eff Cancer Research Results

eff, efficacy: Click to Expand ⟱
Source:
Type:
Power to enhance an anti cancer effect
Scientific Papers found: Click to Expand⟱
4384- ,    Silver nanoparticles: synthesis, properties, and therapeutic applications
- Review, Var, NA
AntiCan↑, AgNPs are employed in newly emerging applications as photosensitizers/radiosensitizers, antiviral and anticancer agents.
RadioS↑,
CellMemb↑, underlying anticancer mechanisms of AgNPs include (1) disruption of cell membranes, and (2) production of reactive oxygen species and Ag+ to damage protein or DNA.
ROS↑,
DNAdam↑,
PhotoS↑, photosensitizing mechanism of AgNPs is based on nonradiative decay converting photo energy to thermal energy.
eff↑, Smaller particles have a larger surface area and, therefore, have greater toxic potential

2325- 2DG,    Research Progress of Warburg Effect in Hepatocellular Carcinoma
- Review, Var, NA
HK2↓, 2-Deoxyglucose (2-DG) is a widely studied HK2 inhibitor that has been reported to inhibit glycolysis by inhibiting hexokinase
Glycolysis↓,
PKM2↓, In rat HCC models, 2-DG was shown to reduce PKM2 and LDHA expression, leading to decreased aerobic glycolysis and tumor cell death
LDHA↓,
TumCD↑,
ChemoSen↑, Combining 2-DG with sorafenib demonstrated superior antitumor effects compared to sorafenib alone, suggesting its potential for synergistic action with other anticancer drugs
eff↑, Moreover, DHA combined with 2-DG can reportedly induce apoptosis in A549 and PC-9 cells

2327- 2DG,    2-Deoxy-d-Glucose and Its Analogs: From Diagnostic to Therapeutic Agents
- Review, Var, NA
Glycolysis↓, 2-DG inhibits glycolysis due to formation and intracellular accumulation of 2-deoxy-d-glucose-6-phosphate (2-DG6P), inhibiting the function of hexokinase and glucose-6-phosphate isomerase, and inducing cell death
HK2↓,
mt-ROS↑, 2-DG-mediated glucose deprivation stimulates reactive oxygen species (ROS) production in mitochondria, also leading to AMPK activation and autophagy stimulation.
AMPK↑,
PPP↓, 2-DG has been shown to block the pentose phosphate shunt
NADPH↓, Decreased levels of NADPH correlate with reduced glutathione levels, one of the major cellular antioxidants.
GSH↓,
Bax:Bcl2↑, Valera et al. also observed that in bladder cancer cells, 2-DG treatment modulates the Bcl-2/Bax protein ratio, driving apoptosis induction
Apoptosis↑,
RadioS↑, 2-DG radiosensitization results from its effect on thiol metabolism
eff↓, (NAC) treatment, downregulated glutamate cysteine ligase activity, or overexpression of ROS scavenging enzymes
Half-Life↓, its plasma half-life was only 48 min [117]) make 2-DG a rather poor drug candidate
other↝, Adverse effects of 2-DG administration in humans include fatigue, sweating, dizziness, and nausea, mimicking the symptoms of hypoglycemia
eff↓, Moreover, 2-DG has to be used at relatively high concentrations (≥5 mmol/L) in order to compete with blood glucose

1340- 3BP,    Safety and outcome of treatment of metastatic melanoma using 3-bromopyruvate: a concise literature review and case study
- Review, NA, NA
Glycolysis↓, inhibiting key glycolysis enzymes
HK2↓,
LDH↓,
OXPHOS↓, inhibits mitochondrial oxidative phosphorylation
angioG↓,
H2O2↑, induces hydrogen peroxide generation in cancer cells (oxidative stress effect)
eff↑, Concurrent use of a GSH depletor(paracetamol) with 3BP killed resistant melanoma cells

1341- 3BP,    The HK2 Dependent “Warburg Effect” and Mitochondrial Oxidative Phosphorylation in Cancer: Targets for Effective Therapy with 3-Bromopyruvate
- Review, NA, NA
Glycolysis↓, second-generation glycolysis inhibitor.
OXPHOS↓,
*toxicity↓, Normal cells remain unharmed
ROS↑, well known that this compound generates ROS
GSH↓,
eff↑, 3BP demonstrates synergistic activity with other compounds that reduce intracellular levels of GSH

5282- 3BP,  Rad,    3-Bromopyruvate-mediated MCT1-dependent metabolic perturbation sensitizes triple negative breast cancer cells to ionizing radiation
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468
Glycolysis↓, Metabolomic analyses showed that 3BP causes inhibition of glycolysis
RadioS↑, Overall, MCT1-mediated metabolic perturbation in combination with radiotherapy is shown to be a promising strategy for the treatment of glycolytic tumors such as TNBC, overcoming the selectivity challenges of targeting glycolysis with glucose analogs
eff↑, 3BP is selectively toxic to cells expressing MCT1
GAPDH↓, 3BP inhibits GAPDH but not hexokinase
PPP↑, Pentose phosphate pathway is upregulated in response to 3BP
GSH↓, Glutathione and NADH are depleted at early time points
ECAR↓, prolonged incubation with 20 μM 3BP for 24 h resulted in a statistically significant selective decrease in ECAR

5278- 3BP,    effect-of-3-bromopyruvate-on-human-colorectal">The effect of 3-bromopyruvate on human colorectal cancer cells is dependent on glucose concentration but not hexokinase II expression
- in-vitro, CRC, HCT116 - in-vitro, CRC, Caco-2 - in-vitro, CRC, SW48
ATP↓, 3-Bromopyruvate (3BP) is a pyruvate analogue with alkylating properties that depletes cellular ATP levels and induces rapid cell death in neoplastic cells with limited cytotoxic effects against normal cells.
TumCD↑,
selectivity↑,
toxicity↓, 3BP treatment led to eradication of tumours of hepatocellular carcinoma cell origin in rats without apparent cytotoxic effects [19]
OS↑, first human case report suggested that 3BP was able to prolong survival in a cancer patient diagnosed with hepatocellular carcinoma in 2012 [19,20].
HK2?, 3BP is able to dissociate and inhibit mitochondrial HKII function, thereby reducing ATP production. 3BP binding also frees up binding sites previously occupied by HKII
Cyt‑c↑, llowing pro-apoptotic molecules (such as BAX and BAD) to promote the release of cytochrome c into the cytosol and induce eventual cell death
eff↑, Raji lymphoma cells grown under hypoxic conditions were more sensitive to 3BP than in normoxia
p‑Akt↑, 3BP induces rapid AKT phosphorylation at residue Thr-308

5274- 3BP,    ME3BP-7 is a targeted cytotoxic agent that rapidly kills pancreatic cancer cells expressing high levels of monocarboxylate transporter MCT1
- in-vitro, PC, NA
eff↑, novel microencapsulated formulation of 3BP (ME3BP-7), which is effective against a variety of PDAC cells in vitro and remains stable in serum.
TumCG↓, Furthermore, systemically administered ME3BP-7 significantly reduces pancreatic cancer growth and metastatic spread in multiple orthotopic models of pancreatic cancer with manageable toxicity.
TumMeta↓,
toxicity↝,
Glycolysis↓, The anticancer effects of 3BP were initially attributed to inhibition of glycolysis (Ganapathy-Kanniappan et al., 2009;
toxicity↓, Our previous work demonstrated that microencapsulation of 3BP reduces its toxicity (Chapiro et al., 2014).
Dose↝, we were only able to reliably deliver multiple doses of the drug intravenously (i.v.), and the number of injections and time periods over which we could administer the drug were limited.

5272- 3BP,    The efficacy of the anticancer 3-bromopyruvate is potentiated by antimycin and menadione by unbalancing mitochondrial ROS production and disposal in U118 glioblastoma cells
- in-vitro, GBM, U87MG - in-vitro, Nor, HEK293
Glycolysis↓, We used the antiglycolytic 3-bromopyruvate (3BP) as a metabolic modifier to treat U118 glioblastoma cell
ROS↑, ROS generated in mitochondria were enhanced at 30 μM 3BP, possibly by unbalancing their generation and their disposal because of glutathione peroxidase inhibition.
GPx↓,
eff↓, Indeed, the scavenger of mitochondrial superoxide MitoTEMPO counteracted 3BP-induced cyt c release and weakened the potentiating effect of 3BP/
OXPHOS↓, (3BP) is a reactive non-specific drug that can act as a metabolic modifier by interfering with glycolysis and oxidative phosphorylation in cancer cells
HK2↓, The mitochondrial hexokinase-II is the main target since its activity is specifically blocked by the formation of a pyruvinyl adduct after reacting with 3BP at the surface of the outer mitochondrial membrane
ATP↓, In malignant tumour cell lines, 3BP inhibits ATPase activity, reduces ATP levels, and reverses chemoresistance by antagonizing drug efflux by acting on the ATP-binding cassette transporters (
ROS↑, Furthermore, 3BP increases the production of reactive oxygen species (ROS) (Ihrlund et al., 2008; Kim et al., 2008; Macchioni et al., 2011a), induces ER stress,
ER Stress↑,
BioAv↓, Unfortunately, prolonged treatment with the drug reduces ROS levels and confers resistance by inducing regulatory genes that act on antioxidant systems.
Cyt‑c↑, 3BP induces cytochrome c release without triggering an apoptotic cascade in U118 cells
eff↑, The ROS enhancers antimycin and menadione sensitize U118 cells to 3BP

5263- 3BP,  CET,    3-Bromopyruvate overcomes cetuximab resistance in human colorectal cancer cells by inducing autophagy-dependent ferroptosis
- in-vitro, CRC, DLD1 - NA, NA, HCT116
eff↑, Our results demonstrated that the co-treatment of 3-BP and cetuximab synergistically induced an antiproliferative effect in both CRC cell lines
Ferroptosis↓, co-treatment induced ferroptosis, autophagy, and apoptosis.
TumAuto↑,
Apoptosis↑,
FOXO3↑, co-treatment inhibited FOXO3a phosphorylation and degradation and activated the FOXO3a/AMPKα/pBeclin1 and FOXO3a/PUMA pathways, leading to the promotion of ferroptosis, autophagy, and apoptosis in DLD-1
AMPKα↑,
p‑Beclin-1↑,
HK2↓, 3-Bromopyruvate (3-BP), also known as hexokinase II inhibitor II, has shown promise as an anticancer agent against various types of cancer
ATP↓, 3-BP exerts its anticancer effects by manipulating cell energy metabolism and regulating oxidative stress, as evidenced by the accumulation of reactive oxygen species (ROS) [13,14,15,16].
ROS↑,
Dose↝, Eight days postinoculation, xenografted mice were randomly divided into four groups and intraperitoneally injected with PBS, 3-BP, cetuximab, or a combination of 3-BP and cetuximab every four days for five injections.
TumVol↓, 3-BP alone or co-treatment with 3-BP and cetuximab significantly reduced the tumor volume and tumor weight on Day 28, but co-treatment showed a greater reduction than 3-BP alone
TumW↓,
xCT↑, The protein level of SLC7A11 was significantly upregulated in all three cell lines following co-treatment (Fig. 2B).
GSH↓, co-treatment with 3-BP and cetuximab led to glutathione (GSH) depletion (Fig. 2D), reactive oxygen species (ROS) production
eff↓, Knockdown of either ATG5 or Beclin1 attenuated the cell death and MDA production induced by co-treatment
MDA↑,

5259- 3BP,    Advanced cancers: eradication in all cases using 3-bromopyruvate therapy to deplete ATP
- in-vivo, HCC, NA
ATP↓, Advanced cancers (2-3cm) developed and were treated with the alkylating agent 3-bromopyruvate, a lactate/pyruvate analog shown here to selectively deplete ATP and induce cell death.
TumCD↑,
toxicity↓, In all 19 treated animals advanced cancers were eradicated without apparent toxicity or recurrence.
eff↑, These findings attest to the feasibility of completely destroying advanced, highly glycolytic cancers.
tumCV↓, The chemical agent 3-BrPA depletes ATP stores and inhibits HCC cell viability
Dose↝, administered eight treatments on successive days with 1 ml of 2 mM 3-BrPA, also in 1· PBS, pH 7.5. Injection of 3-BrPA was into the tumor.

5260- 3BP,    Systemic Delivery of Microencapsulated 3-Bromopyruvate for the Therapy of Pancreatic Cancer
- in-vivo, PC, NA
TumCG↓, In vivo, animals treated with β-CD–3-BrPA demonstrated minimal or no tumor progression as evident by the BLI signal
toxicity↓, In contrast to animals treated with free 3-BrPA, no lethal toxicity was observed for β-CD–3-BrPA.
BioAv↝, It is possible that in the microencapsulated formulation, 3-BrPA, is more bioavailable for uptake into tumor cells and less available to the normal cells that apparently mediate its toxicity
GAPDH↓, 3-Bromopyruvate (3-BrPA), a highly potent small-molecular inhibitor of the enzyme GAPDH, represents the only available antiglycolytic drug candidate that is able to enter cancer cells selectively through the monocarboxylate transporter 1 (MCT1; refs.
toxicity↑, However, due to its alkylating properties, 3-BrPA is associated with significant toxicity when delivered systemically in therapeutic doses, which has impeded the clinical development and use of this drug in patients with cancer
Dose↝, Encapsulation of 3-BrPA in β-CD was achieved by portionwise addition of 3-BrPA (166 mg, 1 mmol/L) to a stirring solution of β-CD (1,836 mg in 30 mL DI water). The resulting solution was sonicated for 1 hour at room temperature and then shaken overnig
ATP↓, ability of microencapsulated 3-BrPA (β-CD-3-BrPA) to achieve dose-dependent ATP depletion and cell death, two human pancreatic cancer cell lines were employed.
eff↑, both PDAC cell lines were more sensitive to the drugs when hypoxic (Fig. 2)
TumCI↓, MiaPaCa-2 and Suit-2 cells showed a reduction in invasion at drug concentrations as low as 12.5 µmol/L.
MMP9↓, marked reduction in the secretion of MMP-9 was detected in both cell lines.
toxicity↓, No organ toxicities or tissue damage was observed in animals treated with β-CD–3-BrPA

5261- 3BP,    The cytotoxicity of 3-bromopyruvate in breast cancer cells depends on extracellular pH
- in-vitro, BC, NA
eff↑, Transport of the anti-cancer agent 3-bromopyruvate (3BP) in breast cancer cells is mediated by monocarboxylate transporter (MCT)-1 activated by glycosylated chaperone cluster of differentiation (CD) 147. T
eff↓, The extracellular acidic pH increases the affinity for 3BP uptake enhancing its selective cytotoxic effect in tumour cells.

5269- 3BP,    The anti-metabolite KAT/3BP has in vitro and in vivo anti-tumor activity in lymphoma models.
- in-vitro, HCC, NA
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.

5264- 3BP,    Candidate cancer drug suspected after death of three patients at an alternative medicine clinic
- Review, Var, NA
toxicity↑, German police took action on 4 August after two patients from the Netherlands and one from Belgium died shortly after undergoing treatment at the Biological Cancer Centre, run by alternative practitioner Klaus Ross in the town of Brüggen, Germany
Glycolysis↓, It is believed to "starve" tumor cells to death by inhibiting glycolysis, the breakdown of glucose molecules to provide cells with energy.
eff↑, experiments on human cancer cell lines showed that combining another chemotherapeutic with 3BP increased its efficacy.
OS↑, the patient "was able to survive a much longer period than expected with an improved quality of life, which is clearly attributable to the treatment with 3BP,
QoL↑,
toxicity↝, Vogl says doctors should "absolutely" not perform systemic infusions, in which the drug circulates through the entire body. "

5266- 3BP,    3-bromopyruvate-based agent KAT-101
- Review, Var, NA
eff↑, Upon oral administration of 3-BP-based agent KAT-101, the 3-BP derivative, being structurally similar to lactic acid, specifically binds to and enters cancer cells through monocarboxylic acid transporters (MCTs)
Glycolysis↓, KAT-101 interferes with both glycolysis and mitochondrial oxidative phosphorylation (OxPhos), thereby depleting adenosine triphosphate (ATP) levels and thus limits energy supply needed by cancer cells to proliferate.
OXPHOS↓,
ATP↓,
TumCP↓,
Apoptosis↑, This induces cancer cell apoptosis and prevents cancer cell proliferation.
HK2↓, In addition, KAT-101 is able to release mitochondrial-bound hexokinase (HK) II (HK2)
MPT↑, increases the formation of mitochondrial permeability transition pores (MPTPs), which induces apoptosis.
LDH↓, KAT-101 also inhibits a variety of enzymes, including lactate dehydrogenase (LDH), pyruvate dehydrogenase (PDH) and pyruvate dehydrogenase kinase (PDHK).
PDH↓,

3452- 5-ALA,    5-ALA Is a Potent Lactate Dehydrogenase Inhibitor but Not a Substrate: Implications for Cell Glycolysis and New Avenues in 5-ALA-Mediated Anticancer Action
- in-vitro, GBM, T98G - in-vitro, GBM, LN-18 - in-vitro, GBM, U87MG
Glycolysis↓, we found that 5-ALA, a natural precursor of heme, can hinder cell glycolysis, which is the main path of energy production for most cancer cells.
LDH↓, ore specifically, we found that 5-ALA can block an enzyme involved in glycolysis, called lactate dehydrogenase (LDH)
eff↝, We found that 5-ALA has a potency of LDH inhibition comparable to other established LDH inhibitors, such as oxamate or tartronic acid
ECAR↓, a marked decrease in extracellular acidification rate (ECAR) was registered as a consequence of administering 5-ALA,

4774- 5-FU,  TQ,  CoQ10,    Exploring potential additive effects of 5-fluorouracil, thymoquinone, and coenzyme Q10 triple therapy on colon cancer cells in relation to glycolysis and redox status modulation
- in-vitro, CRC, NA
AntiCan↑, All treatments resulted in anticancer effects depicted by cell cycle arrest and apoptosis, with TQ demonstrating greater efficacy than CQ10, both with and without 5-FU.
TumCCA↑,
Apoptosis↑,
eff↑,
Bcl-2↓, However, 5-FU/TQ/CQ10 triple therapy exhibited the most potent pro-apoptotic activity in all cell lines, portrayed by the lowest levels of oncogenes (CCND1, CCND3, BCL2, and survivin)
survivin↓,
P21↑, and the highest upregulation of tumour suppressors (p21, p27, BAX, Cytochrome-C, and Cas- pase-3).
p27↑,
BAX↑,
Cyt‑c↑,
Casp3↑,
PI3K↓, The triple therapy also showed the strongest suppression of the PI3K/AKT/mTOR/HIF1α pathway, with a concurrent increase in its endogenous inhibitors (PTEN and AMPKα) in all cell lines used.
Akt↓,
mTOR↓,
Hif1a↓,
PTEN↑,
AMPKα↑,
PDH↑, triple therapy favoured glucose oxidation by upregulating PDH, while decreasing LDHA and PDHK1 enzymes.
LDHA↓,
antiOx↓, most significant decline in antioxidant levels and the highest increases in oxidative stress markers
ROS↑,
AntiCan↑, This study is the first to demonstrate the superior anticancer effects of TQ compared to CQ10, with and without 5-FU, in CRC treatment.

3941- 5HT,  dietMed,  VitB12,  FA,  VitC  Nutrition strategies that improve cognitive function
- Review, AD, NA
*other↑, Low glycemic index foods seem to improve attention, memory and functional capacity, while those rich in simple sugars are associated with difficulty in concentration and attention.
*other↓, Low levels of serotonin have been linked to decreased learning, reasoning and memory.
*cognitive↑, It is advisable to consume diets with an adequate ratio (5:1) of omega-6: 3 fatty acids (Mediterranean diet) given that they are associated with better memory capacity and lower risk of cognitive deterioration.
*eff↑, Vitamins B1, B6, B12, B9 (folic acid) and D, choline, iron and iodine exert neuroprotective effects and improve intellectual performance.
*eff↑, In parallel, antioxidants (vitamins C, E, A, zinc, selenium, lutein and zeaxanthin) have a very important role in the defense against oxidative stress associated with mental deterioration and in the improvement of cognition.

3968- ACNs,    Enhanced Neuronal Activation with Blueberry Supplementation in Mild Cognitive Impairment
- Human, AD, NA
*BOLD↑, Following daily supplementation for 16 weeks, blueberry-treated participants exhibited increased BOLD activation in the left pre-central gyrus, left middle frontal gyrus, and left inferior parietal lobe during working memory load conditions
*cognitive?, consistent with prior trials showing neurocognitive benefit with blueberry supplementation in this at-risk population.
*eff↑, High-flavanol cocoa treatment has been associated with enhancement of cerebral blood flow, [9] Concord grape juice [10] and pomegranate juice [11] supplementation with increased regional brain activation, and resveratrol treatment with enhanced hippo

3972- ACNs,    Recent Research on the Health Benefits of Blueberries and Their Anthocyanins
- Review, AD, NA - Review, Park, NA
*cardioP↑, Epidemiological studies associate regular, moderate intake of blueberries and/or anthocyanins with reduced risk of cardiovascular disease, death, and type 2 diabetes, and with improved weight maintenance and neuroprotection.
*neuroP↑,
*Inflam↓, Among the more important healthful aspects of blueberries are their anti-inflammatory and antioxidant actions and their beneficial effects on vascular and glucoregulatory function
*antiOx↓,
*GutMicro↑, Blueberry phytochemicals may affect gastrointestinal microflora and contribute to host health
*Half-Life↑, However, >50% of the 13C still remained in the body after 48 h
*LDL↓, controlled study of 58 diabetic patients, blueberry intake led to a decline in LDL cholesterol, triglycerides, and adiponectin and an increase in HDL cholesterol
*adiP↓,
*HDL↑,
*CRP↓, reduction was documented in inflammatory markers, including serum high-sensitivity C-reactive protein, soluble vascular adhesion molecule-1, and plasma IL-1β
*IL1β↓,
*Risk↓, lower Parkinson disease risk was associated with the highest quintile of anthocyanin (RR: 0.76) and berry (RR: 0.77) intake
*Risk↓, Nurse's Health Study, greater intake of blueberries and strawberries was associated with slower rates of cognitive decline in older adults, with an estimated delay in decline of about 2.5 y
*cognitive↑, Cognitive performance in elderly adults improved after 12 wk of daily intake of blueberry (94) or Concord grape (95) juice.
*memory↑, Better task switching and reduced interference in memory was found in healthy older adults after 90 d of blueberry supplementation
*other↑, After 12 wk of blueberry consumption, greater brain activity was detected using magnetic resonance imaging in healthy older adults during a cognitive challenge.
*BOLD↑, Similarly, during a memory test, regional blood oxygen level-dependent activity detected by MRI (99) was enhanced in the subjects taking blueberry, but not in those taking placebo.
*NO↓, 50–200 mg/d bilberry showed a dose-dependent decrease in neurotoxic NO and malondialdehyde, combined with an increase in neuroprotective antioxidant capacity due to glutathione, vitamin C, superoxide dismutase, and glutathione peroxidase
*MDA↓,
*GSH↑,
*VitC↑,
*SOD↑,
*GPx↑,
*eff↓, The percentage loss of blueberry anthocyanins during −18°C storage was 12% after 10 mo of storage
*eff↓, Freeze-dried blueberry powder loses anthocyanins in a temperature-dependent manner with a half-life of 139, 39, and 12 d when stored at 25, 42, and 60°C, respectively
*eff↓, Blueberries are low in ascorbic acid and high in anthocyanins (187), and notably anthocyanins are readily degraded by ascorbic acid
*eff↝, Shelf-stable blueberry products like jam (196), juice (197), and extracts (198) can lose polyphenolic compounds when stored at ambient temperature whereas refrigeration mitigates losses.
*Risk↓, It can be safely stated that daily moderate intake (50 mg anthocyanins, one-third cup of blueberries) can mitigate the risk of diseases and conditions of major socioeconomic importance in the Western world.

3973- ACNs,    Saskatoon and wild blueberries have higher anthocyanin contents than other Manitoba berries
- Analysis, AD, NA
eff↑, Saskatoon berry and wild blueberry showed a high content of total anthocyanins (562.4 and 558.3 mg/100 g, respectively) that were not significantly (P>0.05) different from each other.

5459- AF,    Auranofin Induces Lethality Driven by Reactive Oxygen Species in High-Grade Serous Ovarian Cancer Cells
- in-vitro, Ovarian, NA
ROS↑, AF primarily functions as a pro-oxidant by inhibiting thioredoxin reductase (TrxR), an antioxidant enzyme overexpressed in ovarian cancer.
TrxR↓, The primary mechanism of action of auranofin is to act as a pro-oxidative agent, increasing the production of reactive oxygen species (ROS) as a consequence of inhibiting the thioredoxin reductase (TrxR) anti-oxidant system
MMP↓, triggers the depolarization of the mitochondrial membrane, and kills HGSOC cells by inducing apoptosis.
Apoptosis↑,
eff↓, Notably, AF-induced cell death was abrogated by the ROS-scavenger N-acetyl cysteine (NAC).
Casp3↑, lethality of AF was associated with the activation of caspases-3/7 and the generation of DNA damage
Casp7↑,
DNAdam↑,
eff↑, Finally, when AF and L-BSO were combined, we observed synergistic lethality against HGSOC cells, which was mediated by a further increase in ROS and a decrease in the levels of the antioxidant GSH.
GSH↓,
angioG↓, Additionally, auranofin has been shown to inhibit angiogenesis
ChemoSen↑, In this study, we identified the mechanisms of cytotoxicity induced by auranofin in HGSOC cells that have different clinical sensitivities to platinum.
cl‑PARP↑, the cleavage of poly-ADP ribose polymerase (PARP), and the polyubiquitination of proteins
eff↑, synergistic lethal interaction between auranofin and a second pro-oxidant agent, the glutathione (GSH) inhibitor, L-buthionine sulfoximine (L-BSO);

5464- AF,    Inhibition of Thioredoxin-Reductase by Auranofin as a Pro-Oxidant Anticancer Strategy for Glioblastoma: In Vitro and In Vivo Studies
- vitro+vivo, GBM, NA
TrxR↓, Gold derivatives are irreversible inhibitors of TrxR. Among them, auranofin (AF), a selective TrxR inhibitor, has proven its effectiveness as a drug for the treatment of rheumatoid arthritis
BioAv↓, further clinical application of AF could be challenging due to the low solubility and insufficient delivery to glioblastoma.
ROS↑, The inhibition of TrxR1, which leads to increased ROS levels, is currently recognized as the primary mechanism of AF cytotoxicity [106]. In vitro studies have also shown that AF inhibits other thioredoxin reductases, such as TrxR2 and TrxR3
eff↝, The literature indicates that not all cancer tumors exhibit the same level of TrxR expression, affecting their sensitivity to AF.
TET1?, AF was shown to inhibit TET1 in T-ALL models
BioAv↑, Encapsulating AF into nanoparticles or combining it with other pharmaceutical excipients can minimize its potential adverse effects, preserve its interaction with serum proteins, and result in greater stability.

5460- AF,    Auranofin radiosensitizes tumor cells through targeting thioredoxin reductase and resulting overproduction of reactive oxygen species
- vitro+vivo, Var, 4T1
RadioS↑, AF at 3–10 μM is a potent radiosensitizer in vitro
ROS↑, . The first one is linked to an oxidative stress, as scavenging of reactive oxygen species (ROS)
eff↓, N-acetyl cysteine counteracted radiosensitization. (NAC)
mt-OCR↓, We also observed a decrease in mitochondrial oxygen consumption with spared oxygen acting as a radiosensitizer under hypoxic conditions.
DNAdam↑, Overall, radiosensitization was accompanied by ROS overproduction, mitochondrial dysfunction, DNA damage and apoptosis
Apoptosis↑,
TrxR↓, targeting thioredoxin reductase (TrxR)
eff↑, a simultaneous disruption of the thioredoxin and glutathione systems by the combination of AF and buthionine sulfoximine was shown to significantly improve tumor radioresponse.

5469- AF,    Ligand supplementation restores the cancer therapy efficacy of the antirheumatic drug auranofin from serum inactivation
- in-vitro, CRC, HCT116
eff↑, Synergistic effect of pantethine on auranofin
Half-Life↑, The gold ions can be maintained for a relatively long period in the blood (plasma half-lives of auranofin gold of 1.8 days in rats, 19.5 days in dogs, and 17 days in humans)37,71,72.

5458- AF,    Auranofin reveals therapeutic anticancer potential by triggering distinct molecular cell death mechanisms and innate immunity in mutant p53 non-small cell lung cancer
- in-vitro, NSCLC, NA
TrxR↓, Auranofin (AF) is an FDA-approved antirheumatic drug with anticancer properties that acts as a thioredoxin reductase 1 (TrxR) inhibitor.
AntiCan↓,
GPx4↓, Although functionally AF appeared a potent inhibitor of GPX4 in all NCI–H1299 cell lines, the induction of lipid peroxidation and consequently ferroptosis was limited to the p53 R273H expressing cells.
DNAdam↑, AF mainly induced large-scale DNA damage and replication stress, leading to the induction of apoptotic cell death rather than ferroptosis.
toxicity↓, AF is an orally available, lipophilic, organogold compound with a well-known safety profile that was approved by the U.S. Food and Drug Administration (FDA) for the treatment of rheumatoid arthritis (RA).
eff↝, AF represents a potential novel therapeutic strategy to efficiently kill mutant p53 NSCLC tumor cells through distinct immunogenic cell death pathways.

5472- AF,    Auranofin induces apoptosis and necrosis in HeLa cells via oxidative stress and glutathione depletion
- in-vitro, Cerv, HeLa
TrxR↓, Auranofin (Au), an inhibitor of thioredoxin reductase, is a known anti‑cancer drug
AntiCan↑,
TumCG↓, Au inhibited the growth of HeLa cells with an IC50 of ~2 µM at 24 h.
Apoptosis↑, This agent induced apoptosis and necrosis, accompanied by the cleavage of poly (ADP‑ribose) polymerase and loss of mitochondrial membrane potential.
necrosis↑,
cl‑PARP↑,
MMP↓,
ROS↑, With respect to the levels of ROS and GSH, Au increased intracellular O2•- in the HeLa cells and induced GSH depletion.
GSH↓,
eff↓, The antioxidant, N‑acetyl cysteine, not only attenuated apoptosis and necrosis in the Au‑treated HeLa cells, but also decreased the levels of O2•- and GSH depletion in the cells.

5468- AF,    The gold complex auranofin: new perspectives for cancer therapy
- Review, Var, NA
TrxR↓, Auranofin mainly targets the anti-oxidative system catalyzed by thioredoxin reductase (TrxR), which protects the cell from oxidative stress and death in the cytoplasm and the mitochondria.
ROS↑, Inhibiting TrxR dysregulates the intracellular redox state causing increased intracellular reactive oxygen species levels, and stimulates cellular demise
eff↑, TrxR is over-expressed in many cancers as an adaptive mechanism for cancer cell proliferation, rendering it an attractive target for cancer therapy, and auranofin as a potential therapeutic agent for cancer.
Apoptosis↑, promotion of ASK-induced apoptosis, and blockage of cell growth, proliferation, and survival due to reduced AKT activity and NF-kB- and p53-mediated transcription.
TumCG↓,
TumCP↓,
Akt↓,
NF-kB↓,
DNAdam↑, DNA damage
eff↝, auranofin inhibits TrxR1 in a p53-independent manner
eff↓, Pre-treatment with NAC counteracted the cancer cell killing effects of auranofin,
PI3K↓, auranofin induces cytotoxicity in human pancreatic adenocarcinoma and non-small cell lung cancer via the inhibition of the PI3K/AKT/mTOR pathway
Akt↓,
mTOR↓,
Hif1a↓, auranofin inhibits the cancer cell response to hypoxia, demonstrated by a decrease in HIF-1 𝛼 expression and VEGF secretion upon auranofin treatment under hypoxic conditions
VEGF↓,
Casp3↑, auranofin was shown to induce caspase-3-mediated apoptosis in human ovarian carcinoma SKOV-3 cells
CSCs↓,
ATP↓, it was found that auranofin inhibits ABCG2 function by depleting cellular ATP via inhibition of glycolysis [96]
Glycolysis↓,
eff↑, auranofin synergizes with another Trx1 inhibitor, piperlongumine, in killing gastric cancer cells in association with ROS-mediated ER stress response and mitochondrial dysfunction.
eff↑, when the gold complex is combined with either selenite or tellurite [104]
MMP↓, Increased ROS induced by AUR causes decreased membrane potential in the mitochondrial membrane, resulting in a decrease in anti-apoptotic proteins, caspase-dependent cell death, and translocation of apoptosis-inducing factor (AIF)
AIF↑,
toxicity↓, Auranofin is considered safe for human use in treating rheumatoid arthritis; thus, this gold derivative can reach the clinic for other diseases relatively quickly and at a low cost

5467- AF,    Auranofin Inhibition of Thioredoxin Reductase Sensitizes Lung Neuroendocrine Tumor Cells (NETs) and Small Cell Lung Cancer (SCLC) Cells to Sorafenib as well as Inhibiting SCLC Xenograft Growth
- in-vitro, Lung, NA
TrxR↓, AF treatment decreased TrxR activity and clonogenic survival in small cell lung cancer (SCLC) cell lines (DMS273 and DMS53) as well as the lung atypical (neuroendocrine tumor) NET cell line H727.
eff↑, AF treatment also significantly sensitized DMS273 and H727 cell lines in vitro to sorafenib, a multi-kinase inhibitor that was shown to decrease intracellular glutathione.
Dose↝, AF was administered intraperitoneally at 2 mg/kg or 4 mg/kg (IP) once (QD) or twice daily (BID) for 1 to 5 days in mice with DMS273 xenografts.
OS↑, When this daily AF treatment was extended for 14 days a significant prolongation of median survival from 19 to 23 days (p=0.04, N=30 controls, 28 AF) was observed without causing changes in animal bodyweight, CBCs, bone marrow toxicity, blood urea ni
eff↑, We also demonstrated that suppressing TrxR with AF can sensitize breast cancer stem cells to ROS induced stem cell transitions associated with EMT and cytotoxicity associated with 2-deoxyglucose treatment.

1900- AF,    Potential Anticancer Activity of Auranofin
- Review, Var, NA
TrxR↓, Auranofin inhibits the activity of thioredoxin reductase (TrxR
ROS↑, TrxR inhibition leads to an increase in cellular oxidative stress and induces apoptosis
Apoptosis↓,
TumCP↓, TrxR1 knockdown also inhibits cancer cell proliferation and DNA replication
eff↑, cytotoxicity of cisplatin is increased in cells expressing high levels of TrxR1 compared with cells expressing low levels

5444- AG,    A Systematic Review of Phytochemistry, Pharmacology and Pharmacokinetics on Astragali Radix: Implications for Astragali Radix as a Personalized Medicine
- Review, Var, NA
*Imm↑, AR possesses various biological functions, including potent immunomodulation, antioxidant, anti-inflammation and antitumor activities.
*antiOx↑,
*Inflam↓,
AntiTum↑,
eff↑, characteristics of increasing curative effect and reducing the toxicity of chemotherapeutic drugs [11 , 118].
chemoP↑,
Dose↝, main bioactive compounds responsible for the anti-cancer effects of AR mainly include formononetin, AS-IV and APS. S
TumCMig↓, AS-IV could inhibit the migration and proliferation of non-small cell lung cancer (NSCLC
TumCP↓,
Akt↓, h via inhibition of the Akt/GSK-3β/β-catenin signaling axis.
GSK‐3β↓,
MMP2↓, downregulating the expression of matrix metalloproteases (MMP)-2 and -9
MMP9↓,
EMT↓, AS-IV could inhibit TGF-B1 induced EMT through inhibition of PI3K/AKT/NF-KB
PI3K↓,
Akt↓,
NF-kB↓,
Inflam↓,
TGF-β1↓,
TNF-α↓,
IL6↓,
Fas↓, reduced FAS/FasL
FasL↓,
NOTCH1↓, decressing notch1
JNK↓, inactivating JNK pathway [145]
TumCG↓, The results showed that the AR water extract could inhibit the growth of colorectal cancer in vivo without apparent toxicity and side effect, which suggests that AR is a potential therapeutic drug for colorectal cancer

5431- AG,    Advances in research on the anti-tumor mechanism of Astragalus polysaccharides
- Review, Var, NA
AntiTum↑, APS has been increasingly used in cancer therapy owing to its anti-tumor ability as it prevents the progression of prostate, liver, cervical, ovarian, and non-small-cell lung cancer by suppressing tumor cell growth and invasion and enhancing apoptosi
TumCG↓,
TumCI↓,
Apoptosis↑, after APS treatment, the apoptosis of HepG2 cells is accelerated (57).
Imm↑, APS enhances the sensitivity of tumors to antineoplastic agents and improves the body’s immunity
Bcl-2↓, Huang et al. proposed that APS induces H22 (a hepatocellular cancer [HCC] cell line) apoptosis by downregulating Bcl-2 and upregulating Bax expression (56).
BAX↑,
Wnt↓, downregulating the Wnt/β-catenin signaling pathway.
β-catenin/ZEB1↓,
TumCG↓, APS effectively inhibited the growth of MDA-MB-231 (a human breast cancer [BC] cell line) graft tumor (58)
miR-133a-3p↑, apoptosis rate of human osteosarcoma MG63 cells increased owing to the upregulation of miR-133a and inactivation of the JNK signaling pathways (71).
JNK↓,
Fas↑, Li and Shen found that APS can induce apoptosis by activating the Fas death receptor pathway.
P53↑, Zhang et al. showed that APS could activate p53 and p21 and inhibit the expression of Notch1 and Notch3 in vitro, ultimately inhibiting cell proliferation and promoting their apoptosis
P21↑,
NOTCH1↓,
NOTCH3↓,
TumCP↓,
TumCCA↑, Liu et al. found that APS induced the cell cycle of bladder cancer UM-UC-3 to stop in the G0/G1 phase, thus inhibiting its proliferation
GPx4↓, APS was found to reduce GPX4 expression, inhibit the activity of the light chain subunit SLC7A11 (xCT), and promote the formation of BECN1-xCT complex by activating AMPK/BECN1 signaling.
xCT↓,
AMPK↑,
Beclin-1↑,
NF-kB↓, APS could control the proliferation of lung cancer cells (A549 and NCI-H358 cells) by inhibiting the NF-κB signaling pathway (97)
EMT↓, APS treatment led to reduced EMT markers (vimentin, AXL) and MIF levels in cells.
Vim↓,
TumMeta↓, APS inhibits Lewis lung cancer growth and metastasis in mice by significantly reducing VEGF and EGFR expression in cancerous tissues
VEGF↓,
EGFR↓,
eff↑, Nano-drug delivery systems can increase efficiency and reduce toxicity
eff↑, Jiao et al. developed selenium nanoparticles modified with macromolecular weight APS and observed positive results in hepatoma treatment
MMP↓, Subsequent investigations revealed that APS can decrease the ΔΨm values and Bcl-2, p-PI3K, P-gp, and p-AKT levels while elevating Bax expression.
P-gp↓,
MMP9↓, downregulation of MMP-9 expression,
ChemoSen↑, Li et al. observed that APS could enhance the sensitivity of SKOV3 ovarian cancer cells to CDDP treatment by activating the mitochondrial apoptosis pathway and JNK1/2 signaling pathway
SIRT1↓, APS significantly suppressed SIRT1 and SREBP1 expression, decreased cholesterol and triglyceride levels in PC3 and DU145, and attenuated cell proliferation.
SREBP1↓,
TumAuto↑, APS can induce autophagy in colorectal cancer cells by inhibiting the PI3K/AKT/mTOR axis and the development of cancer cells.
PI3K↓,
mTOR↓,
Casp3↑, Shen found that APS elevated caspase-9, caspase-3, and Bax protein levels, decreased Bcl-2 protein expression, and inhibited CD133 and CD44 co-positive colon cancer stem cell proliferation time
Casp9↑,
CD133↓,
CD44↓,
CSCs↓,
QoL↑, QOL was significantly improved as indicated by the reduction in pain and improvement in appetite

5432- AG,    Astragalus polysaccharides combined with radiochemotherapy for cervical cancer: a systematic review and meta-analysis of randomized controlled studies
- Review, Cerv, NA
ChemoSen↑, review aims to determine the clinical efficacy and safety of Astragalus Polysaccharide Injection (APS) combined with chemoradiotherapy for cervical cancer based on existing data.
eff↑, APS combined with chemoradiotherapy improved the objective response rate (ORR, RR = 1.43, 95% CI: 1.24–1.64) and disease control rate (
RadioS↑, APS can enhance the clinical efficacy of radiotherapy and chemotherapy for cervical cancer, respectively.
CEA↓, APS further reduced tumor marker levels: CEA (MD = −1.24, 95% CI: −1.58 to −0.89, p < 0.00001; heterogeneity: χ2 = 1.75, p = 0.19, I2 = 43%), SCC (
Wnt↓, Specifically, APS inhibits the cisplatin resistance pathway and regulates the cell cycle by suppressing the Wnt/β-catenin pathway via the PPARD/CDC20 axis (Liu et al., 2025)
β-catenin/ZEB1↓,
γH2AX↑, APS also influences autophagy and upregulates γH2AX expression, thereby enhancing cervical cancer sensitivity to radiotherapy
ER Stress↑, APS alleviates endoplasmic reticulum stress and promotes mitochondrial autophagy, thereby enhancing apoptosis and mitigating cisplatin-induced toxicity
mt-TumAuto↑,
QoL↑, suggested that APS combination therapy improves short-term clinical efficacy, quality of life, and immune function
Imm↑,

5434- AG,    Recent Advances in the Mechanisms and Applications of Astragalus Polysaccharides in Liver Cancer Treatment: An Overview
- Review, Liver, NA
AntiCan↑, Preclinical studies indicate that APS exerts significant anti-liver cancer effects through multiple biological actions, including the promotion of apoptosis, inhibition of proliferation, suppression of epithelial–mesenchymal transition, regulation of
Apoptosis↑,
TumCP↓,
EMT↓,
Imm↑, improving host immune response
ChemoSen↑, APS exhibits synergistic effects when combined with conventional chemotherapeutics and interventional treatments such as transarterial chemoembolisation, improving efficacy and reducing toxicity.
BioAv↓, limitations such as low bioavailability and a lack of large-scale clinical trials remain challenges for clinical translation.
TumCG↓, APS significantly inhibited tumour growth in H22-bearing mice with a dose-dependent effect (100, 200, 400 mg/kg), with the 400 mg/kg group achieving a tumour inhibition rate of 59.01%
IL2↑, APS enhance the thymus and spleen indices and elevates the key cytokines, including IL-2, IL-12, and TNF-α.
IL12↑,
TNF-α↑,
P-gp↓, APS reversed chemoresistance by downregulating P-glycoprotein and MDR1 mRNA expression
MDR1↓,
QoL↑, These effects contributed to improved treatment tolerance and enhanced quality of life [39].
Casp↑, APS can activate both the intrinsic and extrinsic apoptotic pathways, leading to caspase activation and DNA fragmentation
DNAdam↑,
Bcl-2↓, Mechanistically, APS downregulate antiapoptotic proteins such as Bcl-2 while upregulating proapoptotic proteins such as Bax and cleaved caspase-3.
BAX↑,
MMP↓, APS have been shown to disrupt the mitochondrial membrane potential and promote the release of cytochrome c, thereby enhancing apoptotic cascades in hepatocellular carcinoma models.
Cyt‑c↑,
NOTCH1↓, APS (0.1, 0.5, and 1.0 mg/mL) were shown to reduce both mRNA and protein levels of Notch1 in a concentration-dependent manner.
GSK‐3β↓, APS significantly inhibited the proliferation of HepG2 cells by downregulating the expression of glycogen synthase kinase-3β (GSK-3β), with 200 μg/mL being the most effective concentration.
TumCCA↑, APS exerted these effects by inducing cell cycle arrest at the G2/M and S phases, thereby impeding tumour cell proliferation [35].
GSH↓, HepG2 cells. APS also reduced intracellular glutathione (GSH) levels, increased reactive oxygen species (ROS) and lipid peroxidation levels, and elevated intracellular iron ion concentrations—all in a dose-dependent manner.
ROS↑,
lipid-P↑,
c-Iron↑,
GPx4↓, APS treatment led to the downregulation of GPX4 and upregulation of ACSL4, indicating that APS promotes ferroptosis in liver cancer cells.
ACSL4↑,
Ferroptosis↑,
Wnt↓, inhibit the expression of key proteins involved in the Wnt/β-catenin signalling pathway
β-catenin/ZEB1↓,
cycD1/CCND1↓, by downregulating the key oncogenic targets, including β-catenin, C-myc, and cyclin D1, which subsequently reduces Bcl-2 expression and activates the apoptotic cascade in HepG2 liver cancer cells.
Akt↓, It also inhibited the Akt/p-Akt signalling pathway.
PI3K↓, APS inhibit the PI3K/AKT/mTOR signalling pathway, which is a central negative regulator of autophagy.
mTOR↓,
CXCR4↓, PS upregulated the epithelial marker E-cadherin while downregulating the mesenchymal marker vimentin and the chemokine receptor CXCR4 at both mRNA and protein levels, suggesting that APS suppress liver cancer cell growth and metastasis by inhibiting
Vim↓,
PD-L1↓, APS interfere with immune checkpoint signalling by downregulating Programmed death-ligand 1 (PD-L1) expression on tumour cells.
eff↑, The preparation of polysaccharide–SeNP composites typically involves using sodium selenite (Na2SeO3) as the precursor and ascorbic acid (Vc) as the reducing agent, with synthesis carried out via a chemical reduction method in a polysaccharide solutio
eff↑, Mechanistic investigations revealed that AASP–SeNPs elevated intracellular ROS levels and reduced the mitochondrial membrane potential (∆Ψm).
ChemoSen↑, APS enhance doxorubicin-induced endoplasmic reticulum (ER) stress by reducing O-GlcNAcylation levels, thereby promoting apoptosis of liver cancer cells.
ChemoSen↑, APS inhibited BEL-7404 human liver cancer cell growth in a concentration-dependent manner and showed stronger cytotoxicity when combined with cisplatin.
chemoP↑, APS protects against chemotherapy-induced liver injury, particularly that caused by CTX, through antiapoptotic mechanisms

5441- AG,  Chemo,    Astragalus-containing Chinese herbal combinations for advanced non-small-cell lung cancer: a meta-analysis of 65 clinical trials enrolling 4751 patients
- Review, Lung, NA
eff↑, We found a large treatment effect of adding astragalus-based herbal treatment to standard chemotherapy regimens.
ChemoSen↑,

5236- AgNPs,    Adaptive regulations of Nrf2 alleviates silver nanoparticles-induced oxidative stress-related liver cells injury
- in-vitro, Liver, HepG2 - in-vitro, Nor, L02
tumCV↓, AgNPs induced a concentration-dependent decline in HepG2 and L02 cells viability.
ROS↑, • AgNPs induced ROS increase and apoptosis in HepG2 and L02 cells.
*ROS↑,
DNAdam↑, AgNPs induced DNA damage, autophagy and cell cycle arrest in HepG2 and L02 cells.
*DNAdam↑,
eff↓, N-acetylcysteine (NAC)alleviated AgNPs-induced cytotoxicity in HepG2 and L02 cells.
selectivity↑, Interestingly, HepG2 cells were more sensitive to AgNPs than L02 cells, and this may be related to the different ROS generation and responses to AgNPs by cancer cells and normal cells.

5237- AgNPs,    Nrf2 Activation Mitigates Silver Nanoparticle-Induced Ferroptosis in Hepatocytes
- in-vitro, Liver, HepG2
Ferroptosis↑, we provide evidence that AgNPs trigger ferroptosis in both mouse hepatocytes and HepG2 cells
p62↑, AgNPs increased p62 expression, which in turn stabilized Nrf2 by suppressing its interaction with Keap1.
NRF2↝,
eff↓, Upon activation, Nrf2 enhances the transcription of key antioxidant enzymes, including NQO1 and HO-1, thereby alleviating ferroptosis.

1907- AgNPs,  GoldNP,  Cu,    In vitro antitumour activity of water soluble Cu(I), Ag(I) and Au(I) complexes supported by hydrophilic alkyl phosphine ligands
- in-vitro, Lung, A549 - in-vitro, BC, MCF-7 - in-vitro, Melanoma, A375 - in-vitro, Colon, HCT15 - in-vitro, Cerv, HeLa
TrxR↓, In particular, [Au(PTA)4]PF6 was able to decrease by 50% TrxR activity at 4.2 nM
eff↓, C 50 value calculated for [Ag(PTA) 4]PF6 was 10.3 nM.
eff↓, Conversely, [Cu(PTA)4]PF6 was found to be much less effective in inhibiting this cytosolic selenoenzyme, with an IC50 value of 89.5 nM, roughly from 9 to 21 times higher than those calculated for silver and gold derivatives,
other∅, To the best of our knowledge, this is the first example of a phosphino silver complex acting as TrxR inhibitor.

1906- AgNPs,  GoldNP,  Cu,    Current Progresses in Metal-based Anticancer Complexes as Mammalian TrxR Inhibitors
- Review, Var, NA
TrxR↓, 183(Au) was able to decrease TrxR activity by 50% at 4.20 nM
eff↓, IC 50 value calculated for 184(Ag) was 10.30 nM
eff↓, Conversely, 185(Cu) was found to be much less effective in inhibiting TrxR activity, with an IC 50 value of 89.50 nM

1903- AgNPs,    Novel Silver Complexes Based on Phosphanes and Ester Derivatives of Bis(pyrazol-1-yl)acetate Ligands Targeting TrxR: New Promising Chemotherapeutic Tools Relevant to SCLC Managemen
- in-vitro, Lung, U1285
TrxR↓, accumulate into cancer cells and to selectively target Thioredoxin (TrxR),
eff↝, 2 µM was able to decrease TrxR enzyme activity by about 68%, compared with auranofin, which at the same concentration
ROS↑, cellular production of reactive oxygen species (ROS)

4403- AgNPs,    Silver Nanoparticles Decorated UiO-66-NH2 Metal-Organic Framework for Combination Therapy in Cancer Treatment
- in-vitro, GBM, U251 - in-vitro, GBM, U87MG - in-vitro, GBM, GL26 - in-vitro, Cerv, HeLa - in-vitro, CRC, RKO
AntiCan↑, Among the various NPs, silver nanoparticles (AgNPs) have garnered attention due to their cytotoxic and genotoxic properties in cancer cells.
eff↑, Our results demonstrate that UiO-66-NH2@AgNPs@Cis-Pt and its combinations exhibit enhanced cytotoxicity compared to individual components such as AgNPs and Cis-Pt.
EPR↑, Their nanometric structure allows them to easily penetrate and accumulate in tumour tissues either actively, via targeting systems [6,7,8], or passively, by taking advantage of tumour angiogenesis and the enhanced permeation and retention (EPR) effe
selectivity↑,
ROS↑, Once inside, AgNPs induce an increase in the production of reactive oxygen species (ROS) and cause mitochondrial dysfunctions, caspases activation, apoptosis, autophagy, and DNA damage
Casp↑,
Apoptosis↑,
DNAdam↑,
tumCV↓, figure 8
eff↑, One of the primary characteristics of AgNPs is their ability to release Ag+ ions from their surface in response to low pH or oxidation.

4404- AgNPs,  Rad,    Main Approaches to Enhance Radiosensitization in Cancer Cells by Nanoparticles: A Systematic Review
- Review, Var, NA
eff↑, Asharani et al compared the toxicity between 3–10 nm Pt, 5–35 nm Ag, and 15–35 nm Au NPs covered with PVA, and concluded that Ag NPs were the most toxic,
ROS↑, been suggested by different biological studies that they can produce ROS, and therefore can affect the concentration of intracellular calcium, activate transcription factors, and induce cytokine production

4400- AgNPs,  Rad,    Differential cytotoxic and radiosensitizing effects of silver nanoparticles on triple-negative breast cancer and non-triple-negative breast cells
- in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549 - in-vivo, BC, MDA-MB-231
ROS↑, AgNPs is known to cause dose-dependent toxicities, including induction of oxidative stress and DNA damage, which can lead to cell death.
DNAdam↑,
selectivity↑, We show that AgNPs are highly cytotoxic toward TNBC cells at doses that have little effect on nontumorigenic breast cells or cells derived from liver, kidney, and monocyte lineages.
TumCG↓, reduce TNBC growth and improve radiation therapy.
RadioS↑,
Dose↝, s 23±14 nm: particles were diluted to 40 μg/mL. 25 μg/mL AgNP dilution for 24 hours. zeta potential of AgNPs in water at pH 7 was approximately −36 mV, indicating good colloidal stability.
selectivity↑, Depending on AgNP dose, all three TNBC cell lines were 5- to 10-fold more sensitive to AgNP exposure than the nontumorigenic breast cells.
other↝, this study demonstrate that the cytotoxicity was dependent on exposure of cells to intact AgNPs and not due to Ag+ ions
eff↓, toxicity of AgNPs was significantly reduced in MDA-MB-231, MCF-7, and MCF-10A cells following pretreatment with GSH
eff↑, Selective depletion of GSH by BSO resulted in increased AgNP toxicity in all cell lines.
γH2AX↑, AgNPs significantly increased γH2AX in these cells compared to radiation alone.
Dose↓, Strikingly, an AgNP dose of as little as 1 μg/mL resulted in a dose enhancement of IR treatment (approximately 2-fold at the 2 Gy dose) f
eff↑, Moreover, intratumoral injection of AgNPs with or without radiation treatment can inhibit the growth of TNBC xenografts in mice

4399- AgNPs,  Chit,    Silver nanoparticles impregnated alginate-chitosan-blended nanocarrier induces apoptosis in human glioblastoma cells
- in-vitro, GBM, U87MG
DNAdam↑, extensive DNA damage.
ROS↑, Elevation in reactive oxygen species level indicates induction of oxidative stress in treated cells.
MMP↓, Mitochondrial dysfunction in cell death is evident from the depolarization of mitochondrial membrane potential (ΔΨm ).
eff↑, induction of apoptosis at low concentration of Ag NPs present in Ag NPs-Alg-Chi NC in comparison with free Ag NPs makes it a promising tool for cancer therapy.

4398- AgNPs,    Induction of apoptosis in cancer cells at low silver nanoparticle concentrations using chitosan nanocarrier
- in-vitro, Colon, HT29
Apoptosis↑, The involvement of mitochondrial pathway of cell death in the Ag-CS NCs induced apoptosis was evident from the depolarization of mitochondrial membrane potential (ΔΨ(m)).
MMP↓,
Casp3↑, up-regulation of caspase 3 expression
ROS↑, increased production of intracellular ROS due to Ag-CS NCs treatment indicated that the oxidative stress could augment the induction of apoptosis in HT 29 cells
eff↑, use of significantly low concentration of Ag NPs impregnated in chitosan nanocarrier is a much superior approach in comparison to the use of free Ag NPs in cancer therapy.

4392- AgNPs,    Hepatocurative activity of biosynthesized silver nanoparticles fabricated using Andrographis paniculata
- in-vivo, LiverDam, NA
*antiOx↑, strong antioxidant effect of the AgNPs compared to 5% aqueous leaf extract.
*eff?, effective in revival of all biological parameters to near normal in all intoxicated groups indicating the curing effects on CCl(4) induced liver injury.

4423- AgNPs,    Pongamia pinnata seed extract-mediated green synthesis of silver nanoparticle loaded nanogel for estimation of their antipsoriatic properties
- in-vivo, PSA, NA
*eff↑, Pongamia pinnata seed extracts loaded with nanogel formulations (AgNPs CUD NG) to improve the retention, accumulation, and the penetration of AgNPs into the epidermal layer of psoriasis.
*other↑, AgNPs CUD NG enhanced the retention of AgNPs on the psoriatic skin compared to normal skin

4421- AgNPs,    Effect of Biologically Synthesized Silver Nanoparticles on Human Cancer Cells
- in-vitro, Cerv, NA
selectivity↑, IC50: ≤4.25 μg/ml for normal and ≤32.5 μg/ml cerival cancer cells
eff↝, in vitro cytotoxicity assessment of the AgNPs has significant correlation with the total protein concentration in treated cells.
other↝, In the present study, silver nanoparticles were biologically synthesized using pure enzyme α-amylase and the other one by using soluble proteins of neem leaf extracts.

4424- AgNPs,    Understanding the prospective of nano-formulations towards the treatment of psoriasis
- in-vivo, PSA, NA
*eff↑, nano-formulations remain established as a promising modality for treating psoriasis treatment as they propose better penetration, targeted delivery, enhanced safety, and efficacy


Showing Research Papers: 1 to 50 of 1186
Page 1 of 24 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1186

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   Ferroptosis↓, 1,   Ferroptosis↑, 2,   GPx↓, 1,   GPx4↓, 3,   GSH↓, 7,   H2O2↑, 1,   c-Iron↑, 1,   lipid-P↑, 1,   MDA↑, 1,   NRF2↝, 1,   OXPHOS↓, 4,   ROS↑, 20,   mt-ROS↑, 1,   TrxR↓, 11,   xCT↓, 1,   xCT↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 2,   ATP↓, 7,   MMP↓, 7,   MPT↑, 1,   mt-OCR↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACSL4↑, 1,   AMPK↑, 2,   ECAR↓, 2,   GAPDH↓, 2,   Glycolysis↓, 12,   HK2?, 1,   HK2↓, 7,   LDH↓, 3,   LDHA↓, 2,   NADPH↓, 1,   PDH↓, 1,   PDH↑, 1,   PKM2↓, 1,   PPP↓, 1,   PPP↑, 1,   SIRT1↓, 1,   SREBP1↓, 1,  

Cell Death ⓘ

Akt↓, 6,   p‑Akt↑, 1,   Apoptosis↓, 1,   Apoptosis↑, 13,   BAX↑, 3,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   Casp↑, 2,   Casp3↑, 5,   Casp7↑, 1,   Casp9↑, 1,   Cyt‑c↑, 4,   Fas↓, 1,   Fas↑, 1,   FasL↓, 1,   Ferroptosis↓, 1,   Ferroptosis↑, 2,   JNK↓, 2,   necrosis↑, 1,   p27↑, 1,   survivin↓, 1,   TumCD↑, 3,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 2,  

Transcription & Epigenetics ⓘ

other↝, 3,   other∅, 1,   PhotoS↑, 1,   tumCV↓, 3,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 2,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   p‑Beclin-1↑, 1,   p62↑, 1,   TumAuto↑, 2,   mt-TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 10,   P53↑, 1,   cl‑PARP↑, 2,   γH2AX↑, 2,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↑, 2,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CD44↓, 1,   CSCs↓, 2,   EMT↓, 3,   FOXO3↑, 1,   GSK‐3β↓, 2,   mTOR↓, 4,   NOTCH1↓, 3,   NOTCH3↓, 1,   PI3K↓, 5,   PTEN↑, 1,   TumCG↓, 9,   Wnt↓, 3,  

Migration ⓘ

CEA↓, 1,   miR-133a-3p↑, 1,   MMP2↓, 1,   MMP9↓, 3,   TET1?, 1,   TGF-β1↓, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 6,   TumMeta↓, 2,   Vim↓, 2,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   EGFR↓, 1,   EPR↑, 1,   Hif1a↓, 2,   VEGF↓, 2,  

Barriers & Transport ⓘ

CellMemb↑, 1,   P-gp↓, 2,  

Immune & Inflammatory Signaling ⓘ

CXCR4↓, 1,   IL12↑, 1,   IL2↑, 1,   IL6↓, 1,   Imm↑, 3,   Inflam↓, 1,   NF-kB↓, 3,   NK cell↑, 1,   PD-L1↓, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 8,   Dose↓, 1,   Dose↝, 8,   eff↓, 16,   eff↑, 41,   eff↝, 7,   Half-Life↓, 1,   Half-Life↑, 1,   MDR1↓, 1,   RadioS↑, 6,   selectivity↑, 6,  

Clinical Biomarkers ⓘ

CEA↓, 1,   EGFR↓, 1,   IL6↓, 1,   LDH↓, 3,   PD-L1↓, 1,  

Functional Outcomes ⓘ

AntiCan↓, 1,   AntiCan↑, 6,   AntiTum↑, 3,   chemoP↑, 2,   OS↑, 3,   QoL↑, 4,   toxicity↓, 8,   toxicity↑, 4,   toxicity↝, 2,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 152

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 2,   GPx↑, 1,   GSH↑, 1,   HDL↑, 1,   MDA↓, 1,   ROS↑, 1,   SOD↑, 1,   VitC↑, 1,  

Core Metabolism/Glycolysis ⓘ

adiP↓, 1,   LDL↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,   other↑, 3,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling ⓘ

CRP↓, 1,   IL1β↓, 1,   Imm↑, 1,   Inflam↓, 2,  

Drug Metabolism & Resistance ⓘ

eff?, 1,   eff↓, 3,   eff↑, 5,   eff↝, 1,   Half-Life↑, 1,  

Clinical Biomarkers ⓘ

CRP↓, 1,   GutMicro↑, 1,  

Functional Outcomes ⓘ

BOLD↑, 2,   cardioP↑, 1,   cognitive?, 1,   cognitive↑, 2,   memory↑, 1,   neuroP↑, 1,   Risk↓, 3,   toxicity↓, 1,  
Total Targets: 34

Scientific Paper Hit Count for: eff, efficacy
65 Silver-NanoParticles
58 Magnetic Fields
43 Sulforaphane (mainly Broccoli)
38 Curcumin
35 Vitamin C (Ascorbic Acid)
32 Thymoquinone
30 Chemotherapy
28 Shikonin
25 immunotherapy
25 Piperlongumine
24 Artemisinin
23 EGCG (Epigallocatechin Gallate)
23 Selenite (Sodium)
22 Baicalein
22 Quercetin
21 Resveratrol
20 Copper and Cu NanoParticles
20 Ashwagandha(Withaferin A)
20 Berberine
19 Radiotherapy/Radiation
18 Magnetic Field Rotating
17 Apigenin (mainly Parsley)
17 Phenylbutyrate
17 Selenium NanoParticles
17 Dichloroacetate
16 diet FMD Fasting Mimicking Diet
16 Gambogic Acid
16 Bicarbonate(Sodium)
15 Selenium
15 Lycopene
14 Propolis -bee glue
14 Exercise
14 Phenethyl isothiocyanate
13 3-bromopyruvate
12 Citric Acid
12 Metformin
12 Betulinic acid
12 Caffeic acid
12 Fisetin
11 Folic Acid, Vit B9
11 Auranofin
11 chitosan
11 borneol
11 salinomycin
11 Rosmarinic acid
10 Alpha-Lipoic-Acid
10 Melatonin
10 Luteolin
10 Atorvastatin
10 Capsaicin
10 Vitamin K2
10 Silymarin (Milk Thistle) silibinin
10 diet Methionine-Restricted Diet
10 doxorubicin
10 Honokiol
10 VitK3,menadione
9 SonoDynamic Therapy UltraSound
9 Boron
9 Vitamin D3
9 Ellagic acid
9 Disulfiram
9 Hydrogen Gas
9 Urolithin
8 Gold NanoParticles
8 Hyperthermia
8 Cisplatin
8 Chrysin
8 Plumbagin
8 Parthenolide
7 Piperine
7 Electrical Pulses
6 5-fluorouracil
6 Coenzyme Q10
6 Vitamin B12
6 Photodynamic Therapy
6 Fenbendazole
6 Allicin (mainly Garlic)
6 beta-glucans
6 Bifidobacterium
6 HydroxyCitric Acid
6 Spermidine
6 Juglone
5 Astragalus
5 Akkermansia
5 Bevacizumab (brand Avastin)
5 Docetaxel
5 Ascorbyl Palmitate
5 Astaxanthin
5 Berbamine
5 beta-carotene(VitA)
5 Boswellia (frankincense)
5 diet Plant based
5 MCToil
5 Magnolol
5 Moringa oleifera
4 2-DeoxyGlucose
4 almonertinib
4 Andrographis
4 Aspirin -acetylsalicylic acid
4 Dipyridamole
4 Bortezomib
4 Butyrate
4 Cannabidiol
4 diet Short Term Fasting
4 Propyl gallate
4 Pterostilbene
4 Sulfasalazine
4 Whole Body Vibration
3 Anthocyanins
3 Gemcitabine (Gemzar)
3 Anti-oxidants
3 Aloe anthraquinones
3 Biochanin A
3 bempedoic acid
3 Lutein
3 Zeaxanthin
3 Bufalin/Huachansu
3 temozolomide
3 Chlorogenic acid
3 capecitabine
3 Calorie Restriction Mimetics
3 erastin
3 Ginseng
3 Lecithin
3 nicotinamide adenine dinucleotide
3 Naringin
3 Radio Frequency
3 Taurine
3 Vitamin B1/Thiamine
2 5-Aminolevulinic acid
2 Glucose
2 Zinc
2 Aromatherapy
2 Arsenic trioxide
2 Baicalin
2 brusatol
2 Caffeic Acid Phenethyl Ester (CAPE)
2 Caffeine
2 Calcium
2 Choline
2 Oxygen, Hyperbaric
2 Emodin
2 ferumoxytol
2 Kaempferol
2 hydroxychloroquine
2 Genistein (soy isoflavone)
2 γ-linolenic acid (Borage Oil)
2 Orlistat
2 Potassium
2 Methylene blue
2 metronomic chemo
2 Methylsulfonylmethane
2 Mushroom Lion’s Mane
2 Niclosamide (Niclocide)
2 Nimbolide
2 Phosphatidylserine
2 Aflavin-3,3′-digallate
1 cetuximab
1 Serotonin, 5-hydroxytryptamine
1 dietMediterranean
1 Anzaroot, Astragalus fasciculifolius Bioss
1 Trichostatin A
1 wortmannin
1 Resiquimod
1 Ajoene (compound of Garlic)
1 Acetyl-l-carnitine
1 Amodiaquine
1 Vitamin A, Retinoic Acid
1 Sorafenib (brand name Nexavar)
1 Trastuzumab
1 D-limonene
1 Huperzine A/Huperzia serrata
1 probiotics
1 Brucea javanica
1 Bacopa monnieri
1 Bromelain
1 Bruteridin(bergamot juice)
1 Rutin
1 urea
1 Carnosine
1 Cannabichromene
1 Cinnamon
1 Camptothecin
1 irinotecan
1 Black phosphorus
1 chemodynamic therapy
1 Dichloroacetophenone(2,2-)
1 Date Fruit Extract
1 diet Fermented Foods
1 diet Ketogenic
1 PXD, phenoxodiol
1 Ferulic acid
1 Vitamin E
1 flavonoids
1 Flickering Light Stimulation
1 verapamil
1 Garcinol
1 tamoxifen
1 Hydroxycinnamic-acid
1 HydroxyTyrosol
1 itraconazole
1 Laetrile B17 Amygdalin
1 lambertianic acid
1 Docosahexaenoic Acid
1 Matrine
1 Methyl Jasmonate
1 carboplatin
1 methotrexate
1 Magnesium
1 Methylglyoxal
1 Mushroom Reishi
1 Myricetin
1 Oleocanthal
1 sericin
1 Paclitaxel
1 Psoralidin
1 enzalutamide
1 Oxaliplatin
1 Scoulerine
1 polyethylene glycol
1 acetaminophen
1 Formononetin
1 acetazolamide
1 Iron
1 Squalene
1 Glutathione
1 statins
1 Sutherlandioside D
1 triptolide
1 Tumor Treating Fields
1 Ursolic acid
1 Vitamin B3,Niacin
1 Vitamin B5,Pantothenic Acid
1 Vitamin B6,pyridoxine
1 Wogonin
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#:961  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

Home Page