Catalase Cancer Research Results

Catalase, Catalase: Click to Expand ⟱
Source:
Type:
Caspases are a cysteine protease that speed up a chemical reaction via pointing their target substrates following an aspartic acid residue.1 They are grouped into apoptotic (caspase-2, 3, 6, 7, 8, 9 and 10) and inflammatory (caspase-1, 4, 5, 11 and 12) mediated caspases.
Caspase-1 may have both tumorigenic or antitumorigenic effects on cancer development and progression, but it depends on the type of inflammasome, methodology, and cancer.
Catalase is an enzyme found in nearly all living cells exposed to oxygen. Its primary role is to protect cells from oxidative damage by catalyzing the conversion of hydrogen peroxide (H₂O₂), a potentially damaging byproduct of metabolism, into water (H₂O) and oxygen (O₂). This detoxification process is crucial because excess H₂O₂ can lead to the formation of reactive oxygen species (ROS) that damage proteins, lipids, and DNA.

Catalase and Cancer
Oxidative Stress and Cancer:
Cancer cells often experience increased levels of oxidative stress due to rapid proliferation and metabolic changes. This stress can lead to DNA damage, promoting tumorigenesis.
Catalase helps mitigate oxidative stress, and its expression can influence the survival and proliferation of cancer cells.
Expression Levels in Different Cancers:
Overexpression: In some cancers, such as breast cancer and certain types of leukemia, catalase may be overexpressed. This overexpression can help cancer cells survive in oxidative environments, potentially leading to more aggressive tumor behavior.
Downregulation: Conversely, in other cancers, such as colorectal cancer, reduced catalase expression has been observed. This downregulation can lead to increased oxidative stress, contributing to tumor progression and metastasis.
Prognostic Implications:
Survival Rates: Studies have shown that high levels of catalase expression can be associated with poor prognosis in certain cancers, as it may enable cancer cells to resist apoptosis (programmed cell death) induced by oxidative stress.

Some types of cancer cells have been reported to exhibit lower catalase activity, possibly increasing their vulnerability to oxidative damage under certain conditions. This vulnerability has even been exploited in some therapeutic strategies (for example, approaches that generate excess H₂O₂ or other ROS specifically targeting cancer cells have been researched).
Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


Scientific Papers found: Click to Expand⟱
5680- BML,    Anticancer properties of bromelain: State-of-the-art and recent trends
- Review, Var, NA
*Inflam↓, *Bacteria↓, *Pain↓, *Diar↓, *Wound Healing↑, ERK↓, JNK↓, XIAP↓, HSP27↓, β-catenin/ZEB1↓, HO-1↓, lipid-P↓, ACSL4↑, ROS↑, SOD↑, Catalase↓, GSH↓, MDA↓, Casp3↓, Casp9↑, DNAdam↑, Apoptosis↑, NF-kB↓, P53↑, MAPK↓, APAF1↑, Cyt‑c↓, CD44↓, Imm↑, ATG5↑, LC3I↑, Beclin-1↑, IL2↓, IL4↓, IFN-γ↓, COX2↓, iNOS↓, ChemoSen↑, RadioS↑, Dose↝, other↓,
2652- CAP,    Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence
- Review, Var, NA
chemoPv↑, AntiCan↑, ROS↑, TumCG↓, ROS↑, MMP↑, Apoptosis↑, TumCCA↑, JNK↑, SOD↓, Catalase↓, GPx↓, other↓, SIRT1↓, NADPH↑, FOXO3↑,
2654- CUR,    Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence
- Review, Var, NA
ROS↑, Catalase↓, SOD1↓, GLO-I↓, NADPH↓, TumCCA↑, Apoptosis↑, Akt↓, ER Stress↑, JNK↑, STAT3↓, BioAv↑,
1656- FA,    Ferulic Acid: A Natural Phenol That Inhibits Neoplastic Events through Modulation of Oncogenic Signaling
- Review, Var, NA
tyrosinase↓, CK2↓, TumCP↓, TumCMig↓, FGF↓, FGFR1↓, PI3K↓, Akt↓, VEGF↓, FGFR1↓, FGFR2↓, PDGF↓, ALAT↓, AST↓, TumCCA↑, CDK2↓, CDK4↓, CDK6↓, BAX↓, Bcl-2↓, MMP2↓, MMP9↓, P53↑, PARP↑, PUMA↑, NOXA↑, Casp3↑, Casp9↑, TIMP1↑, lipid-P↑, mtDam↑, EMT↓, Vim↓, E-cadherin↓, p‑STAT3↓, COX2↓, CDC25↓, RadioS↑, ROS↑, DNAdam↑, γH2AX↑, PTEN↑, LC3II↓, Beclin-1↓, SOD↓, Catalase↓, GPx↓, Fas↑, *BioAv↓, cMyc↓, Beclin-1↑, LC3‑Ⅱ/LC3‑Ⅰ↓,
5115- JG,    Natural Products to Fight Cancer: A Focus on Juglans regia
- Review, Var, NA
Casp3↑, Casp9↑, MMP↓, AR↓, PSA↓, E-cadherin↑, N-cadherin↓, Vim↓, Akt↓, GSK‐3β↓, EMT↑, TumCI↓, MMP9↓, VEGF↓, MMP2↓, TumCCA↑, ROS↑, Apoptosis↑, GSH↓, Catalase↓, SOD↓, GPx↓, DNAdam↑, γH2AX↑, eff↑, BAX↑, Fas↑, Pin1↓,
2919- LT,    Luteolin as a potential therapeutic candidate for lung cancer: Emerging preclinical evidence
- Review, Var, NA
RadioS↑, ChemoSen↑, chemoP↑, *lipid-P↓, *Catalase↑, *SOD↑, *GPx↑, *GSTs↑, *GSH↑, *TNF-α↓, *IL1β↓, *Casp3↓, *IL10↑, NRF2↓, HO-1↓, NQO1↓, GSH↓, MET↓, p‑MET↓, p‑Akt↓, HGF/c-Met↓, NF-kB↓, Bcl-2↓, SOD2↓, Casp8↑, Casp3↑, PARP↑, MAPK↓, NLRP3↓, ASC↓, Casp1↓, IL6↓, IKKα↓, p‑p65↓, p‑p38↑, MMP2↓, ICAM-1↓, EGFR↑, p‑PI3K↓, E-cadherin↓, ZO-1↑, N-cadherin↓, CLDN1↓, β-catenin/ZEB1↓, Snail↓, Vim↑, ITGB1↓, FAK↓, p‑Src↓, Rac1↓, Cdc42↓, Rho↓, PCNA↓, Tyro3↓, AXL↓, CEA↓, NSE↓, SOD↓, Catalase↓, GPx↓, GSR↓, GSTs↓, GSH↓, VitE↓, VitC↓, CYP1A1↓, cFos↑, AR↓, AIF↑, p‑STAT6↓, p‑MDM2↓, NOTCH1↓, VEGF↓, H3↓, H4↓, HDAC↓, SIRT1↓, ROS↑, DR5↑, Cyt‑c↑, p‑JNK↑, PTEN↓, mTOR↓, CD34↓, FasL↑, Fas↑, XIAP↓, p‑eIF2α↑, CHOP↑, LC3II↑, PD-1↓, STAT3↓, IL2↑, EMT↓, cachexia↓, BioAv↑, *Half-Life↝, *eff↑,
2916- LT,    Antioxidative and Anticancer Potential of Luteolin: A Comprehensive Approach Against Wide Range of Human Malignancies
- Review, Var, NA - Review, AD, NA - Review, Park, NA
proCasp9↓, CDC2↓, CycB/CCNB1↓, Casp9↑, Casp3↑, Cyt‑c↑, cycA1/CCNA1↑, CDK2↓, APAF1↑, TumCCA↑, P53↑, BAX↑, VEGF↓, Bcl-2↓, Apoptosis↑, p‑Akt↓, p‑EGFR↓, p‑ERK↓, p‑STAT3↓, cardioP↑, Catalase↓, SOD↓, *BioAv↓, *antiOx↑, *ROS↓, *NO↓, *GSTs↑, *GSR↑, *SOD↑, *Catalase↑, *lipid-P↓, PI3K↓, Akt↓, CDK2↓, BNIP3↑, hTERT/TERT↓, DR5↑, Beclin-1↑, TNF-α↓, NF-kB↓, IL1↓, IL6↓, EMT↓, FAK↓, E-cadherin↑, MDM2↓, NOTCH↓, MAPK↑, Vim↓, N-cadherin↓, Snail↓, MMP2↓, Twist↓, MMP9↓, ROS↑, MMP↓, *AChE↓, *MMP↑, *Aβ↓, *neuroP↑, Trx1↑, ROS↓, *NRF2↑, NRF2↓, *BBB↑, ChemoSen↑, GutMicro↑,
4092- MF,    Mechanisms and therapeutic effectiveness of pulsed electromagnetic field therapy in oncology
- Review, Var, NA
Apoptosis↑, selectivity↑, ROS↑, Catalase↓, TumVol↓, angioG↓,
4643- OLE,  HT,    Use of Oleuropein and Hydroxytyrosol for Cancer Prevention and Treatment: Considerations about How Bioavailability and Metabolism Impact Their Adoption in Clinical Routine
- Review, Var, NA
TumCCA↑, Apoptosis↑, ER Stress↑, UPR↑, CHOP↑, ROS↑, Bcl-2↓, NOX4↑, Hif1a↓, MMP2↓, MMP↓, VEGF↓, Akt↓, NF-kB↓, p65↓, SIRT3↓, mTOR↓, Catalase↓, SOD2↓, FASN↓, STAT3↓, HDAC2↓, HDAC3↓, BAD↑, BAX↑, Bak↑, Casp3↑, Casp9↑, PARP↑, P53↑, P21↑, p27↑, Half-Life↝, BioAv↓, BioAv↓, selectivity↑, RadioS↑, *ROS↓, *GSH↑, *MDA↓, *SOD↑, *Catalase↑, *NRF2↑, *chemoP↑, *Inflam↓, PPARγ↑,

Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 9,   CYP1A1↓, 1,   GPx↓, 4,   GSH↓, 4,   GSR↓, 1,   GSTs↓, 1,   HO-1↓, 2,   lipid-P↓, 1,   lipid-P↑, 1,   MDA↓, 1,   NOX4↑, 1,   NQO1↓, 1,   NRF2↓, 2,   ROS↓, 1,   ROS↑, 10,   SIRT3↓, 1,   SOD↓, 5,   SOD↑, 1,   SOD1↓, 1,   SOD2↓, 2,   Trx1↑, 1,   VitC↓, 1,   VitE↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   CDC2↓, 1,   CDC25↓, 1,   FGFR1↓, 2,   MMP↓, 3,   MMP↑, 1,   mtDam↑, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

ACSL4↑, 1,   ALAT↓, 1,   cMyc↓, 1,   FASN↓, 1,   GLO-I↓, 1,   NADPH↓, 1,   NADPH↑, 1,   PPARγ↑, 1,   SIRT1↓, 2,  

Cell Death ⓘ

Akt↓, 5,   p‑Akt↓, 2,   APAF1↑, 2,   Apoptosis↑, 7,   BAD↑, 1,   Bak↑, 1,   BAX↓, 1,   BAX↑, 3,   Bcl-2↓, 4,   Casp1↓, 1,   Casp3↓, 1,   Casp3↑, 5,   Casp8↑, 1,   Casp9↑, 5,   proCasp9↓, 1,   CK2↓, 1,   Cyt‑c↓, 1,   Cyt‑c↑, 2,   DR5↑, 2,   Fas↑, 3,   FasL↑, 1,   HGF/c-Met↓, 1,   hTERT/TERT↓, 1,   iNOS↓, 1,   JNK↓, 1,   JNK↑, 2,   p‑JNK↑, 1,   MAPK↓, 2,   MAPK↑, 1,   MDM2↓, 1,   p‑MDM2↓, 1,   NOXA↑, 1,   p27↑, 1,   p‑p38↑, 1,   PUMA↑, 1,  

Transcription & Epigenetics ⓘ

H3↓, 1,   H4↓, 1,   other↓, 2,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,   p‑eIF2α↑, 1,   ER Stress↑, 2,   HSP27↓, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   Beclin-1↓, 1,   Beclin-1↑, 3,   BNIP3↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↓, 1,   LC3I↑, 1,   LC3II↓, 1,   LC3II↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 3,   P53↑, 4,   PARP↑, 3,   PCNA↓, 1,   γH2AX↑, 2,  

Cell Cycle & Senescence ⓘ

CDK2↓, 3,   CDK4↓, 1,   cycA1/CCNA1↑, 1,   CycB/CCNB1↓, 1,   P21↑, 1,   TumCCA↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

CD34↓, 1,   CD44↓, 1,   cFos↑, 1,   EMT↓, 3,   EMT↑, 1,   ERK↓, 1,   p‑ERK↓, 1,   FGF↓, 1,   FGFR2↓, 1,   FOXO3↑, 1,   GSK‐3β↓, 1,   HDAC↓, 1,   HDAC2↓, 1,   HDAC3↓, 1,   mTOR↓, 2,   NOTCH↓, 1,   NOTCH1↓, 1,   PI3K↓, 2,   p‑PI3K↓, 1,   PTEN↓, 1,   PTEN↑, 1,   p‑Src↓, 1,   STAT3↓, 3,   p‑STAT3↓, 2,   p‑STAT6↓, 1,   TumCG↓, 1,   tyrosinase↓, 1,  

Migration ⓘ

AXL↓, 1,   Cdc42↓, 1,   CEA↓, 1,   CLDN1↓, 1,   E-cadherin↓, 2,   E-cadherin↑, 2,   FAK↓, 2,   ITGB1↓, 1,   MET↓, 1,   p‑MET↓, 1,   MMP2↓, 5,   MMP9↓, 3,   N-cadherin↓, 3,   PDGF↓, 1,   Rac1↓, 1,   Rho↓, 1,   Snail↓, 2,   TIMP1↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   Twist↓, 1,   Tyro3↓, 1,   Vim↓, 3,   Vim↑, 1,   ZO-1↑, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↑, 1,   p‑EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 5,  

Immune & Inflammatory Signaling ⓘ

ASC↓, 1,   COX2↓, 2,   ICAM-1↓, 1,   IFN-γ↓, 1,   IKKα↓, 1,   IL1↓, 1,   IL2↓, 1,   IL2↑, 1,   IL4↓, 1,   IL6↓, 2,   Imm↑, 1,   NF-kB↓, 4,   p65↓, 1,   p‑p65↓, 1,   PD-1↓, 1,   PSA↓, 1,   TNF-α↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 2,   CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 2,   ChemoSen↑, 3,   Dose↝, 1,   eff↑, 1,   Half-Life↝, 1,   RadioS↑, 4,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AR↓, 2,   AST↓, 1,   CEA↓, 1,   EGFR↑, 1,   p‑EGFR↓, 1,   GutMicro↑, 1,   hTERT/TERT↓, 1,   IL6↓, 2,   NSE↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   cachexia↓, 1,   cardioP↑, 1,   chemoP↑, 1,   chemoPv↑, 1,   Pin1↓, 1,   TumVol↓, 1,  
Total Targets: 207

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 3,   GPx↑, 1,   GSH↑, 2,   GSR↑, 1,   GSTs↑, 2,   lipid-P↓, 2,   MDA↓, 1,   NRF2↑, 2,   ROS↓, 2,   SOD↑, 3,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,  

Cell Death ⓘ

Casp3↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL10↑, 1,   IL1β↓, 1,   Inflam↓, 2,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   eff↑, 1,   Half-Life↝, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   neuroP↑, 1,   Pain↓, 1,   Wound Healing↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,   Diar↓, 1,  
Total Targets: 30

Scientific Paper Hit Count for: Catalase, Catalase
2 Luteolin
1 Bromelain
1 Capsaicin
1 Curcumin
1 Ferulic acid
1 Juglone
1 Magnetic Fields
1 Oleuropein
1 HydroxyTyrosol
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:26  Cells:%  prod#:%  Target#:46  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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