γH2AX Cancer Research Results

γH2AX, gamma-H2AX: Click to Expand ⟱
Source:
Type:
γH2AX (gamma-H2AX) is a histone protein that plays a crucial role in the repair of DNA double-strand breaks (DSBs). It is a phosphorylated form of the H2AX protein, which is a component of chromatin.

γH2AX is often used as a biomarker for DNA damage and genomic instability. When DNA is damaged, the H2AX protein is phosphorylated, forming γH2AX, which recruits and activates DNA repair proteins to the site of damage.
γ-H2AX, a marker for DNA double-strand breaks.

Cancer cells often exhibit increased levels of γH2AX due to their high rate of DNA replication and repair errors.

Gamma-H2AX, on the other hand, refers to a phosphorylated form of H2AX.
Scientific Papers found: Click to Expand⟱
2907- LT,    Protective effect of luteolin against oxidative stress‑mediated cell injury via enhancing antioxidant systems
- in-vitro, Nor, NA
*ROS↓, Intracellular ROS levels and damage to cellular components such as lipids and DNA in H2O2-treated cells were significantly decreased by luteolin pretreatment.
*Casp9↓, Luteolin suppressed active caspase-9 and caspase-3 levels while increasing Bcl-2 expression and decreasing Bax protein levels.
*Casp3↓,
*Bcl-2↑,
*BAX↓,
*GSH↑, luteolin restored levels of glutathione that was reduced in response to H2O2.
*SOD↑, luteolin enhanced the activity and protein expressions of superoxide dismutase, catalase, glutathione peroxidase, and heme oxygenase-1.
*Catalase↑,
*GPx↑,
*HO-1↑,
*antiOx↑, upregulating antioxidant enzymes.
*lipid-P↓, protective effect of luteolin against lipid peroxidation
*p‑γH2AX↓, showed that luteolin pretreatment diminished expression levels of phospho-H2A.X in H2O2-exposed cells
eff↑, promising therapeutic agent for management and treatment of conditions such as COPD and pulmonary fibrosis.

3277- Lyco,    Recent trends and advances in the epidemiology, synergism, and delivery system of lycopene as an anti-cancer agent
- Review, Var, NA
antiOx↑, lycopene provides a strong antioxidant activity that is 100 times more effective than α-tocopherol and more than double effective that of β-carotene
TumCP↓, In vivo and in vitro experiments have demonstrated that lycopene at near physiological levels (0.5−2 μM) could inhibit cancer cell proliferation [[22], [23], [24]], induce apoptosis [[25], [26], [27]], and suppress metastasis [
Apoptosis↑,
TumMeta↑,
ChemoSen↑, lycopene can increase the effect of anti-cancer drugs (including adriamycin, cisplatin, docetaxel and paclitaxel) on cancer cell growth and reduce tumour size
BioAv↓, low water solubility and bioavailability of lycopene
Dose↝, The concentration of lycopene in plasma (daily intake of 10 mg lycopene) is approximately 0.52−0.6 μM
BioAv↓, significant decrease in lycopene bioavailability in the elderly
BioAv↑, oils and fats favours the bioavailability of lycopene [80], while large molecules such as pectin can hinder the absorption of lycopene in the small intestine due to their action on lipids and bile salt molecules
SOD↑, GC: 50−150 mg/kg BW/day ↑SOD, CAT, GPx ↑IL-2, IL-4, IL-10, TNF-α ↑IgA, IgG, IgM ↓IL-6
Catalase↑,
GPx↑,
IL2↑, lycopene treatment significantly enhanced blood IL-2, IL-4, IL-10, TNF-α levels and reduced IL-6 level in a dose-dependent manner.
IL4↑,
IL1↑,
TNF-α↑,
GSH↑, GC: ↑GSH, GPx, GST, GR
GPx↑,
GSTA1↑,
GSR↑,
PPARγ↑, ↑GPx, SOD, MDA ↑PPARγ, caspase-3 ↓NF-κB, COX-2
Casp3↑,
NF-kB↓,
COX2↓,
Bcl-2↑, AGS cells Lycopene 5 μM ↑Bcl-2 ↓Bax, Bax/Bcl-2, p53 ↓Chk1, Chk2, γ-H2AX, DNA damage ↓ROS Phase arrest
BAX↓,
P53↓,
CHK1↓,
Chk2↓,
γH2AX↓,
DNAdam↓,
ROS↓,
P21↑, CRC: ↑p21 ↓PCNA, β-catenin ↓COX-2, PGE2, ERK1/2 phosphorylated
PCNA↓,
β-catenin/ZEB1↓,
PGE2↓,
ERK↓,
cMyc↓, AGS cells: ↓Wnt-1, c-Myc, cyclin E ↓Jak1/Stat3, Wnt/β-catenin alteration ↓ROS
cycE/CCNE↓,
JAK1↓,
STAT3↓,
SIRT1↑, Huh7: ↑SIRT1 ↓Cells growth ↑PARP cleavage ↓Cyclin D1, TNFα, IL-6, NF-κB, p65, STAT3, Akt activation ↓Tumour multiplicity, volume
cl‑PARP↑,
cycD1/CCND1↓,
TNF-α↓,
IL6↓,
p65↓,
MMP2↓, SK-Hep1 human hepatoma cells Lycopene 5, 10 μM ↓MMP-2, MMP-9 ↓
MMP9↓,
Wnt↓, AGS cells Lycopene 0.5 μM, 1 μM ↓Wnt-1, c-Myc, cyclin E ↓Jak1/Stat3, Wnt/β-catenin alteration ↓ROS


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 2,   GSH↑, 1,   GSR↑, 1,   GSTA1↑, 1,   ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   PPARγ↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   BAX↓, 1,   Bcl-2↑, 1,   Casp3↑, 1,   Chk2↓, 1,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   DNAdam↓, 1,   P53↓, 1,   cl‑PARP↑, 1,   PCNA↓, 1,   γH2AX↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   STAT3↓, 1,   Wnt↓, 1,  

Migration ⓘ

MMP2↓, 1,   MMP9↓, 1,   TumCP↓, 1,   TumMeta↑, 1,   β-catenin/ZEB1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL1↑, 1,   IL2↑, 1,   IL4↑, 1,   IL6↓, 1,   JAK1↓, 1,   NF-kB↓, 1,   p65↓, 1,   PGE2↓, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 1,   ChemoSen↑, 1,   Dose↝, 1,   eff↑, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  
Total Targets: 50

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   ROS↓, 1,   SOD↑, 1,  

Cell Death ⓘ

BAX↓, 1,   Bcl-2↑, 1,   Casp3↓, 1,   Casp9↓, 1,  

DNA Damage & Repair ⓘ

p‑γH2AX↓, 1,  
Total Targets: 13

Scientific Paper Hit Count for: γH2AX, gamma-H2AX
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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