PrxII Cancer Research Results

PrxII, Peroxiredoxin II: Click to Expand ⟱
Source:
Type:
Prx II is a peroxidase that reduces hydrogen peroxide and organic hydroperoxides. Higher levels of Prx II in cancer cells enhance their ability to detoxify reactive oxygen species (ROS).
• This protection against oxidative damage enables tumor cells to survive in a stressful microenvironment characterized by high metabolic activity and inflammation.
Prx II is often upregulated in several types of cancers. For example, increased expression of Prx II has been reported in breast, lung, colorectal, and gastric cancers, among others. This upregulation is generally viewed as an adaptive response of cancer cells to the increased oxidative stress associated with rapid proliferation and a hostile tumor microenvironment.
- Higher Prx II expression has been associated with unfavorable clinical outcomes.

• Many cancer therapies, including chemotherapy and radiation therapy, rely on the generation of ROS to induce cancer cell death. Elevated levels of Prx II can reduce the efficacy of these treatments by neutralizing ROS, thereby contributing to resistance.
Scientific Papers found: Click to Expand⟱
5948- Cela,    Recent Trends in anti-tumor mechanisms and molecular targets of celastrol
TumCP↓, mechanism of action of celastrol in terms of inhibition of cell proliferation and regulation of the cell cycle, regulation of apoptosis and autophagy, inhibition of cell invasion and metastasis, anti-inflammation, regulation of immunotherapy, and an
TumCCA↑,
Apoptosis↑,
TumAuto↑,
TumCI↓,
TumMeta↓,
Imm↝,
angioG↓,
Cyt‑c↑, release of cytochrome c (CytC)
ROS↑, increasing ROS levels, and activating the mitochondrial apoptosis pathway
BAX↑, upregulating the expression of CytC and the pro-apoptotic protein Bax, activating caspase-3 and caspase-9, and leading to the cleavage of PARP
Casp3↑,
Casp9↑,
cl‑PARP↑,
PrxII↓, binds to peroxiredoxin-2 (Prdx2) and inhibits its enzyme activity,
ER Stress↑, resulting in ROS-dependent endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and apoptosis in gastric cancer cells
mtDam↑,
CHOP↑, celastrol upregulates the expression of CHOP, Bip, XBP1s, and IRE1 proteins,
Inflam↓, Anti-inflammatory properties of celastrol
NF-kB↓, Celastrol additionally obstructed NF-κB and its downstream gene products, such as CXCR4 and MMP9, and reduced serum IL-6 and TNF-α levels to inhibit cell invasion and migration in vivo
CXCR4↓,
MMP9↓,
IL6↓,
TNF-α↓,
HSP90↓, accumulation may be due to the inhibition of HSP90 and the stress response
neuroP↑, Our mass spectrometry research also showed that celastrol directly binds to HSP90 and HSP70, exerting antitumor and neuroprotective effects
STAT3↓, Celastrol exerts anti-tumor activity by inhibiting STAT3
Prx↓, celastrol binds directly to Prdx1, Prdx2, Prdx4, and Prdx6 via active cysteine sites, inhibiting their antioxidant activity without affecting protein expression
HO-1↑, Celastrol also targeted heme oxygenase-1 (HO-1), increasing its expression in activated hematopoietic stem cells
eff↑, Research has indicated that celastrol, combined with 17-N-Allylamino-17-demethoxygeldanamycin (17-AAG), inhibits the toxic stress response of HSP90-targeted proteins, reduces the sensitization of human glioblastomas to celastrol treatment, an
eff↑, celastrol, when combined with EGFR tyrosine kinase inhibitors (EGFR-TKIs), effectively inhibits the growth and invasion of T790M mutant human lung cancer H1975
BioAv↑, nano-delivery systems present a novel pathway for the development and clinical application of celastrol, potentially overcoming existing limitations and maximizing its therapeutic potential.
toxicity↑, several significant challenges, including its pronounced hepatic and renal toxicity and potential for causing immunosuppression
CardioT↑, celastrol, which includes hepatotoxicity, cardiotoxicity, infertility toxicity, hematopoietic system toxicity and nephrotoxicity.
hepatoP↓,

1942- PL,    Piperlongumine inhibits antioxidant enzymes, increases ROS levels, induces DNA damage and G2/M cell cycle arrest in breast cell lines
- in-vitro, BC, MCF-7
ROS↑, PLN increased ROS levels and expression of the SOD1 antioxidant enzyme
SOD1↑,
Trx1↓, PLN inhibited the expression of the antioxidant enzymes catalase, TRx1, and PRx2.
Catalase↓,
PrxII↓,
ROS↑, ability of PLN to inhibit antioxidant enzyme expression was associated with the oxidative stress response
GADD45A↑, upregulated the levels of GADD45A mRNA and p21 protein.
P21↑,
DNAdam↑, In response to elevated ROS levels and DNA damage induction, the cells were arrested at the G2/M phase
TumCCA↑, arrested at the G2/M phase


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 ⓘ

Catalase↓, 1,   HO-1↑, 1,   Prx↓, 1,   PrxII↓, 2,   ROS↑, 3,   SOD1↑, 1,   Trx1↓, 1,  

Mitochondria & Bioenergetics ⓘ

mtDam↑, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 1,   HSP90↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   GADD45A↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

STAT3↓, 1,  

Migration ⓘ

MMP9↓, 1,   TumCI↓, 1,   TumCP↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Immune & Inflammatory Signaling ⓘ

CXCR4↓, 1,   IL6↓, 1,   Imm↝, 1,   Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   eff↑, 2,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

CardioT↑, 1,   hepatoP↓, 1,   neuroP↑, 1,   toxicity↑, 1,  
Total Targets: 41

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PrxII, Peroxiredoxin II
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#:1085  State#:%  Dir#:1
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