Thiols Cancer Research Results
Thiols, Thiols: Click to Expand ⟱
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"Thiols" generally refer to compounds containing sulfhydryl (–SH) groups, with glutathione (GSH) being one of the most abundant and well-studied cellular thiols. Thiol groups play essential roles in maintaining redox balance, detoxifying reactive oxygen species (ROS), and modulating protein function via post-translational modifications.
• Elevated levels of glutathione and related thiols have been associated with enhanced resistance to chemotherapy and radiation, as these treatments often work by inducing oxidative damage.
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Scientific Papers found: Click to Expand⟱
AntiCan↑, 3BP exhibited strong anticancer effects in both preclinical and human studies e.g. energy depletion, oxidative stress, anti-angiogenesis, anti-metastatic effects, targeting cancer stem cells and antagonizing the Warburg effect.
ROS↑,
angioG↓,
CSCs↓,
Warburg↓,
GSH↓, Reported decrease in endogenous cellular GSH content upon 3BP treatment was confirmed to be due to the formation of 3BP-GSH complex i
Thiols↓, Being a thiol blocker, 3BP may attack thiol groups in tissues and serum proteins e.g. albumin and GSH.
AntiCan↑, Allicin not only protects against tumors but also alleviates the adverse effects of anticancer treatment and enhances the chemotherapeutic response under certain conditions.
ChemoSen↑,
angioG↓, DATS works against tumors by blocking the cell cycle, inhibiting tumor cell proliferation, and inhibiting angiogenesis
chemoP↑,
*GutMicro↑, In addition to against bacteria, allicin has also been shown to modulate the composition of gut microbiota (GM) and increase the diversity of beneficial bacteria in animal models
*antiOx↑, allicin was confirmed to have strong antioxidant properties
other↝, Allicin is a reactive sulfur species (RSS) and a potent thiol-trapping reagent, rapidly reacting with glutathione (GSH) to yield S-allylmercaptoglutathione (GSSA)
GSH↓, Thus, allicin depletes the intracellular GSH pool and reacts with cysteine thiols available in proteins through S-thioallylation
Thiols↓, This reaction is the key to the biological activity of allicin, and the reversible oxidation and reduction of protein-thiols is the core of many processes in cells
*ROS↓, In a hypertrophic heart mouse model, the clearance of intracellular ROS by allicin was measured, and has been shown to reduce the production of ROS and block ROS-dependent ERK1/2, JNK1/2, AKT, NF-κB and Smad signaling, which leads to the inhibition o
*hepatoP↑, Moreover, allicin has been proven to play a hepatoprotective role against acetaminophen (APAP)-induced liver injury by reducing oxidative stress
*Inflam↓, OSCs in garlic has been shown to inhibit the tumor-mediated pro-inflammatory activity by modulating the cytokine pattern in a way that leads to an overall inhibition of NF-κB
*NF-kB↓,
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Nor, |
3T3 |
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BC, |
MCF-7 |
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Lung, |
A549 |
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in-vitro, |
CRC, |
HT-29 |
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Thiols↓, Garlic produces the thiol-reactive defence substance, allicin, upon wounding.
tumCV↓, Allicin reduced cell viability and cell proliferation in a concentration dependent manner.
TumCP↓, Allicin Inhibits Cell Proliferation
GSH↓, allicin reacts with and depletes the GSH pool.
GSSG↑, Allicin is a thiol-reagent and reacts easily with glutathione, forming S-allylmercaptoglutathione (GSSA) and leading to an increased production of GSSG
ROS↑, Allicin oxidizes thiols and causes oxidative stress in its own right.
*Bacteria?, Allicin in its pure form was found to exhibit i) antibacterial activity against a wide range of Gram-negative and Gram-positive bacteria, including multidrug-resistant enterotoxicogenic strains of Escherichia coli
*Thiols↓, The main antimicrobial effect of allicin is due to its chemical reaction with thiol groups of various enzymes, e.g. alcohol dehydrogenase, thioredoxin reductase, and RNA polymerase
*TrxR↓,
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AML, |
Jurkat |
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Nor, |
L929 |
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necrosis↑, Allicin induces apoptosis or necrosis in a dose-dependent manner but biocompatible doses influence cellular metabolism and signalling cascades.
Thiols↓, Oxidation of protein thiols and depletion of the glutathione pool are thought to be responsible for allicin's physiological effects.
GSH↓,
ENO1↓, allicin caused inhibition of enolase activity, an enzyme considered a cancer therapy target.
Zn2+↑, Allicin leads to Zn2+ release in murine EL-4 cells
Glycolysis↓, suggests that allicin can inhibit glycolysis which provides electron donors for ATP generation required for cellular biosynthesis pathways and growth of the cells.
ATP↓,
BioAv↓, achieving therapeutically relevant concentrations of allicin via the oral route is therefore unlikely and more direct routes of application to the desired site of action need to be considered
TumCP↓, Eugenol clearly decreased the proliferation rate and increased LDH release in a concentration- and time-dependent manner.
LDH↝, (50–1000 µM) of eugenol on LDH release from HeLa cells for 24 h (cytotoxicity) i
ChemoSen↑, It showed synergistic effects with cisplatin and X-rays.
RadioS↑,
Casp3↑, Eugenol increased caspase-3 activity and the expression of Bax, cytochrome c (Cyt-c), caspase-3, and caspase-9 and decreased the expression of B-cell lymphoma (Bcl)-2, cyclooxygenase-2 (Cox-2), and interleukin-1 beta (IL-1β)
BAX↑,
Cyt‑c↑,
Casp9↑,
Bcl-2↓,
COX2↓,
IL1β↓,
ROS↑, pro-oxidant action that kills cancer cells by affecting several signaling pathways
NF-kB↓, nhibits nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, downregulates prostaglandin synthesis, decreases cyclooxygenase-2 (Cox-2) activity, produces cell cycle arrest in the S phase, increases the generation of reac
COX2↓,
TumCCA↓,
Thiols↓, In human colon cancer HT-29 cells, eugenol increased ROS, while decreasing thiol levels
GSH↓, eugenol also induced apoptosis of human breast cancer MCF-7 cells, accompanied by exhaustion in glutathione (GSH) and an increase in ROS
Dose↝, Eugenol, a significant bioactive compound, is found in cloves and other traditional Indian medicinal plants, such as cinnamon, tulsi, ginger, turmeric, and Japanese star anise, which have been reported to have significant anticancer properties.
AntiCan↑,
*Inflam↓, also exhibits different pharmacological effects (anti-inflammatory, cardio-protection, and neuroprotection).
*cardioP↑,
*neuroP↑,
angioG↓, eugenol exhibits anti-apoptotic, anti-angiogenic, and anti-metastatic properties in cancer cell lines and in vivo animal models, which we discuss in this review.
TumMeta↓,
*BioAv↑, Oral administration of eugenol promoted rapid absorption by different organs and metabolism in the liver. encapsulation is required to address the issues of early absorption, increased water solubility, and improved efficiency
*eff↑, Eugenol encapsulation as an inclusion with β-cyclodextrin, chitosan, and 2-hydroxypropyl-β-cyclodextrin nanoparticles improves its thermal stability
*toxicity↝, Eugenol at lower doses displayed minimal adverse effects, including contact dermatitis, local irritation, and rare allergic responses. However, at its higher doses, it can lead to liver and kidney damage, tissue injury, sudden onset of seizures, and
antiNeop↑, exhibit antineoplastic properties against different cancers by triggering cell cycle arrest and apoptosis in cancer cells
TumCCA↑,
Apoptosis↑,
*antiOx↑, Eugenol exhibits its antioxidant property due to its unique structural configuration, specifically the presence of an allyl group, as revealed by electron spin resonance
*lipid-P↓, Eugenol prevents lipid peroxidation (Nagababu and Lakshmaiah 1994), hexanal oxidation (Lee and Shibamoto 2001), copper-dependent LDL oxidation, and nonenzymatic peroxidation in liver mitochondria
*ROS↓, Eugenol exhibited 58–81 % DPPH radical scavenging potential in its 0.25–1.0 µM/ml concentration
*SOD↑, Eugenol protects against oxidative damage by increasing the levels of certain antioxidant enzymes, such as SOD, CAT, GST, and GPx (Huang et al. 2015).
*Catalase↑,
*GSTs↑,
*GPx↑,
*iNOS↓, Eugenol pre-treatment increased the levels of antioxidant enzymes and decreased the expression of iNOS, COX2, IL-6, and tumor necrosis factor-α (TNF-α) (Kaur et al. 2010).
*COX2↓,
*IL6↓,
*TNF-α↓,
*AntiArt↑, Administration of eugenol at 33 mg/kg dose in arthritis-induced male Sprague-Dawley rats decreased the swelling of paws and joints (
*Bacteria↓, Along with cinnamaldehyde and thymol, Li et al. determined eugenol's antibacterial activity against E. coli and S. aureus.
TumAuto↑, eugenol activated apoptosis and autophagy through the PI3K/AKT/FOXO3a pathway in cancer cells(breast cancer cells).
PI3K↓, PI3K/Akt/mTOR pathway inhibition
Akt↓,
FOXO3↝,
BAX↑,
mTOR↓, PI3K/Akt/mTOR pathway inhibition
NF-kB↓, NF-κB signaling pathway inhibition
P53↑, In some cancers, eugenol has been shown to upregulate p53, thereby inhibiting cancer growth.
TumCG↓,
CSCs↓, eugenol downregulated certain signaling cascades of the Wnt signaling pathway and specific cancer stem cell markers, including CD44, EpCAM, Notch1, and Oct4, in breast cancer cell lines treated with eugenol.
CD44↓,
EpCAM↓,
NOTCH1↓,
OCT4↓,
Bcl-2↓, Eugenol also downregulates the protein expressions of p85, BCL-2, PDK1, HER2, AKT, BAD, Cyclin D1, and NF-KB.
PDK1↓,
HER2/EBBR2↓,
BAD↓,
cycD1/CCND1↓,
ROS↑, EUG-medium chain triglyceride nanoemulsions Liver cancer HB8065 cells Increased the levels of ROS generation to initiated the apoptotic cell death
Casp3↑, apoptosis initiated by Caspase-3
protein upregulation
selectivity↑, Eugenol was not cytotoxic to MCF10A cells; however, it displayed cytotoxic activity in the transformed MCF10A cells (MCF10A-ras).
MMP2↓, A significant decline in matrix metalloproteinase (MMP-2, MMP-9) levels and an increase in tissue inhibitor of metalloproteinase-1 (TIMP-1) expression were also observed.
MMP9↓,
TIMP1↑,
VEGF↓, Eugenol also inhibits metastatic invasion and angiogenesis, as evident from the downregulation of MMP-2, MMP-9, VEGF, and VEGFR1, along with the upregulation of RECK and TIMP-2
VEGFR1↓,
RECK↑,
TIMP2↑,
DNAdam↑, Eugenol demonstrated an apoptosis-inducing effect in HL-60 cells, as evidenced by DNA fragmentation and a DNA ladder assay.
MMP↓, It is accompanied by a decline in mitochondrial membrane potential and thiol levels, early disruption of the lipid layer, DNA fragmentation, and activation of proapoptotic markers (Caspase-3, PARP, p53)
Thiols↓,
PARP↑,
*Pain↓, eugenol nanoemulsion may significantly reduce pain-associated arteriovenous fistula (AVF)
E2Fs↓, t interferes with several critical cancer signaling pathways, including the Wnt/b-Catenin pathway, PI3K/AKT pathway, MAPK/ERK pathway, E2F1/survivin pathway, JNK/STAT3 pathway, and NF-κB signaling pathway, among others.
survivin↓, cause E2F1/survivin downregulation, which activates apoptosis in breast cancer cells
ROS↑, sOMF
mitResp↓, Inhibit Mitochondrial Respiration
mtDam↑, Produce Loss of Mitochondrial Integrity
Dose↝, Repeated intermittent sOMF was applied for 2 hours at a specific frequency, in the 200-300 Hz frequency range, with on-off epochs of 250 or 500 ms duration.
MMP?, ROS generation has been shown to be driven, in part, by elevated mitochondrial membrane chemiosmotic potential (ΔΨ) and ubiquinol (QH2)
OCR↓, Immediately after cessation of field rotation we observe a loss of mitochondrial integrity (labeled LMI), with a very rapid increase in O2 consumption
mt-H2O2↑, We have previously demonstrated that sOMF treatment of cells generates superoxide/hydrogen peroxide in the mitochondrial matrix
eff↓, we repeated the same experiment in the presence of Trolox, which protects thiols from ROS oxidation (47). sOMF treatment of RLM in State 3u pre-treated with Trolox (15 μM), show minimal inhibition,
SDH↓, SDH Inhibition by sOMF in State 3u RLM Is Caused by ROS Generation
Thiols↓, suggest that thiol oxidation in SDH may result from sOMF.
GSH↓, Glutathione in the mitochondrial matrix can provide some protection from ROS, but after solubilizing the mitochondria, this protection is lost and the SDH becomes more sensitive to sOMF.
TumCD↑, sOMF is highly effective at killing non-dividing GBM cell cultures,
Casp3↑, caspase-3 activation 1 h after sOMF
Casp7↑, rapid activation of caspase-3/7
MPT↑, OMF-treated cell that causes near simultaneous MPT, release of cytochrome c and other apoptosis-inducing factors, resulting in caspase-3/7 activation in these GBM cells.
Cyt‑c↑,
selectivity↑, differential sensitivity to sOMF of cancer cells over ‘normal’ cells becomes apparent. rapid increase in the reactive oxygen species (ROS) in the mitochondria to cytotoxic levels only in cancer cells, and not in normal human cortical neurons
GSH/GSSG↓, increasing GSSG/GSH ratio
ETC↓, completely arrest electron transport in isolated, respiring, rat liver mitochondria and patient derived glioblastoma (GBM)
TumCP↓, Plumbagin inhibited activation, proliferation, cytokine production, and graft-versus-host disease in lymphocytes and inhibited growth of tumor cells
TumCG↓,
NF-kB↓, by suppressing nuclear factor-κB (NF-κB)
ROS↑, Plumbagin was also shown to induce reactive oxygen species (ROS) generation in tumor cells via an unknown mechanism
GSH↓, Plumbagin depleted glutathione (GSH) levels that led to increase in ROS generation
eff↓, production by plumbagin was abrogated by thiol antioxidants but not by non-thiol antioxidants confirming that thiols but not ROS play an important role in biological activity of plumbagin.
i-Thiols↓, Plumbagin depleted intracellular thiols (mainly GSH)
GSH/GSSG↓, plumbagin also induced GSH to GSSG conversion
*GSH↓, In this report, for the first time we show GSH depletion as a source of ROS generation in normal lymphocytes following plumbagin treatment.
*ROS↑, plumbagin-induced increase in ROS levels in lymphocytes
Apoptosis↑, parthenolide has shown to induce apoptosis in cancer cells
GSH↓, Parthenolide rapidly depleted intracellular thiols, including both free glutathione (GSH) and protein thiols.
ROS↑, ncreases in intracellular reactive oxygen species (ROS) and calcium levels
Ca+2↑,
GRP78/BiP↑, Increased expression of GRP78 protein, a marker for endoplasmic reticulum stress was also detected
ER Stress↑,
eff↓, pretreatment with N-acetylcysteine, a precursor of GSH synthesis, protected the cells from parthenolide-induced thiol depletion, ROS production, cytosolic calcium increase and completely blocked parthenolide-induced apoptosis.
eff↑, pretreatment of buthionine sulfoximine, an inhibitor of GSH synthesis sensitized the cell to apoptosis
Thiols↓, Parthenolide rapidly depleted intracellular thiols
toxicity↝, selenite is safe and tolerable with an unexpectable high maximum tolerated dose (MTD) and short half-life.
Half-Life↝, half-life was short (18.5 h)
ROS↑, Selenide efficiently redox cycles with oxygen, producing reactive oxygen species (ROS) until the system is exhausted of thiols and/or NADPH
Thiols↓,
NADPH↓,
toxicity↝, trimethylselenonium may serve as a urinary biomarker for both excessive selenium intake and body burden as well as a toxic dose of selenium
other↝, Selenoprotein P (SELENOP) is a proven biomarker of Se status
Showing Research Papers: 1 to 11 of 11
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
GSH↓, 8, GSH/GSSG↓, 2, GSSG↑, 1, mt-H2O2↑, 1, ROS↑, 8, Thiols↓, 9, i-Thiols↓, 1,
Metal & Cofactor Biology ⓘ
Zn2+↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 1, ETC↓, 1, mitResp↓, 1, MMP?, 1, MMP↓, 1, MPT↑, 1, mtDam↑, 1, OCR↓, 1, SDH↓, 1,
Core Metabolism/Glycolysis ⓘ
ENO1↓, 1, Glycolysis↓, 1, LDH↝, 1, NADPH↓, 1, PDK1↓, 1, Warburg↓, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↑, 2, BAD↓, 1, BAX↑, 2, Bcl-2↓, 2, Casp3↑, 3, Casp7↑, 1, Casp9↑, 1, Cyt‑c↑, 2, necrosis↑, 1, survivin↓, 1, TumCD↑, 1,
Kinase & Signal Transduction ⓘ
HER2/EBBR2↓, 1,
Transcription & Epigenetics ⓘ
other↝, 2, tumCV↓, 1,
Protein Folding & ER Stress ⓘ
ER Stress↑, 1, GRP78/BiP↑, 1,
Autophagy & Lysosomes ⓘ
TumAuto↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 1, P53↑, 1, PARP↑, 1,
Cell Cycle & Senescence ⓘ
cycD1/CCND1↓, 1, E2Fs↓, 1, TumCCA↓, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
CD44↓, 1, CSCs↓, 2, EpCAM↓, 1, FOXO3↝, 1, mTOR↓, 1, NOTCH1↓, 1, OCT4↓, 1, PI3K↓, 1, TumCG↓, 2, Zn2+↑, 1,
Migration ⓘ
Ca+2↑, 1, MMP2↓, 1, MMP9↓, 1, RECK↑, 1, TIMP1↑, 1, TIMP2↑, 1, TumCP↓, 3, TumMeta↓, 1, VEGFR1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 3, VEGF↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, IL1β↓, 1, NF-kB↓, 3,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, ChemoSen↑, 2, Dose↝, 2, eff↓, 3, eff↑, 1, Half-Life↝, 1, RadioS↑, 1, selectivity↑, 2,
Clinical Biomarkers ⓘ
HER2/EBBR2↓, 1, LDH↝, 1,
Functional Outcomes ⓘ
AntiCan↑, 3, antiNeop↑, 1, chemoP↑, 1, toxicity↝, 2,
Total Targets: 86
Pathway results for Effect on Normal Cells:
NA, unassigned ⓘ
AntiArt↑, 1,
Redox & Oxidative Stress ⓘ
antiOx↑, 2, Catalase↑, 1, GPx↑, 1, GSH↓, 1, GSTs↑, 1, lipid-P↓, 1, ROS↓, 2, ROS↑, 1, SOD↑, 1, Thiols↓, 1, TrxR↓, 1,
Cell Death ⓘ
iNOS↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL6↓, 1, Inflam↓, 2, NF-kB↓, 1, TNF-α↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, eff↑, 1,
Clinical Biomarkers ⓘ
GutMicro↑, 1, IL6↓, 1,
Functional Outcomes ⓘ
cardioP↑, 1, hepatoP↑, 1, neuroP↑, 1, Pain↓, 1, toxicity↝, 1,
Infection & Microbiome ⓘ
Bacteria?, 1, Bacteria↓, 1,
Total Targets: 29
Scientific Paper Hit Count for: Thiols, Thiols
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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