CD8+, and NK cells, enhanced tumor-associated macrophage infiltration, and reduced local immunosuppression
*LDL↓, Indeed, clinical studies on healthy subjects have evidenced that standardized garlic treatment (900 mg/day) significantly reduces total cholesterol (TC) and low-density lipoprotein cholesterol (c-LDL).
*antiOx↑, Multiple studies have focused on allicin therapeutic potential as an antioxidant (inducing antioxidant product production),
AntiCan↑, anticancer (triggering cancer cells apoptosis and inhibiting tumor growth),
*cardioP↑, cardioprotective (decreasing angiogenesis and inducing vasorelaxation)
*BP↓, Conversely, aged garlic extract supplementation was shown to be more effective than the placebo in lowering systolic blood pressure
*Weight↓, Garlic powder supplementation (800 mg/daily) resulted in a significant decrease in body weight and body fat mass (
NK cell↑, Actually, aged garlic administration in patients with advanced cancer of the digestive system led to an improvement of natural killer (NK) cell activity but did not cause improvement in QoL
*AntiDiabetic↑, Actually, daily garlic allicin supplementation (0.05–1.5 g) displayed a positive and sustained role in blood glucose, total cholesterol (TC), and high/low density lipoprotein (HDL-c/LDL-c) regulation in type 2 diabetes mellitus (T2DM) management
*GSH↑, 2-month application of coated garlic powder tablets (900 mg with alliin and allicin contents of 1.3% and 0.6%, respectively), the glutathione (GSH) concentration significantly increased in circulating human erythrocytes
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Nor, |
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IBD, |
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Diabetic, |
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*Wound Healing↑, Traditionally recognized for its anti-inflammatory and antimicrobial effects, which are very important in wound healing, the Aloe Vera relies on its polysaccharides
*Imm↑, which confer immunomodulatory, antioxidant, and tissue-regenerative properties.
*antiOx↑,
*AntiDiabetic↑, graphical abstract
*AntiCan↑,
*Inflam↓, The anti-inflammatory properties of Aloe Vera polysaccharides are primarily mediated through the inhibition of key inflammatory pathways.
*NF-kB↓, Acemannan and other polysaccharides suppress the activation of nuclear factor-kappa B (NF-κB), a transcription factor that regulates the expression of pro-inflammatory genes.
*COX2↓, By inhibiting NF-κB [48,49], Aloe Vera polysaccharides reduce the production of cyclooxygenase-2 (COX-2) and lipoxygenase (LOX),
*5LO↓,
*IL1β↓, Aloe Vera polysaccharides downregulate the expression of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α, while upregulating anti-inflammatory cytokines such as IL-10
*IL6↓,
*TNF-α↓,
*IL10↑,
*other↓, This dual action helps to mitigate inflammation in conditions such as arthritis, dermatitis, and inflammatory bowel disease (IBD)
*ROS↓, Aloe Vera polysaccharides exhibit potent antioxidant activity by scavenging reactive oxygen species (ROS) and free radicals,
*SOD↑, The polysaccharides enhance the activity of endogenous antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), which neutralize oxidative stress and protect cells from damage [17,63].
*Catalase↑,
*GPx↑,
*lipid-P↓, This property is particularly beneficial in preventing lipid peroxidation, DNA damage, and protein oxidation, processes associated with chronic diseases and aging
*DNAdam↓,
*GutMicro↑, Aloe Vera polysaccharides support gastrointestinal health, acting as prebiotics and promoting the growth of beneficial gut microbiota such as Lactobacillus and Bifidobacterium species [64].
*ZO-1↑, enhance the integrity of the intestinal epithelial barrier by upregulating the expression of tight junction proteins such as occludin and zonula occludens-1 (ZO-1) [51,54].
AntiTum↑, Certain polysaccharides in Aloe Vera, including acemannan, have demonstrated antitumoral effects by inducing apoptosis (programmed cell death) in cancer cells.
Casp3↑, This is achieved through the activation of caspase-3 and caspase-9, key enzymes in the apoptotic pathway [45,48].
Casp9↑,
angioG↓, Aloe Vera polysaccharides also inhibit angiogenesis and metastasis by downregulating matrix metalloproteinases (MMPs) and VEGF [75].
MMPs↓,
VEGF↓,
NK cell↑, Moreover, these polysaccharides enhance the immune system’s ability to recognize and destroy cancer cells through stimulating natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) [43,55].
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
Apoptosis↑, Mechanistically, CBD induced apoptosis through pathways such as PPAR-γ activation, mitochondrial dysfunction, and oxidative stress.
PPARγ↓,
mtDam↑,
ROS↑, Induced cell death via apoptosis and increased ROS levels.
EMT↓, It inhibited epithelial-to-mesenchymal transition (EMT), downregulated invasive markers, and modulated the tumor microenvironment by enhancing CD8 + T cell and NK cell activity.
CD8+↑,
NK cell↑,
ChemoSen↑, CBD showed synergistic effects with conventional therapies (e.g., cisplatin, radiotherapy) by increasing drug uptake and overcoming resistance.
ATP↓, CBD decreases intracellular ATP and glucose levels
glucose↓,
Ca+2↑, CBD enhances calcium influx (mediated by TRPV2) and elevates p-ERK expression in CIK cells
TRPV2↑,
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.
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↑,
angioG↓, Both chitosan and its various derivatives have been reported to selectively permeate through the cancer cell membranes and show anticancer activity through the cellular enzymatic, antiangiogenic, immunoenhancing, antioxidant defense mechanism, and ap
*Imm↑,
*antiOx↑,
selectivity↑, They get sequestered from noncancer cells and provide their enhanced bioavailability in cancer cells in a sustained release manner.
other↝, The degree of deacetylation (DDA) of chitin ranges from 60 to 100 % and molecular weight of commercially obtained chitosan ranges from 3800 to 20,000 Daltons.
toxicity↓, The degree of deacetylation (DDA) of chitin ranges from 60 to 100 % and molecular weight of commercially obtained chitosan ranges from 3800 to 20,000 Daltons.
BioAv↑,
eff↝, exert anticancer activity with minimal toxicity on noncancer cells [13] and such activity against different cancer cell lines significantly depends upon molecular weight and DDA [
Half-Life↑, Sustained Release Mechanism
MPT↑, Chitosan MDA-MB-231 Permeation enhancement, lowering of MMP9 activity
MMP9↓,
lipid-P↑, induction of lipid peroxidation, enhanced permeation and retention (EPR) effect
EPR↑,
NK cell↑, Immunoenhancement through increase in activity of NK cells, T cells, killer lymphocytes and cytokins.
Casp3↑, Cellular apoptosis, activation of caspase-3 and caspase-8,
Casp8↑,
TumCCA↑, Cytokine signaling cell cycle arrest, ROS activation
ROS↑,
DDS↑, CMCS has been prepared as a carrier of anticancer drug such as 5- fluorouracil, curcumin, and doxorubicin
VEGF↓, decrease in VEGF level and increase in TIMP1 level after 14-day treatment of mouse serum with CMCS in vivo.
TIMP1↑,
ChemoSen↑, The paclitaxel loaded modified glycol chitosan nanoparticles in the size of 400 nm has been found to show sustained release of paclitaxel to bring about the inhibition of MCF-7 tumor growth due to EPR effect in vitro
eff↑, Chitosan-curcumin nanoformulation has been found to show anticancer activity following the apoptotic pathways associated with DNA damage, cell-cycle blockage, and elevation of ROS levels in vivo
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Lung, |
H460 |
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Lung, |
H1299 |
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Lung, |
A549 |
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Lung, |
PC9 |
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MDSCs↓,
TregCell↓,
IL10↓,
NK cell↑,
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↑,
OS↑, In 2008, a cohort study of breast cancer survivors identified that patients who consistently exercised for greater than 2.5 hours per week following diagnosis had a greater than 60% reduction in the risk of all deaths compared with patients who were
IGF-1↓, Table 1, IGF1 Decreased levels, IGFBP3 Increased levels
IGFBP3↑,
BRCA1↑, BRCA1 Increased expression
BRCA2↑, BRCA2 Increased expression
RAS↓, RAS family oncogenes Suppressed activity
P53↑, P53 Enhanced activity
HSPs↑, Heat shock proteins Enhanced activity
Leptin↓, Leptin Reduced activity
Irisin↓, Irisin Enhanced activity
Resistin↓, Resistin Reduced activity
NK cell↑, NK cells Enhanced activity
CRP↓, C-reactive protein, interleukin-6, TNFα Reduced activity
IL6↓,
TNF-α↓,
PGE1↓, Prostaglandins Reduced activity
COX2↓, Cox-2 Reduced activity
*GSH↑, Glutathione, Catalase and Superoxide dismutase Increased activity
*Catalase↑,
*SOD↑,
*monoA↑, Monoamines Higher levels
*EndoR↑, Endorphins Increased release
*testos↑, testosterone increases immediately after vigorous exercise in some but not all studies. lasting for 20–60 minutes post-exercise
ROS↑, Physical activity, especially if strenuous, produces reactive oxidative species (ROS)
QoL↑, Adverse cancer-related symptoms, which have been shown to be alleviated by exercise, include fatigue, muscle weakness, thromboembolism, weight gain, loss of bone density, quality of life (QOL), psychological distress, incontinence and sexual dysfunct
BMD↑, the rate of decline in BMD was significantly less in the resistance exercise group, with a greater benefit seen in the aerobic exercise group
BowelM↑, Exercise reduces bowel transit time and ameliorates constipation and its associated abdominal cramps
AntiCan↑, involvement of melatonin in different anticancer mechanisms
Apoptosis↑, apoptosis induction, cell proliferation inhibition, reduction in tumor growth and metastases
TumCP↓,
TumCG↑,
TumMeta↑,
ChemoSideEff↓, reduction in the side effects associated with chemotherapy and radiotherapy, decreasing drug resistance in cancer therapy,
radioP↑,
ChemoSen↑, augmentation of the therapeutic effects of conventional anticancer therapies
*ROS↓, directly scavenge ROS and reactive nitrogen species (RNS)
*SOD↑, melatonin can regulate the activities of several antioxidant enzymes like superoxide dismutase, glutathione reductase, glutathione peroxidase, and catalase
*GSH↑,
*GPx↑,
*Catalase↑,
Dose∅, demonstrated that 1 mM melatonin concentration is the pharmacological concentration that is able to produce anticancer effects
VEGF↓, downregulatory action on VEGF expression in human breast cancer cells
eff↑, tumor-bearing mice were treated with (10 mg/kg) of melatonin and (5 mg/kg) of cisplatin. The results have shown that melatonin was able to reduce DNA damage
Hif1a↓, MDA-MB-231-downregulation of the HIF-1α gene and protein expression coupled with the production of GLUT1, GLUT3, CA-IX, and CA-XII
GLUT1↑,
GLUT3↑,
CAIX↑,
P21↑, upregulation of p21, p27, and PTEN protein is another way of melatonin to promote cell programmed death in uterine leiomyoma
p27↑,
PTEN↑,
Warburg↓, FIGURE 3
PI3K↓, in colon cancer cells by downregulation of PI3K/AKT and NF-κB/iNOS
Akt↓,
NF-kB↓,
cycD1/CCND1↓,
CDK4↓,
CycB/CCNB1↓,
CDK4↓,
MAPK↑,
IGF-1R↓,
STAT3↓,
MMP9↓,
MMP2↓,
MMP13↓,
E-cadherin↑,
Vim↓,
RANKL↓,
JNK↑,
Bcl-2↓,
P53↑,
Casp3↑,
Casp9↑,
BAX↑,
DNArepair↑,
COX2↓,
IL6↓,
IL8↓,
NO↓,
T-Cell↑,
NK cell↑,
Treg lymp↓,
FOXP3↓,
CD4+↑,
TNF-α↑,
Th1 response↑, FIGURE 3
BioAv↝, varies 1% to 50%?
RadioS↑, melatonin’s radio-sensitizing properties
OS↑, In those individuals taking melatonin, the overall tumor regression rate and the 5-year survival were elevated
QoL↑, melatonin combined with standard chemotherapy lines would derive, at least, a better quality of life for breast cancer patients
OS↑, Moreover, regular doses of 20 mg/day seemed to increase partial response and 1-year survival rates.
Dose∅, regular doses of 20 mg/day
antiOx↑, melatonin possesses antioxidant properties, which may help to protect cells from damage caused by free radicals
ROS↑, elimination of free radicals non-enzymatically transforms melatonin into metabolites with greater antioxidant capacity, which enabling the removal of 10 reactive species per molecule
SOD↑, melatonin upregulates various antioxidant enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase
Catalase↑,
GPx↑,
Risk↓, individuals with higher melatonin levels show a lower risk of developing breast cancer, and melatonin supplementation may help inhibit the growth and spread of breast cancer cells
NK cell↑, enhance natural killer cell activity
IL1β↓, inhibit the production of pro-inflammatory cytokines such as interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α)
IL6↓,
TNF-α↓,
radioP↑, protect hematopoietic progenitor cells from radiation therapy and chemotherapy
chemoP↑,
TumVol↓, most frequent observations was the ability of melatonin to reduce tumor size
TumMeta↓, decrease the risk of metastasis
angioG↓,
ChemoSen↑, melatonin can synergistically potentiate drug cytotoxicity.
eff↑, it has been suggested that administering melatonin at the appropriate phase of the circadian cycle may enhance its anti-tumor activity and reduce the side effects of chemotherapy and radiation therapy
ChemoSen↑, lucidum could be administered as an alternative adjunct to conventional treatment
CR3↝, beta‐glucans act on complement receptor type 3 (CR‐3) triggering a series of molecular pathway
eff↑, tudy patients who received G. lucidum treatment in combination with conventional chemotherapy generally responded more positively than those in the standard treatment group.
NK cell↑, use of G. lucidum and showed an increase in NK‐cell activity
T-Cell↑, findings also showed that G. lucidum could be capable of enhancing immunity in cancer patients by stimulating T‐lymphocyte proliferation
QoL↑, QoL was relatively improved in cancer patients with G. lucidum treatment than without.
AntiCan↑, Sodium Bicarbonate “Kills” Cancer Cells
e-pH↑, The utilization of sodium bicarbonate to neutralize the acidity and increase the tumor pHe might control cancer cells progression
TumMeta↓, Sodium bicarbonate reduces the formation of spontaneous metastases and the rate of lymph node involvement in mouse models of metastatic breast cancer.
TumCI↓, administration of 200 mM bicarbonate to 4-week-old TRAMP mice (weaning at 3 weeks) effectively perturbs the in situ evolution of cancer to a microinvasive disease
TumCG↓, sodium bicarbonate significantly controls tumor growth and improves CD8+ T-cell infiltration.
CD8+↑,
NK cell↑, Natural killer (NK) cell activity is also increased in a B-cell lymphoma mouse model following the systemic administration of a buffer therapy.
Remission↑, began a self-administered course of vitamins, supplements, and 60 g of bicarbonate mixed in water daily. As of this submission, he has remained well with stable tumor for 10 months.
eff↑, Therefore, sodium bicarbonate could be used as an adjuvant therapy to enhance the efficacy of conventional treatments.
ChemoSen↑, Surprisingly, extracellular alkalization induced a 2- to 3-fold increase in the efficacy of doxorubicin
ChemoSen↓, it greatly reduces the efficacy of some weak acidic chemotherapeutics, such as chlorambucil.
ChemoSen↑, Ingredients from propolis also ”sensitize“ cancer cells to chemotherapeutic agents
TumCCA↑, cell-cycle arrest and attenuation of cancer cells proliferation
TumCP↓,
Apoptosis↑,
antiOx↓, behave as antioxidants against peroxyl and hydroxyl radicals,
ROS↑, whereas prooxidant activity is observed in the presence of Cu2+.
COX2↑, Propolis, as well as flavonoids derived from propolis, such as galangin, is a potent COX-2 inhibitor
ER(estro)↓, Some flavonoids from propolis, such as galangin, genistein, baicalein, hesperetin, naringenin, and quercetin, suppressed the proliferation of an estrogen receptor (ER)
cycA1/CCNA1↓, by suppressing expressions of cyclin A, cyclin B, and Cdk2 and by stopping proliferation at the G2 phase, by increasing levels of p21 and p27 proteins, and through the inhibition of telomerase reverse transcriptase (hTERT),
CycB/CCNB1↓,
CDK2↓,
P21↑,
p27↑,
hTERT/TERT↓, leukemia cells, propolis successfully reduced hTERT mRNA expression
HDAC↓, by suppressing expressions of cyclin A, cyclin B, and Cdk2 and by stopping proliferation at the G2 phase, by increasing levels of p21 and p27 proteins, and through the inhibition of telomerase reverse transcriptase (hTERT),
ROS⇅, Mexican propolis, demonstrated both pro- and anti-inflammatory effects, depending on the dose applied
Dose?, Mexican propolis, demonstrated both pro- and anti-inflammatory effects, depending on the dose applied
ROS↓, By scavenging free radicals, chelating metal ions (mainly iron and copper), and stimulating endogenous antioxidant defenses, propolis and its flavonoids directly attenuate the generation of ROS
ROS↑, Romanian propolis [99], exhibits prooxidant properties at high concentrations, by mobilizing endogenous copper ions and DNA-associated copper in cells.
DNAdam↑, propolis, i.e., its polyphenolic components, may induce DNA damage in the presence of transition metal ions.
ChemoSen↑, Algerian propolis + doxorubicin decreased cell viability, prevented cell proliferation and cell cycle progression, induced apoptosis by activating caspase-3 and -9 activities, and increased the accumulation of chemotherapeutic drugs in MDA-MB-231 cel
LOX1↓, propolis components inhibited the LOX pathway
lipid-P↓, Croatian propolis improved psoriatic-like skin lesions induced by irritant agents n-hexyl salicylate or di-n-propyl disulfide by decreasing the extent of lipid peroxidation
NO↑, Taken together, propolis may increase the phagocytic index, NO production, and production of IgG antibodies
Igs↑,
NK cell↑, propolis treatment for 3 days increases the cytotoxic activity of NK cells against murine lymphoma.
MMPs↓, extracts of propolis containing artepillin C and CAPE decreased the formation of new vessels and expression of MMPs and VEGF in various cancer cells
VEGF↓,
Hif1a↓, Brazilian green propolis inhibit the expression of the hypoxia-inducible factor-1 (HIF-1) protein and HIF-1 downstream targets such as glucose transporter 1, hexokinase 2, and VEGF-A
GLUT1↓,
HK2↓,
selectivity↑, Portuguese propolis was selectively toxic against malignant cells.
RadioS↑, propolis increased the lifespan of mice that received the radiotherapy with gamma rays
GlucoseCon↓, Portuguese propolis disturbed the glycolytic metabolism of human colorectal cancer cells, as evidenced by a decrease in glucose consumption and lactate production
lactateProd↓,
eff↓, Furthermore, different pesticides or heavy metals can be found in propolis, which can cause unwanted side effects.
*BioAv↓, Due to the low bioavailability and clinical efficacy of propolis and its flavonoids, their biomedical applications remain limited.
Pyro↑, Psoralidin induced pyroptosis and GSDME cleavage in HepG2 and Hepa1–6 cells
TumCG↓, Psoralidin suppressed HCC growth, inducing tumor cell pyroptosis and enhancing the tumor infiltration of T cells and NK cells.
mt-ROS↑, psoralidin induced mitochondrial reactive oxygen species (ROS) production, leading to caspase-3 activation and subsequent GSDME cleavage.
Casp3↑,
cl‑GSDME↑,
IL1β↑, leading to the secretion of interleukin (IL)-1β and IL-18, which promoted natural killer (NK) cell activation
IL18↑,
NK cell↑,
Perforin↑,
GranB↑,
p‑ERK↑,
p‑Akt↑,
NK cell↑, Shikonin had no effect on cells proliferation at 24 h, and enhanced cells proliferation at 48 h and 72 h at the dose of 1.56 ng/ml to 6.25 ng/ml. Meanwhile, Shikonin inhibits the cell proliferation at 100.0 ng/ml
eff↝, Meanwhile, Shikonin inhibits the cell proliferation at 100.0 ng/ml
Imm↑, A less recognized, albeit even more essential role of selenite is in its stimulation of the cellular immune system
angioG↑, certain studies indicate that selenite may inhibit angiogenesis, and help to repair the damaged DNA fragments.
DNArepair↑,
NK cell↑, most important function of this compound in the fighting of cancer may be the direct activation of natural killer (NK) cells.
ROS↑, thus selenite Se4+ exhibits an ability to undergo oxidation and reduction reactions (the so-called redox reactions)
AntiCan↑, It should be emphasized that the use of high doses of sodium selenite exhibits promising anticancer effects, as described in numerous preclinical studies
selectivity↑, Numerous studies demonstrated higher selenite cytotoxicity against cancer cells when compared to normal cells, using a comparable dose of this element
ER Stress↑, sodium selenite can cause cell death by an independent pathway of mitochondrial apoptosis, endoplasmic reticulum stress (caused by the presence of (non)unfolded proteins), processes of autophagy, or necrosis.
TumAuto↑,
necrosis↑,
toxicity↝, Sodium selenite may be toxic when taken orally at higher doses, yet it is well tolerated by other routes such as intravenous, intraperitoneal and/or transdermal
Dose↑, As demonstrated recently by Swedish scientists, considerably higher doses of selenium are well tolerated by patients with cancer, in the case when sodium selenite is administered intravenously.
Risk↑, low blood Se levels were found to be associated with an increased incidence and mortality from various types of cancers
antiOx↑, Se compounds, generally considered to be antioxidants
ROS↑, selenite is not an antioxidant, but possesses oxidizing properties in the presence of specific substrates.
Imm↑, Selenite by virtue of oxidizing cell membrane thiols, can prevent the formation of the coat and consequently makes cancer cells vulnerable to the immune surveillance and destruction.
NK cell↑, selenite may directly activate NK cells, as well as inhibit angiogenesis without undesirable decrease in the oxidative potential of cellular environment.
angioG↓,
toxicity↓, postulated that sodium selenite, in view of its relative low toxicity, might become a drug of choice for many types of cancer including leukemia.
eff↑, Compared to the baseline, at 2 weeks, 75.0% of participants in clinical stage showed improvement, while there was no change in the CTRL group
Inflam↓, Selenite’s effect on lymphedema may be associated with non-antioxidant properties, such as anti-inflammation and immune function.
Imm↑, As sodium selenite is transformed into elemental selenium in cancer, it oxidizes sulfhydryl groups [14], which then disrupts parafibrin, potentially increasing immune recognition towards cancer cells
ROS↑, Effect of Sodium Selenite Supplementation on Blood Parameters is Indicative of Oxidative Stress
*NK cell↑, Oral sodium selenite supplementation (200 μg/day for 8 weeks) in healthy university students increased cytotoxic lymphocytes and NK cell activities
Apoptosis↑, The anticancer power of TQ is accomplished by several aspects; including promotion of apoptosis, arrest of cell cycle and ROS generation.
TumCCA↑,
ROS↑,
*Catalase↑, activation of antioxidant cytoprotective enzymes including, CAT, SOD, glutathione reductase (GR) [80], glutathione-S-transferase (GST) [81] and glutathione peroxidase (GPx) - scavenging H2O2 and superoxide radicals and preventing lipid peroxidation
*SOD↑,
*GR↑,
*GSTA1↓,
*GPx↑,
*H2O2↓,
*ROS↓,
*lipid-P↓,
*HO-1↑, application of TQ to HaCaT (normal) cells promoted the expression of HO-1 in a concentration and time-dependent pattern
p‑Akt↓, TQ could induce ROS which provoked phosphorylation and activation of Akt and AMPK-α
AMPKα↑,
NK cell↑, TQ was outlined to enhance natural killer (NK) cells activity
selectivity↑, Many researchers have noticed that the growth inhibitory potential of TQ is particular to cancer cells
Dose↝, Moreover, TQ has a dual effect in which it can acts as both pro-oxidant and antioxidant in a dose-dependent manner; it acts as an antioxidant at low concentration whereas, at higher concentrations it possess pro-oxidant property
eff↑, Pro-oxidant property of TQ occurs in the presence of metal ions including copper and iron which induce conversion of TQ into semiquinone. This leads to generation of reactive oxygen species (ROS) causing DNA damage and induction of cellular apoptosis
GSH↓, TQ for one hour resulted in three-fold increase of ROS while reduced GSH level by 60%
eff↓, pre-treatment of cells with N-acetylcysteine, counteracted TQ-induced ROS production and alleviated growth inhibition
P53↑, TQ provokes apoptosis in MCF-7 cancer cells by up regulating the expression of P53 by time-dependent manner.
p‑STAT3↓, TQ inhibited the phosphorylation of STAT3
PI3K↑, via up regulation of PI3K and MPAK signalling pathway
MAPK↑,
GSK‐3β↑, TQ produced apoptosis in cancer cells and modulated Wnt signaling by activating GSK-3β, translocating β-catenin
ChemoSen↑, Co-administration of TQ and chemotherapeutic agents possess greater cytotoxic influence on cancer cells.
RadioS↑, Treatment of cells with both TQ and IR enhanced the antiproliferative power of TQ as observed by shifting the IC50 values for MCF7 and T47D cells from ∼104 and 37 μM to 72 and 18 μM, respectively.
BioAv↓, TQ cannot be used as the primary therapeutic agent because of its poor bioavailability [177,178] and lower efficacy
NRF2↑, TQ to HaCaT cells promoted the expression of HO-1 in a concentration and time-dependent pattern. This was achieved via increasing stabilization of Nrf2
eff↑, Our results demonstrate that urolithin A enhances the natural cytotoxicity of PBMCs in a dose-dependent manner
NK cell↑, Urolithin A increased the NK activity of the PBMCs in patients with prostate cancer and healthy subjects
Risk↓, An analysis of 25(OH)D-cancer incidence rates suggests that achieving 80 ng/mL vs. 10 ng/mL would reduce cancer incidence rates by 70 ± 10%.
eff↑, In 1936, Peller reported that people who developed skin cancer from light exposure, such as from their occupation, had lower rates of internal cancers
eff↑, low rates(internal cancer) in three southwest states and high rates in approximately 15 northeast states
Risk↓, Inverse correlations were found for 11 cancers with respect to solar UVB doses for white Americans and several types of cancer for black Americans
Risk↓, It reported an 82% lower risk of breast cancer for 25(OH)D concentration >60 ng/mL versus <20 ng/mL
ChemoSen↑, Sensitization to Apoptosis, Combined Action with Chemotherapy and Radiotherapy
RadioS↑,
Cyt‑c↑, it favors the release of cytochrome C from mitochondria and the activation of caspases 3 and 9 that lead to apoptosis promoted by a variety of signals
Casp3↑,
Casp9↑,
hTERT/TERT↓, by downregulation of telomerase reverse transcriptase (hTERT) via the induction of miR-498
eff↑, In addition, 1,25-(OH)2D3 and metformin have additive/synergistic antiproliferative and proapoptotic effects in colon carcinoma and other types of cells, which are modulated but not hampered by TP53 status
E-cadherin↑, 1,25-(OH)2D3 upregulates an array of intercellular adhesion molecules that are constituents of adherens junctions and tight junctions, including E-cadherin, occludin, claudin-2 and -12, and ZO-1 and -2
CLDN2↑,
ZO-1↑,
Snail↓, 1,25-(OH)2D3 inhibits SNAIL1 and ZEB1 expression in non-small cell lung carcinoma cells
Zeb1↓,
Vim↓, vimentin downregulation
VEGF↓, 1,25-(OH)2D3 alone and more strongly in combination with cisplatin suppresses VEGF activity in ovarian cancer cells
NK cell↑, 1,25-(OH)2D3 is an enhancer of innate immune reactions against infections and tumor cells by activating the responsive cells (macrophages, natural killer (NK) cells, and neutrophils)
Risk↓, vitamin D deficiency promotes gut permeability, colon mucosa bacterial infiltration, and translocation of intestinal pathogens. These effects lead to changes in immune cell populations and gut inflammation, and cancer—an overall condition that is im
eff↑, Combination with immunotherapy
Showing Research Papers: 1 to 25 of 25
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 25
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, antiOx↑, 2, Catalase↑, 1, GPx↑, 1, GSH↓, 1, lipid-P↓, 1, lipid-P↑, 1, NRF2↑, 1, ROS↓, 1, ROS↑, 11, ROS⇅, 1, mt-ROS↑, 1, SOD↑, 1,
Mitochondria & Bioenergetics ⓘ
AIF↓, 1, AIF↑, 1, ATP↓, 1, MPT↑, 1, mtDam↑, 1,
Core Metabolism/Glycolysis ⓘ
CAIX↑, 1, glucose↓, 1, GlucoseCon↓, 1, Glycolysis↓, 2, HK2↓, 3, lactateProd↓, 1, PI3K/Akt↑, 1, PPARγ↓, 1, Warburg↓, 1,
Cell Death ⓘ
Akt↓, 1, p‑Akt↓, 1, p‑Akt↑, 1, Apoptosis↑, 6, BAX↑, 2, Bcl-2↓, 2, Casp3↑, 5, Casp8↑, 1, Casp9↑, 3, Cyt‑c↑, 1, GranB↑, 1, cl‑GSDME↑, 1, hTERT/TERT↓, 2, JNK↑, 1, MAPK↑, 3, necrosis↑, 1, p27↑, 2, Perforin↑, 1, Pyro↑, 1, Telomerase↓, 1,
Kinase & Signal Transduction ⓘ
AMPKα↑, 1, TRPV2↑, 1,
Transcription & Epigenetics ⓘ
BowelM↑, 1, other↝, 3,
Protein Folding & ER Stress ⓘ
ER Stress↑, 1, HSPs↑, 1,
Autophagy & Lysosomes ⓘ
TumAuto↑, 1,
DNA Damage & Repair ⓘ
BRCA1↑, 1, BRCA2↑, 1, DNAdam↑, 1, DNArepair↑, 2, P53↑, 3,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, CDK4↓, 2, cycA1/CCNA1↓, 1, CycB/CCNB1↓, 2, cycD1/CCND1↓, 1, P21↑, 2, TumCCA↑, 4,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, ERK↓, 1, p‑ERK↑, 1, GSK‐3β↑, 1, HDAC↓, 1, IGF-1↓, 2, IGF-1R↓, 1, IGFBP3↑, 1, IGFR↓, 1, PI3K↓, 1, PI3K↑, 1, PTEN↑, 1, RAS↓, 1, STAT3↓, 1, p‑STAT3↓, 1, STAT4↑, 1, TumCG↓, 3, TumCG↑, 1,
Migration ⓘ
Ca+2↑, 1, CLDN2↑, 1, E-cadherin↑, 2, MMP13↓, 1, MMP2↓, 1, MMP9↓, 2, MMPs↓, 2, NFAT↑, 1, Snail↓, 1, TIMP1↑, 1, Treg lymp↓, 1, TregCell↓, 1, TumCI↓, 1, TumCP↓, 2, TumMeta↓, 2, TumMeta↑, 1, Vim↓, 2, Zeb1↓, 1, ZO-1↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 4, angioG↑, 1, EPR↑, 1, Hif1a↓, 2, LOX1↓, 1, NO↓, 1, NO↑, 1, VEGF↓, 5,
Barriers & Transport ⓘ
GLUT1↓, 1, GLUT1↑, 1, GLUT3↑, 1,
Immune & Inflammatory Signaling ⓘ
CD14↓, 1, CD4+↑, 1, COX2↓, 2, COX2↑, 1, CR3↝, 1, CRP↓, 1, DCells↑, 1, FOXP3↓, 1, IFN-γ↑, 4, Igs↑, 1, IL10↓, 1, IL10↑, 1, IL12↑, 1, IL15↑, 1, IL18↑, 1, IL1β↓, 1, IL1β↑, 1, IL2↑, 1, IL6↓, 3, IL8↓, 1, Imm↑, 3, Inflam↓, 1, MDSCs↓, 1, NF-kB↓, 1, NF-kB↑, 2, NK cell↑, 24, PGE1↓, 1, Resistin↓, 1, T-Cell↑, 2, Th1 response↑, 1, TNF-α↓, 2, TNF-α↑, 1,
Cellular Microenvironment ⓘ
e-pH↑, 1,
Hormonal & Nuclear Receptors ⓘ
ER(estro)↓, 1, Irisin↓, 1, Leptin↓, 1, RANKL↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 1, BioAv↝, 1, ChemoSen↓, 1, ChemoSen↑, 10, DDS↑, 2, Dose?, 1, Dose↑, 1, Dose↝, 3, Dose∅, 2, eff↓, 2, eff↑, 16, eff↝, 3, Half-Life↑, 1, RadioS↑, 4, selectivity↑, 4,
Clinical Biomarkers ⓘ
BG↓, 1, BMD↑, 1, BRCA1↑, 1, CRP↓, 1, hTERT/TERT↓, 2, IL6↓, 3,
Functional Outcomes ⓘ
AntiCan↑, 6, AntiTum↑, 2, chemoP↑, 1, ChemoSideEff↓, 1, OS↑, 3, QoL↑, 3, radioP↑, 2, Remission↑, 1, Risk↓, 5, Risk↑, 1, toxicity↓, 3, toxicity↑, 2, toxicity↝, 1, TumVol↓, 1,
Infection & Microbiome ⓘ
CD8+↑, 3,
Total Targets: 188
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 3, Catalase↑, 4, GPx↑, 3, GSH↑, 3, GSTA1↓, 1, H2O2↓, 1, HO-1↑, 1, lipid-P↓, 2, ROS↓, 3, SOD↑, 4,
Core Metabolism/Glycolysis ⓘ
LDL↓, 1,
Transcription & Epigenetics ⓘ
other↓, 1, other↝, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1,
Migration ⓘ
5LO↓, 1, ZO-1↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL10↑, 1, IL1β↓, 1, IL6↓, 1, Imm↑, 3, Inflam↓, 1, NF-kB↓, 1, NK cell↑, 1, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
EndoR↑, 1, monoA↑, 1,
Hormonal & Nuclear Receptors ⓘ
GR↑, 1, testos↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 2, BioAv↝, 1,
Clinical Biomarkers ⓘ
BP↓, 1, GutMicro↑, 1, IL6↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, AntiDiabetic↑, 2, cardioP↑, 1, toxicity↓, 1, Weight↓, 1, Weight↝, 1, Wound Healing↑, 2,
Infection & Microbiome ⓘ
Bacteria↓, 1,
Total Targets: 43
Scientific Paper Hit Count for: NK cell, NK cell activity
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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