Prx Cancer Research Results

Prx, Peroxiredoxin: Click to Expand ⟱
Source:
Type:
also known as Prx
Peroxiredoxins are endogenous antioxidants and redox sensors. Properties of the peroxiredoxins make them suitable as markers of oxidative stress.
Peroxiredoxins (Prxs) are a family of antioxidant enzymes that play a crucial role in cellular redox signaling and the detoxification of reactive oxygen species (ROS). They are involved in various cellular processes, including cell proliferation, differentiation, and apoptosis.
Prx isoforms (such as Prx1 and Prx4) are often overexpressed. This overexpression can help cancer cells cope with increased levels of reactive oxygen species (ROS) generated during rapid cell division and metabolic changes.
Elevated Prx levels have been linked to resistance against chemotherapy and radiation therapy. For example, Prx2 and Prx3 have been implicated in protecting cancer cells from oxidative damage caused by these treatments.
Some Prxs, such as Prx3, can act as tumor suppressors. Their downregulation or loss of function has been associated with increased tumorigenesis and poor prognosis in certain cancers.

PRDX family comprises several isoforms (for example, PRDX1, PRDX2, PRDX3, etc.) that function as antioxidant enzymes to reduce reactive oxygen species (ROS) and maintain redox balance.

PRDX family—especially key isoforms like PRDX1 and PRDX2—are often upregulated in various cancers, correlating with worse prognosis and enhanced tumor cell survival. Through their ROS-detoxifying capabilities, these proteins generally play protumorigenic roles by protecting malignant cells from oxidative stress and supporting resistance to apoptosis and therapy.


Scientific Papers found: Click to Expand⟱
5470- AF,    Exploring a Therapeutic Gold Mine: The Antifungal Potential of the Gold-Based Antirheumatic Drug Auranofin
- Review, Var, NA
TrxR↓, mechanism of action of auranofin was correlated with thioredoxin reductase inhibition,
other↝, but other modes of action such as interference with mitochondrial protein import and NADH kinase were also described and discussed
IL6↑, Conversely, auranofin stimulated IL-6 and IL-8 secretion in monocytes,
IL8↑,
NK cell⇅, NK activation was only observed at low doses of auranofin, while high doses inhibited NK activity
COX2↓, suppression of pro-inflammatory factors such as COX-2 (cyclooxygenase-2), NOS (nitric oxide synthase), NF-κB (nuclear factor-κB), and TrxR, as well as on the activation of peroxyredoxin-1 and Nrf2 (nuclear factor erythroid 2-related factor 2) [19].
NOS2↓,
NRF2↑,
Prx↑,
Half-Life↑, plasma half-lives of 15–25 days [24]
Dose↝, To avoid frequently occurring diarrhea, oral doses of 3–6 mg per day, or below, should also be considered when repurposing auranofin for the treatment of other human diseases.
ROS↑, Imbalances in this system lead to the accumulation of cytotoxic ROS.
NF-kB↓, Auranofin can bind to IKK, which ultimately leads to NF-κB inhibition

3160- Ash,    Withaferin A: A Pleiotropic Anticancer Agent from the Indian Medicinal Plant Withania somnifera (L.) Dunal
- Review, Var, NA
TumCCA↑, withaferin A suppressed cell proliferation in prostate, ovarian, breast, gastric, leukemic, and melanoma cancer cells and osteosarcomas by stimulating the inhibition of the cell cycle at several stages, including G0/G1 [86], G2, and M phase
H3↑, via the upregulation of phosphorylated Aurora B, H3, p21, and Wee-1, and the downregulation of A2, B1, and E2 cyclins, Cdc2 (Tyr15), phosphorylated Chk1, and Chk2 in DU-145 and PC-3 prostate cancer cells.
P21↑,
cycA1/CCNA1↓,
CycB/CCNB1↓,
cycE/CCNE↓,
CDC2↓,
CHK1↓,
Chk2↓,
p38↑, nitiated cell death in the leukemia cells by increasing the expression of p38 mitogen-activated protein kinases (MAPK)
MAPK↑,
E6↓, educed the expression of human papillomavirus E6/E7 oncogenes in cervical cancer cells
E7↓,
P53↑, restored the p53 pathway causing the apoptosis of cervical cancer cells.
Akt↓, oral dose of 3–5 mg/kg withaferin A attenuated the activation of Akt and stimulated Forkhead Box-O3a (FOXO3a)-mediated prostate apoptotic response-4 (Par-4) activation,
FOXO3↑,
ROS↑, the generation of reactive oxygen species, histone H2AX phosphorylation, and mitochondrial membrane depolarization, indicating that withaferin A can cause the oxidative stress-mediated killing of oral cancer cells [
γH2AX↑,
MMP↓,
mitResp↓, withaferin A inhibited the expansion of MCF-7 and MDA-MB-231 human breast cancer cells by ROS production, owing to mitochondrial respiration inhibition
eff↑, combination treatment of withaferin A and hyperthermia induced the death of HeLa cells via a decrease in the mitochondrial transmembrane potential and the downregulation of the antiapoptotic protein myeloid-cell leukemia 1 (MCL-1)
TumCD↑,
Mcl-1↓,
ER Stress↑, . Withaferin A also attenuated the development of glioblastoma multiforme (GBM), both in vitro and in vivo, by inducing endoplasmic reticulum stress via activating the transcription factor 4-ATF3-C/EBP homologous protein (ATF4-ATF3-CHOP)
ATF4↑,
ATF3↑,
CHOP↑,
NOTCH↓, modulating the Notch-1 signaling pathway and the downregulation of Akt/NF-κB/Bcl-2 . withaferin A inhibited the Notch signaling pathway
NF-kB↓,
Bcl-2↓,
STAT3↓, Withaferin A also constitutively inhibited interleukin-6-induced phosphorylation of STAT3,
CDK1↓, lowering the levels of cyclin-dependent Cdk1, Cdc25C, and Cdc25B proteins,
β-catenin/ZEB1↓, downregulation of p-Akt expression, β-catenin, N-cadherin and epithelial to the mesenchymal transition (EMT) markers
N-cadherin↓,
EMT↓,
Cyt‑c↑, depolarization and production of ROS, which led to the release of cytochrome c into the cytosol,
eff↑, combinatorial effect of withaferin A and sulforaphane was also observed in MDA-MB-231 and MCF-7 breast cancer cells, with a dramatic reduction of the expression of the antiapoptotic protein Bcl-2 and an increase in the pro-apoptotic Bax level, thus p
CDK4↓, downregulates the levels of cyclin D1, CDK4, and pRB, and upregulates the levels of E2F mRNA and tumor suppressor p21, independently of p53
p‑RB1↓,
PARP↑, upregulation of Bax and cytochrome c, downregulation of Bcl-2, and activation of PARP, caspase-3, and caspase-9 cleavage
cl‑Casp3↑,
cl‑Casp9↑,
NRF2↑, withaferin A binding with Keap1 causes an increase in the nuclear factor erythroid 2-related factor 2 (Nrf2) protein levels, which in turn, regulates the expression of antioxidant proteins that can protect the cells from oxidative stress.
ER-α36↓, Decreased ER-α
LDHA↓, inhibited growth, LDHA activity, and apoptotic induction
lipid-P↑, induction of oxidative stress, increased lipid peroxidation,
AP-1↓, anti-inflammatory qualities of withaferin A are specifically attributed to its inhibition of pro-inflammatory molecules, α-2 macroglobulin, NF-κB, activator protein 1 (AP-1), and cyclooxygenase-2 (COX-2) inhibition,
COX2↓,
RenoP↑, showing strong evidence of the renoprotective potential of withaferin A due to its anti-inflammatory activity
PDGFR-BB↓, attenuating the BB-(PDGF-BB) platelet growth factor
SIRT3↑, by increasing the sirtuin3 (SIRT3) expression
MMP2↓, withaferin A inhibits matrix metalloproteinase-2 (MMP-2) and MMP-9,
MMP9↓,
NADPH↑, but also provokes mRNA stimulation for a set of antioxidant genes, such as NADPH quinone dehydrogenase 1 (NQO1), glutathione-disulfide reductase (GSR), Nrf2, heme oxygenase 1 (HMOX1),
NQO1↑,
GSR↑,
HO-1↑,
*SOD2↑, cardiac ischemia-reperfusion injury model. Withaferin A triggered the upregulation of superoxide dismutase SOD2, SOD3, and peroxiredoxin 1(Prdx-1).
*Prx↑,
*Casp3?, and ameliorated cardiomyocyte caspase-3 activity
eff↑, combination with doxorubicin (DOX), is also responsible for the excessive generation of ROS
Snail↓, inhibition of EMT markers, such as Snail, Slug, β-catenin, and vimentin.
Slug↓,
Vim↓,
CSCs↓, highly effective in eliminating cancer stem cells (CSC) that expressed cell surface markers, such as CD24, CD34, CD44, CD117, and Oct4 while downregulating Notch1, Hes1, and Hey1 genes;
HEY1↓,
MMPs↓, downregulate the expression of MMPs and VEGF, as well as reduce vimentin, N-cadherin cytoskeleton proteins,
VEGF↓,
uPA↓, and protease u-PA involved in the cancer cell metastasis
*toxicity↓, A was orally administered to Wistar rats at a dose of 2000 mg/kg/day and had no adverse effects on the animals
CDK2↓, downregulated the activation of Bcl-2, CDK2, and cyclin D1
CDK4↓, Another study also demonstrated the inhibition of Hsp90 by withaferin A in a pancreatic cancer cell line through the degradation of Akt, cyclin-dependent kinase 4 Cdk4,
HSP90↓,

3163- Ash,  Rad,    Withaferin A, a steroidal lactone, selectively protects normal lymphocytes against ionizing radiation induced apoptosis and genotoxicity via activation of ERK/Nrf-2/HO-1 axis
*radioP↑, Withaferin A (WA) protected only normal lymphocytes, but not cancer cells, against IR-induced apoptosis
selectivity↑,
*Casp3↓, WA treatment led to significant inhibition of IR-induced caspase-3 activation and decreased IR-induced DNA damage to lymphocytes and bone-marrow cells.
*DNAdam↓,
*ROS↓, WA reduced intracellular ROS and GSH levels
*GSH↓,
*NRF2↑, WA induced pro-survival transcription factor, Nrf-2, and expression of cytoprotective genes HO-1, catalase, SOD, peroxiredoxin-2 via ERK.
*HO-1↑,
*Catalase↑,
*SOD↑,
*Prx↑,
*ERK↑, Activated ERK promotes the nuclear translocation and activity of Nrf2

3250- PBG,    Allergic Inflammation: Effect of Propolis and Its Flavonoids
- Review, NA, NA
*SOD↑, increase in antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, catalase, peroxiredoxin, and heme oxygenase-1
*GPx↑,
*Catalase↑,
*Prx↑,
*HO-1↑,
*Inflam↓, anti-inflammatory properties of propolis may be based on the following mechanisms:
*TNF-α↓, (1) suppression of the release of inflammatory cytokines, such as TNF-α and IL-1β;
*IL1β↓,
*IL4↑, (2) increase in production of anti-inflammatory cytokines such as IL-4 and IL-10;
*IL10↑,
*TLR4↓, (3) prevention of TLR4 activation;
*LOX1↓, (4) suppression of LOX, COX-1 and COX-2 gene expression
*COX1↓,
*COX2↓,
*NF-kB↓, (5) suppression of NF-κB and AP-1 activities;
*AP-1↓,
*ROS↓, CAPE treatment reduced ROS levels in the airway microenvironmen
*GSH↑, GSH level increased after CAPE treatment in an animal allergic asthma model
*TGF-β↓, significantly limiting secretion of eotaxin-1, TGF-β1, TNF-α, IL-4, IL-13, monocyte chemoattractant protein-1, IL-8, matrix metalloproteinase-9, and alpha-smooth muscle actin expression
*IL8↓,
*MMP9↓,
*α-SMA↓,
*MDA↓, (MDA) production and protein carbonyl (PC) levels significantly decreased

3026- RosA,    Modulatory Effect of Rosmarinic Acid on H2O2-Induced Adaptive Glycolytic Response in Dermal Fibroblasts
- in-vitro, Nor, NA
*ROS↓, H2O2 caused a significant ROS increase in the cells, and pre-treatment with rosmarinic acid (5–50 µM) decreased ROS significantly in the presence of glutathione
*ATP↑, The rosmarinic acid also recovered intracellular ATP and decreased NADPH production via the pentose phosphate pathway.
*NADPH↓,
*HK2↓, (HK-2), phosphofructokinase-2 (PFK-2), and lactate dehydrogenase A (LDHA), were downregulated in cells treated with rosmarinic acid
*PFK2↓,
*LDHA↓,
*GSR↑, GSR), glutathione peroxidase-1 (GPx-1), and peroxiredoxin-1 (Prx-1) and redox protein thioredoxin-1 (Trx-1) were upregulated in treated cells compared to control cells.
*GPx↑,
*Prx↑,
*Trx↑,
*antiOx↑, To sum up, the rosmarinic acid could be used as an antioxidant against H2O2-induced adaptive responses in fibroblasts by modulating glucose metabolism, glycolytic genes, and GSH production.
*GSH↑, The pre-treatment of rosmarinic acid could raise intracellular GSH to protect cells from ROS
*ROS↓, rosmarinic acid pre-treatment reduced the amount of ROS in the fibroblasts upon the addition of H2O2
*GlucoseCon↓, both compounds also decreased glucose consumption and lactate production
*lactateProd↓,
*Glycolysis↝, The results indicated that rosmarinic acid is able to shape cellular glucose utilization, glycolysis, and GSH.
*ATP↑, The rosmarinic acid also recovered intracellular ATP and decreased NADPH production via the pentose phosphate pathway.
*NADPH↓,
*PPP↓,

4725- Se,    Prx1_Pathway_with_Selenium_to_Enhance_the_Efficacy_and_Selectivity_of_Cancer_Therapy">Targeting the Nrf2-Prx1 Pathway with Selenium to Enhance the Efficacy and Selectivity of Cancer Therapy
- in-vitro, Lung, A549 - in-vitro, CRC, HT29
AntiCan↑, anti-cancer activity of selenium may in part be mediated by suppressing the Nrf2-Prx1 pathway of a tumor.
NRF2↓, Our study showed that seleni-um suppressed Nrf2 activation and reduced the up-regulation of prx1 in tumor tissues obtained from humanlung cancer A549 and colon cancer HT-29
Prx↓,
ChemoSen↑, how selenium modulation of the Nrf2-Prx1 pathway may enhance the efficacy and selectivity of cancer therapy in both pre-clinical and clinical settings.
*Prx↑, Conversely, increased expression of Prx1 and several other Nrf2 target genes was observed in some normal tissues in the tumor-bearing mice.
*NRF2↑,

3960- Taur,    Versatile Triad Alliance: Bile Acid, Taurine and Microbiota
- Review, AD, NA - Review, Stroke, NA
*ROS↓, prevention of oxidative stress, and inflammation.
*Inflam↓,
*GABA↑, It serves as an agonist of GABAA receptors and, through them, exerts its neuronal inhibitory, anxiolytic, and calming effect
*memory↑, Consequently, taurine promotes emotional learning ability, memory, and cognitive performance
*cognitive↑,
*iNOS↓, It reduces inducible nitric oxide synthase (iNOS), C-reactive protein (CRP),
*CRP↓,
*HO-1↑, In parallel, it increases the expressions of cytoprotective antioxidant proteins, such as heme oxygenase 1 (HO-1), peroxiredoxin (PRX), and thioredoxin (TRX), in macrophages [74].
*Prx↑,
*Trx↑,
*NRF2↑, inhibits reactive oxygen species by Kelch-like ECH-associated protein 1 (Keap-1)/nuclear factor erythroid-2-related factor (Nrf2)/heme oxygenase-1 (HO-1) pathway
*GSH↑, enhanced liver antioxidant capacities via glutathione (GSH), Trolox equivalent antioxidant capacity (TEAC), superoxide dismutase (SOD), and catalase (CAT), decreased lipid peroxidation and malondialdehyde (MDA) levels [
*SOD↑,
*Catalase↑,
*lipid-P↓,
*MDA↓,
*eff↝, Similar to free taurine [62,63,64], TUDCA has proven neuroprotective properties which were researched in the models of Alzheimer’s disease (AD)
*GutMicro↑, taurine has been associated with inhibited growth of harmful bacteria, including Proteobacteria and especially Helicobacter, and also increasing the production of SCFA in mouse feces [351] as well as the metabolism of taurine by microbiota
other↑, Similarly, taurine plays a protective role in acute ischemic stroke

2092- TQ,    Dissecting the Potential Roles of Nigella sativa and Its Constituent Thymoquinone on the Prevention and on the Progression of Alzheimer's Disease
- Review, AD, NA
*iNOS↓, PC12normal: downregulated the iNOS expression along with NO level; (5) had a protective role of intracellular oxidative stress, by restoring the ROS level
*ROS↓,
*GSH↑, SH-SY5Y(normal): increasing the GSH levels.
*neuroP↑, TQ was able to reduce the neurotoxicity induced by Aß in an in vitro model of undifferentiated pheochromocytoma rat cell line, PC-12,
*MMPs↓, reestablishment of the abnormal levels of Matrix metalloproteinases (MMPs) and ROS
*MMP↑, E18, through the inhibition of ROS formation, and mitochondrial membrane depolarization.
*TXNIP↓, TQ was able to downregulate ... Thioredoxin-interacting protein (Txnip) and to upregulate the expression of Peroxiredoxin 1 (Prdx 1)
*Prx↑,
*memory↑, Bargi et al. (2017), reported that TQ was able, yet at lower doses, to improve memory impairments induced by LPS in rats.
*MDA↓, decreased level of markers of oxidative damage in brain tissues such as NOS, malondialdehyde (MDA) as well as an increased activity of SOD and catalase in hippocampus and cortex
*SOD↑,
*Catalase↑,
*BioAv↑, nanoemulsion may enhance the oral bioavailability and brain delivery.


Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ATF3↑, 1,   GSR↑, 1,   HO-1↑, 1,   lipid-P↑, 1,   NQO1↑, 1,   NRF2↓, 1,   NRF2↑, 2,   Prx↓, 1,   Prx↑, 1,   ROS↑, 2,   SIRT3↑, 1,   TrxR↓, 1,  

Mitochondria & Bioenergetics ⓘ

CDC2↓, 1,   mitResp↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

LDHA↓, 1,   NADPH↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Bcl-2↓, 1,   cl‑Casp3↑, 1,   cl‑Casp9↑, 1,   Chk2↓, 1,   Cyt‑c↑, 1,   HEY1↓, 1,   MAPK↑, 1,   Mcl-1↓, 1,   p38↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

H3↑, 1,   other↑, 1,   other↝, 1,  

Protein Folding & ER Stress ⓘ

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

DNA Damage & Repair ⓘ

CHK1↓, 1,   P53↑, 1,   PARP↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   CDK4↓, 2,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 1,   cycE/CCNE↓, 1,   P21↑, 1,   p‑RB1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 1,   FOXO3↑, 1,   NOTCH↓, 1,   STAT3↓, 1,  

Migration ⓘ

AP-1↓, 1,   ER-α36↓, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   N-cadherin↓, 1,   Slug↓, 1,   Snail↓, 1,   uPA↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 1,   PDGFR-BB↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL6↑, 1,   IL8↑, 1,   NF-kB↓, 2,   NK cell⇅, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose↝, 1,   eff↑, 3,   Half-Life↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

E6↓, 1,   E7↓, 1,   IL6↑, 1,   NOS2↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   RenoP↑, 1,  
Total Targets: 82

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 4,   GPx↑, 2,   GSH↓, 1,   GSH↑, 4,   GSR↑, 1,   HO-1↑, 3,   lipid-P↓, 1,   MDA↓, 3,   NRF2↑, 3,   Prx↑, 7,   ROS↓, 6,   SOD↑, 4,   SOD2↑, 1,   Trx↑, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 2,   MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

GlucoseCon↓, 1,   Glycolysis↝, 1,   HK2↓, 1,   lactateProd↓, 1,   LDHA↓, 1,   NADPH↓, 2,   PFK2↓, 1,   PPP↓, 1,  

Cell Death ⓘ

Casp3?, 1,   Casp3↓, 1,   iNOS↓, 2,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,  

Migration ⓘ

AP-1↓, 1,   MMP9↓, 1,   MMPs↓, 1,   TGF-β↓, 1,   TXNIP↓, 1,   α-SMA↓, 1,  

Angiogenesis & Vasculature ⓘ

LOX1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 1,   CRP↓, 1,   IL10↑, 1,   IL1β↓, 1,   IL4↑, 1,   IL8↓, 1,   Inflam↓, 2,   NF-kB↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

GABA↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   eff↝, 1,  

Clinical Biomarkers ⓘ

CRP↓, 1,   GutMicro↑, 1,  

Functional Outcomes ⓘ

cognitive↑, 1,   memory↑, 2,   neuroP↑, 1,   radioP↑, 1,   toxicity↓, 1,  
Total Targets: 58

Scientific Paper Hit Count for: Prx, Peroxiredoxin
2 Ashwagandha(Withaferin A)
1 Auranofin
1 Radiotherapy/Radiation
1 Propolis -bee glue
1 Rosmarinic acid
1 Selenium
1 Taurine
1 Thymoquinone
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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