TAC Cancer Research Results

TAC, total antioxidant capacity: Click to Expand ⟱
Source:
Type:
Total antioxidant capacity (TAC) refers to the ability of a biological sample (such as blood, tissues, or food) to counteract oxidative stress by neutralizing free radicals and reactive oxygen species (ROS).

May have reduced levels in cancers.
Scientific Papers found: Click to Expand⟱
377- AgNPs,    Anticancer Action of Silver Nanoparticles in SKBR3 Breast Cancer Cells through Promotion of Oxidative Stress and Apoptosis
- in-vitro, BC, SkBr3
ROS↑,
Apoptosis↑,
Bax:Bcl2↑,
VEGF↑, VEGF-A
Akt↓,
PI3K↓,
TAC↓,
TOS↑,
OSI↑,
MDA↑,
Casp3↑,
Casp7↑,

5638- BCA,    Investigating the Anticancer Potential of Biochanin A in KB Oral Cancer Cells Through the NFκB Pathway
- in-vitro, Oral, NA
tumCV↓, BCA treatment induced several notable effects on KB cells, including reduced cell viability, altered morphology suggestive of apoptosis, heightened oxidative stress, and alterations in mitochondrial membrane potential.
ROS↑,
MMP↓,
TumCMig↓, BCA treatment demonstrated an inhibitory effect on cell migration.
TAC↓, revealing decreased antioxidant enzyme activities and increased lipid peroxidation across different BCA concentrations
lipid-P↓,
NF-kB↓, downregulated the expression of nuclear factor-κB (
Apoptosis↑, ts demonstrated ability to induce apoptosis, perturb cellular functions, and modulate gene expression within cancer cells underscores its significance.

729- Bor,    Promising potential of boron compounds against Glioblastoma: In Vitro antioxidant, anti-inflammatory and anticancer studies
- in-vitro, GBM, U87MG - in-vivo, Nor, HaCaT
TOS↑,
TumCG↓,
MDA↑,
SOD↑,
Catalase↑,
TAC↓,
GSH↓,
BRAF↑,
MAPK↓,
PTEN↓, BA application was found more favorable because of its inhibitory effect on PIK3CA, PIK3R1, PTEN and RAF1 genes
Raf↓, RAF1
*toxicity↓, We verified the selectivity of the compounds using a normal cell line, HaCaT and found an exact opposite condition after treating HaCaT cells with BA and BX

7567- HYP,    Hyperoside: A review on its sources, biological activities, and molecular mechanisms
- Review, Var, NA
*AntiCan↑, anticancer, anti-inflammatory, antibacterial, antiviral, antidepressant, and organ protective effects.
*Bacteria↓,
*AntiViral↑,
*antiD↓,
*RenoP↑, Kidney protection
*hepatoP↑, Liver protection
*eff↑, treating multiple diseases, such as sepsis, arthritis, colitis, diabetic nephropathy, myocardial ischemia-reperfusion, pulmonary fibrosis, and cancers.
*Sepsis↓,
*AntiArt↑,
*Stroke↓,
TumCMig↓, hyperoside has been shown to inhibit the migration and invasion properties of A549 cells by suppressing the expression of metastasis-associated gene 1 (MTA1), matrix metalloproteinase-2 inhibitor (TIMP-2), matrix metalloproteinase (MMP)-2
TumCI↓,
MTA1↓,
TIMP2↓,
MMP2↓,
MMP↓, disrupted the penetration of the mitochondrial membrane, and triggered mitochondrial cytochrome C and apoptosis inducers into the cytoplasm
Cyt‑c↑,
Akt↓, inhibited the Akt/mTOR/p70S6K signaling pathway in NSCLC cells to promote autophagy and exerted anticancer activity
mTOR↓,
P70S6K↓,
TumAuto↑,
PD-L1↓, thereby inhibiting PD-L1 expression at the transcriptional leve
TNF-α↓, subsequently, inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1b, IL-6 and IL-8, were significantly down-regulated
IL1β↓,
IL6↓,
IL8↓,
Bcl-2↓, Hyperoside was reported to inhibit the over-expression of B-cell lymphoma factor 2 (Bcl)-2 and Bcl-x in lung cancer cells, and up-regulate the preapoptotic factors such as Bax, Bad, and Bak.
Bcl-xL↓,
BAX↑,
BAD↑,
Bak↑,
VEGF↓, decreasing the HeLa cell's vascular endothelial growth factor (VEGF) expression levels in HeLa cells.
Casp3↑, hyperoside promoted apoptosis via enhancing caspase-3 and caspase-8 protein expression, and on the other hand, by promoting tumor suppressor gene P35 expression
Casp8↑,
P53↑,
GSH↓, Hyperoside could also reduce glutathione levels in HeLa cells, superoxide dismutase (SOD), and Catalase (CAT) viability.
SOD↓,
Catalase↓,
TAC↓, reduced the antioxidant capacity and thus to inhibit cancer cell growth
XIAP↓, MCF-7 and 4 T1 cells Decreased the levels of Bcl-2 and XIAP; increased the levels of Bax and cleaved cysteine protease-3; decreased the production of ROS and inhibited NFκB signal pathway
ROS↓,
NF-kB↓,
TLR4↓, MDA-MB-231 cells Inhibited TLR4-NF-κB signaling pathways; decreased the expression of Bcl-2; enhanced the expression of pro-apoptotic Bax and the level of pro-inflammatory cytokine IL-6
P-gp/ABCB1↓, S180 cancer cell Reduced the expression of P-gp, LRP and Bcl-2 and increased the expression of Fas; inhibited bad phosphorylation and increased p27 level
LRP1↓,
Fas↑,
p27/CDKN1B↑,
*cardioP↑, Cardiovascular protection In vivo pulmonary embolism and arterial thrombosis model Prolonged the activated prothrombin time and suppressed thrombin and FXa activities; inhibit the production of PAI-1 induced by TNF-α
*AntiThr↑,
*PAI-1/SERPINE1↓,
*BUN↓, Reduced the contents of serum angiotensin converting enzyme ArgII, ALD, U-mAlb, BUN, SCR, ALT, and AST
*ALAT↓,
*AST↓,
*neuroP?, Neuroprotection


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

MTA1↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   Catalase↑, 1,   GSH↓, 2,   lipid-P↓, 1,   MDA↑, 2,   OSI↑, 1,   ROS↓, 1,   ROS↑, 2,   SOD↓, 1,   SOD↑, 1,   TAC↓, 4,   TOS↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 2,   Raf↓, 1,   XIAP↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Apoptosis↑, 2,   BAD↑, 1,   Bak↑, 1,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp3↑, 2,   Casp7↑, 1,   Casp8↑, 1,   Cyt‑c↑, 1,   Fas↑, 1,   MAPK↓, 1,   p27/CDKN1B↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

BRAF↑, 1,   mTOR↓, 1,   P70S6K↓, 1,   PI3K↓, 1,   PTEN↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

LRP1↓, 1,   MMP2↓, 1,   TIMP2↓, 1,   TumCI↓, 1,   TumCMig↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

VEGF↓, 1,   VEGF↑, 1,  

Barriers & Transport(tgid=15) ⓘ

P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   IL6↓, 1,   IL8↓, 1,   NF-kB↓, 2,   PD-L1↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BRAF↑, 1,   IL6↓, 1,   PD-L1↓, 1,  
Total Targets: 58

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiArt↑, 1,   antiD↓, 1,   Stroke↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   BUN↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

AntiThr↑, 1,  

Migration(tgid=13) ⓘ

PAI-1/SERPINE1↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   cardioP↑, 1,   hepatoP↑, 1,   neuroP?, 1,   RenoP↑, 1,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,   Bacteria↓, 1,   Sepsis↓, 1,  
Total Targets: 19

Scientific Paper Hit Count for: TAC, total antioxidant capacity
1 Silver-NanoParticles
1 Biochanin A
1 Boron
1 Hyperoside
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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