Hydrogen Gas / EZH2 Cancer Research Results

H2, Hydrogen Gas: Click to Expand ⟱
Features:
Hydrogen Gas, Powerful Antioxidant
Mechanistically, H₂ is most defensibly framed as a selective antioxidant + anti-inflammatory signaling modulator (often via Nrf2↑ and NF-κB↓ / NLRP3↓), with strongest clinical relevance in oncology being reduction of treatment toxicities (radiation/CCRT side-effects), with mixed/early evidence for direct anticancer effects.

1.Antioxidant and Nrf2/ARE Pathway: activate Nrf2, which induces antioxidant enzymes.
2.NF-κB Pathway: reported to inhibit NF-κB activation, thereby reducing inflammatory cytokine production
3.Mitochondrial Apoptosis Pathway
4.MAPK (Mitogen-Activated Protein Kinases) Pathway
5.PI3K/Akt/mTOR Pathway
6.Inflammatory Cytokine Signaling: Reducing cytokines (such as IL-6, TNF-α)
7.p53 Pathway
8.Autophagy Pathways: might regulate autophagy, (dual roles in cancer)

Example unit sometimes used in studies
Example Canadian Supplier

Hydrogen gas can be generated in small amount by hydrogenase of certain members of the human gastrointestinal tract microbiota from unabsorbed carbohydrates in the intestine through degradation and metabolism, which then is partially diffused into blood flow and released and detected in exhaled breath, indicating its potential to serve as a biomarker.

Many studies have shown that H2 therapy can reduce oxidative stress. This, however, contradicts radiation therapy and chemotherapy, in which ROS are required to induce apoptosis and combat cancer. Yet many studies show chemoprotective and radioprotective and some even show chemosentizing
Nevertheless there are some papers claiming ROS ↑ for cancer cells

Hydrogen Gas in Water is also used.
- the amount of H2 dissolved in solutions is limited: up to 0.8 mM (1.6 mg/L) H2 can be dissolved in water under atmospheric pressure at room temperature


Hydrogen Gas — molecular hydrogen (H₂) is a small, neutral diatomic gas investigated as a therapeutic medical gas and redox-signaling modulator. It rapidly diffuses across biological membranes and can be administered by inhalation or indirectly as hydrogen-rich water (HRW), hydrogen-rich saline, or hydrogen-releasing materials. H₂ is best classified as an experimental therapeutic gas rather than a conventional antioxidant drug. Standard abbreviations are H₂ for molecular hydrogen and HRW for hydrogen-rich water. Endogenous H₂ is also produced by intestinal microbial fermentation. Its biological effects appear to involve modulation of oxidative stress, inflammation, mitochondrial function, cell-death signaling, and immune metabolism rather than indiscriminate ROS scavenging alone.

Primary mechanisms (ranked):

  1. Redox modulation and selective suppression of highly damaging oxidative/nitrosative stress, with secondary NRF2-dependent antioxidant adaptation.
  2. Suppression of inflammatory signaling, particularly NF-κB and associated cytokine pathways.
  3. Mitochondrial and metabolic modulation, including preservation or remodeling of mitochondrial bioenergetics and PGC-1α-linked signaling.
  4. Immune modulation, including reported restoration of metabolically exhausted CD8+ T-cell function in cancer.
  5. Context-dependent regulation of tumor-cell ROS, apoptosis, pyroptosis, differentiation, proliferation, and PI3K/Akt/mTOR signaling.
  6. Protection of normal tissues from chemotherapy- and radiotherapy-associated oxidative and inflammatory injury.

Bioavailability / PK relevance: H₂ has unusually rapid tissue diffusion because of its very small, nonpolar structure, but tissue exposure is transient because hydrogen is rapidly redistributed and exhaled. Inhalation provides continuing systemic exposure during administration, whereas HRW delivers a comparatively small finite H₂ dose that falls rapidly after preparation and ingestion. At approximately atmospheric pressure and room temperature, water saturation is only about 1.6 mg/L H₂, approximately 0.8 mmol/L. Biological efficacy therefore depends strongly on route, concentration, treatment duration, and proximity of H₂ generation to the target tissue.

In-vitro vs systemic exposure relevance: H₂ does not behave like a conventional concentration-maintained small-molecule drug. Gas-equilibrated cell culture can provide sustained H₂ exposure that is difficult to reproduce with a single oral dose of HRW. Conversely, inhalation can continuously replenish dissolved H₂ during treatment. Results from prolonged gas-equilibrated cultures, high-pressure systems, or locally generated H₂ nanomaterials should therefore not automatically be extrapolated to ordinary hydrogen-water exposure.

Clinical evidence status: Small human studies and randomized adjunctive trials exist, but H₂ is not an established anticancer therapy. The most credible oncology application currently is supportive treatment during chemotherapy or radiotherapy. A 2025 randomized study in cervical-cancer patients receiving concurrent chemoradiotherapy reported reduced acute radiation enteritis and inflammatory responses with adjunctive H₂/O₂ inhalation without an apparent reduction in tumor-control efficacy. Direct antitumor evidence remains predominantly preclinical, observational, or derived from small uncontrolled cancer cohorts. Trials of HRW during glioma radiochemotherapy and other indications remain exploratory. H₂ should therefore be classified as experimental adjunct/supportive therapy rather than standalone cancer treatment.

Hydrogen Gas Cancer-Relevant Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Redox and reactive oxygen species regulation ROS ↑ or ↓ (model-dependent) Excess ROS ↓; oxidative damage ↓ P, R Redox modulation H₂ should not be treated as a simple universal ROS scavenger. Normal-tissue studies predominantly show reduced oxidative injury, whereas some tumor models paradoxically show ROS ↑ and ROS-dependent tumor cell death.
2 NRF2 antioxidant stress response NRF2 ↔ or ↑ (context-dependent) NRF2 ↑; HO-1 ↑; SOD ↑; GSH-associated defenses ↑ R, G Adaptive antioxidant signaling NRF2 activation is mechanistically important mainly for cytoprotection and stress adaptation rather than as a consistent direct anticancer mechanism.
3 NF-κB inflammatory signaling NF-κB ↓ (context-dependent) NF-κB ↓; inflammatory injury ↓ R, G Anti-inflammatory signaling Frequently accompanied by IL-6 ↓, TNF-α ↓ and IL-1β ↓. This pathway is particularly relevant to normal-tissue protection during inflammatory injury and cancer therapy.
4 Mitochondrial bioenergetics and PGC-1α Mitochondrial function ↑ in exhausted immune cells; tumor response model-dependent Mitochondrial damage ↓; ATP homeostasis ↑ R, G Bioenergetic remodeling H₂ can improve mitochondrial resilience. In cancer, an important proposed mechanism is metabolic restoration of exhausted antitumor lymphocytes rather than direct mitochondrial poisoning of tumor cells.
5 CD8 T-cell exhaustion and antitumor immunity Indirect tumor suppression ↑ CD8+ T-cell metabolic fitness ↑ G Immune restoration Clinical observations in colorectal and lung cancer suggest restoration of exhausted CD8+ T-cell function, including mitochondrial and CoQ10-associated effects. Evidence remains preliminary.
6 PI3K Akt mTOR proliferative signaling PI3K ↓; p-Akt ↓; mTOR signaling ↓ (model-dependent) ↔ or context-dependent G Growth suppression Reported particularly in experimental colorectal-cancer models. This is not yet established as a reproducible systemic mechanism in patients.
7 NLRP3 caspase-1 GSDMD pyroptosis ROS ↑; NLRP3 ↑; caspase-1 ↑; GSDMD-mediated pyroptosis ↑ (model-dependent) NLRP3 commonly ↓ during inflammatory injury R, G Context-dependent inflammatory cell death An important example of opposite modulation by biological context. H₂ induced ROS-dependent NLRP3-mediated pyroptosis in an endometrial-cancer model, whereas normal-tissue inflammatory models commonly show NLRP3 suppression.
8 Tumor proliferation and differentiation Proliferation ↓; differentiation ↑ (model-dependent) Generally ↔ G Tumor phenotype modulation Glioblastoma models report differentiation of glioma stem-like cells and reduced tumor growth. Generalization to other cancers is uncertain.
9 Angiogenesis and hypoxic signaling HIF-1α ↓; VEGF ↓ (model-dependent) VEGF responses mixed G Angiogenic suppression Preclinical evidence suggests inhibition in selected tumor models but does not establish a general antiangiogenic clinical effect.
10 Glycolytic metabolism HK2 ↓; PFK ↓; glycolysis ↓; lactate production ↓ (model-dependent) ↔ or context-dependent G Metabolic growth restriction Reported in selected experimental cancer systems and should remain secondary until replicated across models.
11 Chemosensitization Therapeutic response ↑ in selected models Chemotherapy-associated organ injury ↓ G Adjunctive treatment modulation H₂ has produced both chemoprotective normal-tissue effects and occasional tumor chemosensitization. Protection of normal tissues should not be interpreted as established protection of tumors.
12 Radiotherapy tissue protection Tumor control apparently ↔ in limited human data Radiation-associated oxidative and inflammatory injury ↓ R, G Supportive radioprotection A randomized cervical-cancer study reported reduced acute radiation enteritis during chemoradiotherapy without evidence of compromised short-term antitumor efficacy. Larger confirmation is required.
13 Clinical Translation Constraint Direct anticancer efficacy unproven Generally well tolerated in studied protocols G Exposure and evidence limitation H₂ exposure varies substantially with inhaled concentration, flow, duration, HRW concentration, storage, and delivery technology. Gas mixtures containing high H₂ concentrations require engineered control because hydrogen is flammable and explosive in air. No standardized oncology dose or approved anticancer indication exists.

P: 0–30 min     R: 30 min–3 hr     G: >3 hr



Hydrogen Gas and Alzheimer’s disease: Molecular hydrogen has substantial preclinical neuroprotective evidence and limited early human evidence in Alzheimer’s disease and mild cognitive impairment. Proposed mechanisms include oxidative-stress suppression, neuroinflammation reduction, mitochondrial protection, BDNF-related signaling, and reductions in Aβ/BACE-associated pathology and tau phosphorylation. H₂ readily diffuses into the CNS, making delivery biologically plausible, but clinical evidence remains insufficient to classify it as a disease-modifying AD treatment.

Clinical evidence status: Preclinical evidence is extensive relative to the small clinical literature. Human studies include an open-label inhalation pilot in AD, a single-arm biomarker study, and a randomized hydrogen-rich-water study in mild cognitive impairment. Reported cognitive or biomarker improvements are hypothesis-generating; adequately powered randomized trials with validated AD endpoints are still needed.

Hydrogen Gas Alzheimer-Relevant Mechanisms

Rank Pathway / Axis Modulation TSF Primary Effect Notes / Interpretation
1 Oxidative and mitochondrial stress ROS ↓; lipid oxidation ↓; mitochondrial damage ↓ P, R Neuroprotection One of the most consistently reproduced effects in experimental neurodegeneration models.
2 Neuroinflammatory signaling NF-κB ↓; IL-1β ↓; IL-6 ↓; TNF-α ↓ R, G Neuroinflammation suppression Likely interconnected with redox and glial responses.
3 NRF2 antioxidant response NRF2 ↑; HO-1 ↑; endogenous antioxidant defenses ↑ R, G Cellular stress resistance Secondary adaptive mechanism rather than simple chemical radical scavenging.
4 Amyloid beta and BACE signaling Aβ ↓; BACE-associated processing ↓ (model-dependent) G Amyloid pathology reduction Demonstrated mainly in experimental models; human disease-modifying evidence is not established.
5 Tau phosphorylation p-tau ↓ (model-dependent) G Tau pathology attenuation Supported primarily by animal and experimental hydrogen-delivery studies.
6 BDNF and neuronal plasticity BDNF ↑; neuronal plasticity ↑ G Cognitive and synaptic support Reported across several neurologic injury models and investigated as a biomarker in human inhalation studies.
7 NLRP3 inflammasome NLRP3 ↓ R, G Microglial inflammatory suppression Potential connection between oxidative stress, innate immune activation, and neurodegeneration.
8 Cognition and memory Memory ↑; cognitive performance ↑ (model-dependent) G Functional outcome Robust in several animal paradigms but human trials remain small and heterogeneous.
9 Clinical Translation Constraint Evidence insufficient for established AD treatment G Clinical evidence limitation Existing human studies are small, often uncontrolled, or use surrogate endpoints. Optimal concentration, inhalation duration, treatment schedule, and long-term efficacy remain unresolved.

P: 0–30 min     R: 30 min–3 hr     G: >3 hr
EZH2, enhancer of zeste homolog 2 (Drosophila): Click to Expand ⟱
Source: CGL-Driver Genes
Type: Oncogene
EZH2 (Enhancer of Zeste Homolog 2) is a gene that encodes a protein which is a key component of the Polycomb Repressive Complex 2 (PRC2). This complex is involved in the regulation of gene expression through histone methylation, specifically the trimethylation of histone H3 at lysine 27 (H3K27me3), which leads to transcriptional repression of target genes.
EZH2 is often overexpressed in various types of cancers, including breast, prostate, and lymphoma. This overexpression can lead to the silencing of tumor suppressor genes, contributing to uncontrolled cell proliferation and survival.
EZH2 is biology-first; its biomarker value is a readout of epigenetic state.


Scientific Papers found: Click to Expand⟱
7482- H2,    Molecular Hydrogen Therapy: Mechanisms, Delivery Methods, Preventive, and Therapeutic Application
- Review, Var, NA - Review, IBD, NA - Review, Stroke, NA - Review, Sepsis, NA - Review, AD, NA
Dose↝, H2 can be administered exogenously and is also produced endogenously within the intestinal tract.
*Inflam↓, Anti‐Inflammatory Effect
*IL1β↓, diabetes combined with stroke, H₂ intervention downregulates the expression levels of proinflammatory factors (IL‐1β, IL‐6, TNF‐α), while activating the TLR4/NF‐κB signaling pathway to achieve neuroprotective effects
*IL6↓,
*TNF-α↓,
*neuroP↑,
*mTOR↓, sepsis model, H₂ regulates macrophage polarization (inhibiting the M1 phenotype/promoting the M2 phenotype) and inhibits (mTOR) phosphorylation, reducing the release of inflammatory mediators such as IL‐6, TNF‐α, and HMG
*IL10↑, while increasing the levels of anti‐inflammatory factors IL‐10 and Transforming Growth Factor‐beta (TGF‐β)
*TGF-β↑,
*Sepsis↓,
*NRF2↑, whereas Nrf2 induction suppresses these pathways via redox homeostasis modulation
*antiOx↑, figure 1
*Catalase↑,
*SOD↑,
*GPx↑,
*ROS↓, H₂ mediates ROS regulation through Nrf2, inhibiting NF‐κB/NLRP3 inflammasome activation and achieving an antioxidant–anti‐inflammatory synergistic effect
*HO-1↑, H2 can increase the expression of heme oxygenase‐1 (HO‐1) or activate the phosphatidylinositol‐3‐kinase (PI3K)–Akt signaling pathway to improve liver I/R injury
*PI3K↑,
*Akt↑,
*hepatoP↑,
*MPO↓, reduce myeloperoxidase (MPO) activity and IL‐1β/TNF‐α levels to alleviate myocardial injury
*cardioP↑,
CDK4↓, Studies have demonstrated that H2 inhibits CDK4 and CDK6 to restrict lung cancer progression
CDK6↑,
CD47↓, H₂ can reverse immune escape in lung cancer cells by inhibiting the expression of CD47 and activating the apoptosis program
PI3K↓, H2 promotes apoptosis by downregulating Akt phosphorylation and inhibiting the PI3K signaling pathway in non‐small cell lung cancer.
Akt↓,
Hif1a↓, inhalation of H2 suppresses Hypoxia‐Inducible Factor 1 Alpha Subunit (HIF‐1α)/NF‐κB signaling pathway activation and promotes apoptosis in HeLa cells
selectivity↑, This bidirectional regulatory capability allows H₂ to protect normal tissues from excessive apoptosis (such as inflammation‐induced cell death) while selectively inducing apoptosis in tumor cells.
*MMP↑, howed that after treating septic rats with HRS, the decline in mitochondrial membrane potential (MMP) and ATP content was improved.
*ATP↑,
*ER Stress↓, H₂ alleviated inflammation and organ damage by inhibiting ER stress and activating the autophagy pathway in septic mice
*CHOP/DDIT3↓, H2 could downregulate the expression of CHOP, caspase‐12, and GRP78, while inhibiting p38 and c‐Jun N‐terminal kinase (JNK) phosphorylation, and upregulating the LC3‐II/I ratio
*Casp12↓,
*GRP78/BiP↓,
*p38↓,
*p‑JNK↓,
*LC3‑Ⅱ/LC3‑Ⅰ↑,
*p‑eIF2α↓, HRW prevents IBD in mice by reducing levels of p‐eIF2α, ATF4, XBP1, and CHOP, key proteins in ER stress.
*ATF4↓,
*XBP-1↓,
*Imm↑, H₂ exhibit multidimensional characteristics, primarily enhancing immunity by protecting immune organs,
*IFN-γ↓, H2 treatment inhibited several T‐cell effector molecules, such as IFN‐γ, IL‐4, and GZMB
*IL4↓,
*GranB/GZMB↓,
NK cell↑, After inhaling H₂ for 2 weeks, patients with advanced non‐small cell lung cancer showed significant improvement in T‐cell exhaustion. (NK) subgroups was higher than the pretreatment percentag
radioP↑, HRS can protect against radiation‐induced immune dysfunction by restoring the number of CD4+ T and CD8+ T cells in the spleen.
*CD4+↑,
CD8+↑,
*Dose↝, Common delivery methods include inhalation, oral administration of HRW, injection of HRS, promotion of endogenous H2 production
*other↑, H2, which fall within the explosive range at concentrations ranging from 4 to 74%, it is essential to specify the concentration of H2 for inhalation therapy.
*Dose↝, China National Health Commission recommends the administration of oxygen–H2 mixture (33.3% O2 and 66.6% H2)
*antiPs↑, HRW baths exhibit inhibitory effects on inflammation and oxidative stress while demonstrating therapeutic benefits for conditions such as psoriasis
*BioAv↝, the solubility of H2 in water at room temperature and pressure is limited to a maximum of 0.8mM109, resulting in limited efficacy when orally administered.
*GutMicro↑, inhalation of H2 modulates the gut flora to ameliorate acute alcoholic liver injury. H2 altered the composition of the GM, leading to an increase in the relative abundance of Mycobacterium anisopliae and Mycobacterium thickum
Dose↝, CRC cell lines (ROK/SW480/HCT116) and xenograft mouse models,Inhalation of 66% H2 (66% H2 and 33% O2);Duration: 2 h a day for 21 days
*IBI↑, orally administered silicon H2 nanoparticles (SiH NPs) for targeted scavenging of ROS at inflammatory sites, thereby alleviating symptoms of IBD and restoring GM diversity by enhancing the abundance of beneficial bacteria.
TumCP↓, H2 inhibits tumor cell activity, proliferation, invasion, and migration through various molecular mechanisms, in a manner that depends on both dose and time.
TumCI↓,
TumCMig↓,
CD8+↑, H2 Improves Prognosis by Restoring Depleted CD8+ T Cells in Patients with CRC Cancer
PGC-1α↑, It has been shown that H2 can activate PGC‐1α to restore mitochondrial function and rescue depleted CD8+T cells
Akt↓, H2 Inhibits CRC Cell Proliferation by Suppressing the AKT/SCD1 Pathway
SCD1↓,
*MDA↓, The results showed that H2 water alone significantly improved detected antioxidant markers (SOD and CAT) and reduced MDA levels.
Synergy↑, combination of H2 water and 5‐fluorouracil significantly attenuated MDA levels more effectively than 5‐fluorouracil alone
*APP↓, H2 gas significantly inhibited the overexpression of APP, BACE1, and sAP, thereby reducing Aβ production.
*BACE/β-secretase↓,
*Aβ↓,
*cognitive↑, This intervention effectively halted the progression of AD, alleviating cognitive impairment, synaptic deficits, and neuronal death
*neuroP↑, regulation of GM(gutmicrobiome) by HRW considered a key mechanism underlying its neuroprotective effects.
NP/CIPN↓, mice with chemotherapy‐induced neuropathic pain caused by oxaliplatin, drinking HRW significantly reduced inflammation by inhibiting the LPS–TLR4 pathway and decreasing the expression of TNF‐α and IL‐6.
*Stroke↓, inhalation of 2% H2 gas significantly reduced levels of myocardial injury markers, such as creatine kinase‐MB and cardiac troponin‐T, while protecting myocardial tissue from further damage by inhibiting autophagy.
*NLRP3↓, daily inhalation of 2% H2 gas for 3 h over 28 days effectively suppressed the activation of the NLRP3 inflammasome, reduced cardiac fibrosis, and improved cardiac function
*ALAT↓, 4% H2 outperforming 67% H2 in reducing liver enzyme levels Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) and lipid accumulation.
*AST↓,
*LPS↓, inhalation of 4% H2 in an NAFLD rat model significantly lowered plasma LPS levels, inhibited the LPS/TLR4/NF‐κB signaling pathway to reduce liver inflammation
*hepatoP↑, drinking HRW, indicating its hepatoprotective effects
chemoP↑, injecting HRS in rats effectively reduced ALT and AST levels caused by doxorubicin, decreased ROS and MDA production, and regulated the Bax/Bcl‐2 ratio to alleviate inflammation and apoptosis.
*creat↓, mouse model of kidney injury induced by a high‐oxalate diet, HRW consumption markedly improved serum creatinine, blood urea nitrogen, and kidney injury markers such as kidney injury molecule‐1 (KIM‐1)
*Urea↓,
*RenoP↑,
*eff↑, higher concentrations of H2 gas (67%) produced more pronounced improvements in kidney histology and morphology compared with lower concentrations (4%)
Apoptosis↑, H2 gas increased apoptosis in A549 cells while reducing the expression of XIAP and BIRC3 proteins in studies on A549 cells and their nude mouse models.
XIAP↓,
IAP2/BIRC3↓,
TumVol↓, inhalation of 60% H2 gas significantly reduced tumor volume in experimental mice
MALAT1↓, In gastric cancer research, Zhu et al. [10] found that H2 gas downregulated the expression of lncRNA MALAT1 and EZH2 while upregulating miR‐124‐3p
EZH2↓,
miR-124-3p↓,
eff↑, combining platinum nanocolloid (Pt‐nc) with H2 gas effectively inhibited the growth of human promyelocytic leukemia HL60 cells
ChemoSen↑, combining H2 therapy with conventional treatments such as chemotherapy and radiotherapy, demonstrating improved efficacy and reduced side effects
*compII↑, allergic airway inflammation, showing that H2 increased ATP production as well as the activity of mitochondrial respiratory chain complexes I and III
*compIII↑,
*LDL↓, H2‐enriched water in humans, showing that supplementation with H2‐enriched water appeared to reduce serum low‐density lipoprotein cholesterol (LDL‐C) and apolipoprotein B (apoB) levels,
*Obesity↓, H2 may play a beneficial role in the prevention of potential metabolic syndrome
QoL↑, 82 patients with stage III and IV cancers receiving H2 inhalation therapy. They found that H2 inhalation improved the quality of life
PFS↑, Sixteen months of follow‐up found that progression‐free survival in the control group was lower than that in the H2 inhalation group alone, and significantly lower than that in the other three combination therapy groups.
*antiAll↑, therapeutic effects of H2 in these domains are attributed not only to its antioxidant properties but also to its anti‐inflammatory, antiapoptotic, and antiallergic capabilities


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Mitochondria & Bioenergetics(tgid=3) ⓘ

PGC-1α↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

SCD1↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   IAP2/BIRC3↓, 1,   XIAP↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 2,   PI3K↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

EZH2↓, 1,   miR-124-3p↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK4↓, 1,   CDK6↑, 1,  

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

TumCP↓, 1,  

Migration(tgid=13) ⓘ

MALAT1↓, 1,   TumCI↓, 1,   TumCMig↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD47↓, 1,   CD8+↑, 2,   NK cell↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   Dose↝, 2,   eff↑, 1,   selectivity↑, 1,   Synergy↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EZH2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoP↑, 1,   NP/CIPN↓, 1,   PFS↑, 1,   QoL↑, 1,   radioP↑, 1,   TumVol↓, 1,  
Total Targets: 31

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   HO-1↑, 1,   MDA↓, 1,   MPO↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

compII↑, 1,   compIII↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   ATP↑, 1,   LDL↓, 1,  

Cell Death(tgid=5) ⓘ

Casp12↓, 1,   GranB/GZMB↓, 1,   p38↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↑, 1,   p‑JNK↓, 1,   mTOR↓, 1,   PI3K↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

ATF4↓, 1,   other↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↓, 1,   p‑eIF2α↓, 1,   ER Stress↓, 1,   GRP78/BiP↓, 1,   XBP-1↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

LC3‑Ⅱ/LC3‑Ⅰ↑, 1,  

Migration(tgid=13) ⓘ

TGF-β↑, 1,  

Barriers & Transport(tgid=15) ⓘ

IBI↑, 1,   MMP↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   IFN-γ↓, 1,   IL10↑, 1,   IL1β↓, 1,   IL4↓, 1,   IL6↓, 1,   Imm↑, 1,   Inflam↓, 1,   LPS↓, 1,   NLRP3↓, 1,   TNF-α↓, 1,  

Protein Aggregation(tgid=19) ⓘ

APP↓, 1,   Aβ↓, 1,   BACE/β-secretase↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,   Dose↝, 2,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   creat↓, 1,   IL6↓, 1,   Urea↓, 1,  

Functional Outcomes(tgid=23) ⓘ

antiAll↑, 1,   antiPs↑, 1,   cardioP↑, 1,   cognitive↑, 1,   hepatoP↑, 2,   neuroP↑, 2,   Obesity↓, 1,   RenoP↑, 1,   Stroke↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

GutMicro↑, 1,   Sepsis↓, 1,  
Total Targets: 65

Scientific Paper Hit Count for: EZH2, enhancer of zeste homolog 2 (Drosophila)
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#:295  Target#:108  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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