Database Query Results : , , PDKs

PDKs, pyruvate dehydrogenase kinase: Click to Expand ⟱

Source:

Type:

– PDK1 is often upregulated in cancers and is central to the metabolic reprogramming (Warburg effect) that allows tumor cells to favor glycolysis over oxidative phosphorylation.
– Elevated PDK1 expression has been correlated with aggressive tumor behavior and poor prognosis in several cancer types, including non‐small cell lung cancer, ovarian cancer, and gastric cancer.

– Although PDK2 has a similar catalytic role as PDK1, its expression levels and impact may vary.
– Some studies have observed that increased PDK2 expression is associated with more aggressive cancer features and resistance to therapy in certain tumor types.

– PDK3 is often upregulated in response to hypoxic conditions—a common feature of solid tumors—which can further drive metabolic divergence in cancer cells.

– The role of PDK4 appears to be more variable. In some settings, its activity might be lower in tumor cells to favor the use of glycolysis, while in others, it may be upregulated as part of broader metabolic adaptations.

-By upregulating PDKs, cancer cells limit the flux of pyruvate into the mitochondria, thereby promoting glycolysis.

Scientific Papers found: Click to Expand⟱

3271-

ALA,

Decrypting the potential role of α-lipoic acid in Alzheimer's disease

Review,

AD,

*antiOx↑, Alpha-lipoic acid (α-LA), a natural antioxidant
*memory↑, multiple preclinical studies indicating beneficial effects of α-LA in memory functioning, and pointing to its neuroprotective effects
*neuroP↑, α-LA could be considered neuroprotective
*Inflam↓, α-LA shows antioxidant, antiapoptotic, anti-inflammatory, glioprotective, metal chelating properties in both in vivo and in vitro studies.
*IronCh↑, α-LA leads to a marked downregulation in iron absorption and active iron reserve inside the neuron
*NRF2↑, α-LA induces the activity of the nuclear factor erythroid-2-related factor (Nrf2), a transcription factor.
*BBB↑, capable of penetrating the BBB
*GlucoseCon↑, Fig 2, α-LA mediated regulation of glucose uptake
*Ach↑, α-LA may show its action on the activity of the ChAT enzyme, which is an essential enzyme in acetylcholine metabolism
*ROS↓,
*p‑tau↓, decreased degree of tau phosphorylation following treatment with α-LA
*Aβ↓, α-LA possibly induce the solubilization of Aß plaques in the frontal cortex
*cognitive↑, cognitive reservation of α-LA served AD model was markedly upgraded in additional review
*Hif1a↑, α-LA treatment efficaciously induces the translocation and activity of hypoxia-inducible factor-1α (HIF-1α),
*Ca+2↓, research found that α-LA therapy remarkably declines Ca2+ concentration and calpain signaling
*GLUT3↑, inducing the downstream target genes expression, such as GLUT3, GLUT4, HO-1, and VEGF.
*GLUT4↑,
*HO-1↑,
*VEGF↑,
*PDKs↓, α-LA also ameliorates survival in mutant mice of Huntington's disease [150–151], possibly due to the inhibition of the activity of pyruvate dehydrogenase kinase
*PDH↑, α-LA administration enhances PDH expression in mitochondrial hepatocytes by inhibiting the pyruvate dehydrogenase kinase (PDK),
*VCAM-1↓, α-LA inhibits the expression of cell-cell adhesion molecule-1 and VCAM-1 in spinal cords and TNF-α induced neuronal endothelial cells injury
*GSH↑, α-LA may enhance glutathione production in old-aged models
*NRF2↑, activation of the Nrf2 signaling by α-LA
*hepatoP↑, α-LA also protected the liver against oxidative stress-mediated hepatotoxicity
*ChAT↑, α-LA in mice models may prevent neuronal injury possibly due to an increase in ChAT in the hippocampus of animal models

2389-

BA,

Baicalin alleviates lipid accumulation in adipocytes via inducing metabolic reprogramming and targeting Adenosine A1 receptor

in-vitro,

Obesity,

3T3

*ECAR↑, Baicalin promoted metabolic reprogramming in 3T3-L1 preadipocytes, characterized by increased ECAR and decreased OCR
*OCR↓,
*p‑AMPK↑, baicalin significantly altered cellular respiration by reducing mitochondrial oxygen consumption while enhancing glycolytic flux, accompanied by increased phosphorylation of AMPK and ACC, suggesting an adaptation to altered energy availability.
*p‑ACC↑,
*Glycolysis↑, significant enrichment in metabolic pathways such as glycolysis, gluconeogenesis, and lipid metabolism.
*lipidDe↓, inhibited the maturation of sterol regulatory element binding protein 1 (SREBP1) and finally alleviated lipid deposition.
*SREBP1↓,
*FAO↑, baicalin induces metabolic reprogramming of adipocytes by inhibiting glucose aerobic metabolism while enhancing anaerobic glycolysis and FAO.
*HK2↑, baicalin upregulated glycolytic enzymes, such as HK1, HK2, PKM2, and LDHA, while downregulating pyruvate dehydrogenase,
*PKM2↑,
*LDHA↑,
*PDKs↓,
*ACC↓, leading to decreased acetyl-CoA production and enhanced fatty acid β-oxidation.

1889-

DCA,

A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth

Review,

Var,

PDKs↓, Dichloroacetate (DCA) inhibits mitochondrial pyruvate dehydrogenase kinase (PDK)
Glycolysis↓, shifts metabolism from glycolysis to glucose oxidation
mt-H2O2↑, increases mitochondrial H2O2
Apoptosis↑, DCA induces apoptosis, decreases proliferation, and inhibits tumor growth, without apparent toxicity
TumCP↓,
TumCG↓,
toxicity∅,

1887-

DCA,

GSTZ1 expression and chloride concentrations modulate sensitivity of cancer cells to dichloroacetate

in-vitro,

Var,

GSTZ1∅, high levels of GSTZ1 expression confers resistance to the effect of high concentrations of DCA on cell viability
eff↓, These results may have important clinical implications in determining intratumoral metabolism of DCA and, consequently, appropriate oral dosing.
PDKs↓, inhibitor of mitochondrial pyruvate dehydrogenase kinase (PDK), DCA maintains the pyruvate dehydrogenase complex (PDC) in its active, unphosphorylated state
Chl∅, [Cl-] in tumors is often abnormally high compared to the surrounding tissue
eff↓, changes in [Cl-] could have an impact on DCA treatment, because a tumor with high GSTZ1 expression and high [Cl-] could exhibit atypical resistance to the anti-tumor effects of the drug.

1885-

DCA,

Role of SLC5A8, a plasma membrane transporter and a tumor suppressor, in the antitumor activity of dichloroacetate

in-vitro,

CRC,

HCT116

These three cell lines do not express SLC5A8

in-vitro,

CRC,

SW-620

in-vitro,

CRC,

HT-29

SMCT1∅, SLC5A8 transports dichloroacetate very effectively with high affinity. This transporter is expressed in normal cells, but the expression is silenced in tumor cells via epigenetic mechanisms.
eff↓, lack of the SLC5A8 transporter makes tumor cells resistant to the antitumor activity of dichloroacetate.
eff↑, However, if the transporter is expressed in tumor cells ectopically, the cells become sensitive to the drug at low concentrations. This is evident in breast cancer cells, colon cancer cells, and prostate cancer cells.
eff↑, our findings suggest that combining dichloroacetate with a DNA methylation inhibitor would offer a means to reduce the doses of dichloroacetate to avoid detrimental effects associated with high doses but without compromising antitumor activity.
PDKs↓, Dichloroacetate is an inhibitor of pyruvate dehydrogenase kinase (PDK), which phosphorylates the E1α subunit of PDC and inactivates the complex
MMP↓, depolarization of the mitochondrial membrane,
Glycolysis↓, suppression of glycolysis
mitResp↑, enhancement of mitochondrial oxidation
ROS↑, production of reactive oxygen species,
eff↑, In control cells, which did not express the transporter, dichloroacetate did not have any significant effect. However, under identical conditions, SLC5A8-expressing cells underwent apoptosis to a marked extent. This phenomenon was seen in all three c

1882-

DCA,

Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer

Analysis,

NA,

PDKs↓, DCA activates PDH by inhibition of PDK at concentration of 10–250 μM
PDH↑,
lactateProd↓, decrease in lactate levels in both the blood and the cerebrospinal fluid.
Half-Life∅, Although the initial half-life with the first dose is less than one hour, this half-life increases to several hours with subsequent doses.

1878-

DCA,

5-FU,

Synergistic Antitumor Effect of Dichloroacetate in Combination with 5-Fluorouracil in Colorectal Cancer

in-vitro,

CRC,

LS174T

57mM

in-vitro,

CRC,

LoVo

29mM

in-vitro,

CRC,

SW-620

38mM

in-vitro,

CRC,

HT-29

47mM

tumCV↓, DCA inhibited the viability of CRC cells and had synergistic antiproliferation in combination with 5-FU
eff↑, synergistic antiproliferation in combination with 5-FU
PDKs↓, Dichloroacetate (DCA) is a prototypical inhibitor of mitochondrial PDK
lactateProd↓, DCA decreases lactate production by shifting the metabolism of pyruvate from glycolysis towards oxidation in the mitochondria
Glycolysis↓,
mitResp↑, DCA restored mitochondrial function
TumCCA↑, DCA potentiated the cell cycle arrest in G1 phase.
Bcl-2↓, DCA and 5-FU decreased Bcl-2 expression significantly as compared with DCA or 5-FU alone
BAX↑, Bax and caspase-3 were significantly increased in the four CRC cell lines treated with combination of DCA and 5-FU compared to their single usage
Casp3↑,

1877-

DCA,

Non-Hodgkin′s Lymphoma Reversal with Dichloroacetate

Case Report,

lymphoma,

Remission↑, Refusing all suggested chemotherapies, the patient began self-administering dichloroacetate (DCA) 900 mg daily with a PET scan showing complete remission four months later.
p‑PDKs↓, DCA has been shown to block this phosphorylation by PDK at the mitochondrial membrane level and decrease glycolysis in favor of glucose oxidation
Glycolysis↓,
i-Ca+2↓, This return to a normal metabolism of glucose allows for major changes including a decrease in Ca++ intracellularly, and stabilization of the mitochondria allowing a reactivation of caspases in cancer cells leading to apoptosis
toxicity↓, A reversible, minimal nerve damage can be considerably reduced by a daily thiamine intake of several hundred milligrams for humans. thiamine amount varies from 50 mg/day to 100 mg/day depending on whether it is administered orally or injected
Dose∅, A Non-Hodgkin′s lymphoma patient taking 10 mg/kg [750 mg] of dichloroacetate daily of his own accord, had a complete remission of his Non-Hodgkin′s lymphoma cancer after four months

1884-

DCA,

Sal,

Dichloroacetate and Salinomycin Exert a Synergistic Cytotoxic Effect in Colorectal Cancer Cell Lines

in-vitro,

CRC,

DLD1

in-vitro,

CRC,

HCT116

eff↑, The effect of combination of dichloracetate and salinomycin on multicellular spheroid size was stronger than the sum of both monotherapies, particularly in HCT116 cells
pH↓, and in contrast, it is not related to dichloroacetate-induced reduction of intracellular pH
PDKs↓, Dichloroacetate (DCA) is a small synthetic molecule that is known as a pyruvate dehydrogenase kinase inhibitor. Its anticancer properties involve reversing the Warburg effect by switching ATP production back to oxidative phosphorylation
Warburg↓,

1875-

DCA,

Dichloroacetate inhibits neuroblastoma growth by specifically acting against malignant undifferentiated cells

in-vitro,

neuroblastoma,

in-vivo,

NA,

five mice were treated with 2.5 mg/kg/
dose of DCA, 14 mice were treated with 25 mg/kg/dose

mice

selectivity↑, acting specifically on the mitochondria of cancer cells without perturbing the physiology of nonmalignant cells.
AntiCan↑, DCA exhibits an unexpected anticancer effect on NB tumor cells
TumVol↓, growth inhibition became statistically significant when mice were treated with 25 mg/kg/dose of DCA (55% of reduction compared with control group)
PDKs↓, effects of DCA are related to PDK inhibition, mitochondrial oxidative phosphorylation activation and specific mitochondrial hyperpolarization reduction,
mt-OXPHOS↑,
MMP↓,
Glycolysis↓, shifting cellular metabolism from glycolysis to glucose oxidation, without any deleterious effect on normal cells.
toxicity↓, Indeed, more than 40 clinical trials of DCA report that the most significant adverse effect of long-term DCA administration is a reversible peripherical neuropathy.
Warburg↓, indeed, DCA is able to reverse the Warburg effect by inhibiting PDK, restoring mitochondrial membrane potential and increasing ROS production.
ROS↑,
eff↑, DCA was celebrated as the magic bullet against cancer, even if it is currently not yet approved for cancer treatment.

1873-

DCA,

Dual-targeting of aberrant glucose metabolism in glioblastoma

in-vitro,

GBM,

U87MG

in-vitro,

GBM,

U251

PDKs↓, dichloroacetate (DCA), a pyruvate dehydrogenase kinase inhibitor.
eff↑, By combining DCA with PENAO, the two drugs worked synergistically to inhibit cell proliferation (but had no significant effect on non-cancerous cells)
selectivity↑,
MMP↓, induced oxidative stress and depolarized mitochondrial membrane potential, which in turn activated mitochondria-mediated apoptosis
ROS↑,
Apoptosis↑,
Warburg↓, Dichloroacetate (DCA), a pyruvate dehydrogenase kinase (PDK) inhibitor that reverses the Warburg effect
eff↑, DCA has been demonstrated to sensitize cancer cells towards apoptosis and enhance the effects of several anti-cancer agents, including arsenic trioxide [20], cisplatin [22,23] and metformin [24].
Dose∅, IC50 values of DCA were at suprapharmacological millimolar level
toxicity∅, whilst the IC50 values of DCA for non-cancerous cells were not reached (DCA concentration in this study was tested up to 50 mM)

1872-

DCA,

Dichloroacetate, a selective mitochondria-targeting drug for oral squamous cell carcinoma: a metabolic perspective of treatment

in-vitro,

Oral,

HSC2

in-vitro,

Oral,

HSC3

PDKs↓, Dichloroacetate (DCA) is a specific inhibitor of the PDH-regulator PDK proved to foster mitochondrial oxidation of pyruvate.
ROS↑, enhanced production of reactive oxygen species
OCR↑, DCA - a mildly cytotoxic concentration - caused, indeed, an increase of the resting endogenous OCR in all the three OSCC cell lines
other↑, Consequently, the OxPhos/Glycolysis flux ratio increased largely in HSC-2 and scantly in PE15 with an intermediate value for HSC-3

1864-

DCA,

MET,

Dichloroacetate Enhances Apoptotic Cell Death via Oxidative Damage and Attenuates Lactate Production in Metformin-Treated Breast Cancer Cells

in-vitro,

BC,

MCF-7

DCA (2.5 mM) and metformin (1 mM)

in-vitro,

BC,

T47D

in-vitro,

Nor,

MCF10

PDKs↓, Dichloroacetate (DCA) is a well-established drug used in the treatment of lactic acidosis which functions through inhibition of pyruvate dehydrogenase kinase (PDK) promoting mitochondrial metabolism
eff↑, DCA and metformin are used in combination, synergistic induction of apoptosis of breast cancer cells occurs.
ROS↑, Metformin-induced oxidative damage is enhanced by DCA through PDK1 inhibition which also diminishes metformin promoted lactate production.
PDK1↓,
lactateProd↓, also diminishes metformin promoted lactate production.
p‑PDH↑, DCA is an inhibitor of pyruvate dehydrogenase kinase (PDK) which phosphorylates pyruvate dehydrogenase (PDH), rendering it inactive
Dose∅, DCA (2.5 mM) and metformin (1 mM)
OCR↑, DCA treated cells had a significantly higher oxygen consumption rate compared to control cells.
DNA-PK↑,
γH2AX↑, phosphorylatoin of histone H2AX (p-H2AX), which is a useful surrogate marker of such DNA damage
cl‑PARP↑, large increase of cleaved PARP
selectivity↑, Importantly, we also show that this combination of drugs does not kill non-transformed breast epithelial cells MCF10A under the same conditions in which the drugs kill cancer cells.
*toxicity∅, does not kill non-transformed breast epithelial cells MCF10A under the same conditions in which the drugs kill cancer cells.

1867-

DCA,

Chemo,

Sensitization of breast cancer cells to paclitaxel by dichloroacetate through inhibiting autophagy

in-vivo,

BC,

mice

in-vitro,

BC,

TumCG↓, Synergistic inhibition of tumor growth in mice treated with Dox and DCA.
eff↑, DCA markedly enhances Doxorubicin-induced breast cancer cell death and anti-proliferation in vitro.
OS↑, Moreover, the combined therapy of Dox and DCA could significantly inhibit tumor growth in vivo and prolong mouse survival time.
PDKs↓, Dichloroacetate (DCA) is a small inhibitor of pyruvate dehydrogenase kinase (PDK), which activates pyruvate dehydrogenase (PDH), and increases glucose oxidation by promoting influx of pyruvate into the Krebs cycle.
PDH↑,

4901-

DCA,

Sal,

Dichloroacetate and Salinomycin as Therapeutic Agents in Cancer

Review,

NSCLC,

Glycolysis↓, DCA redirects mitochondrial metabolism away from glycolysis to OXPHOS by the inhibition of PDKs
OXPHOS↑,
PDKs↓,
ROS↑, DCA increases reactive oxygen species (ROS), which induce downstream changes in mitochondrial function, causing the selective apoptosis of cancer cells.
Apoptosis↑,
GlucoseCon↓, treatment with DCA decreased glucose consumption and lactate production in vitro in a manner that was statistically significant compared to the controls
lactateProd↓,
RadioS↑, it enhanced the sensitivity of A549 and H1299 cells to X-ray-induced cell killing
TumAuto↑, DCA has been shown to induce autophagy instead of inhibiting it.
mTOR↓, The DCA-induced induction of autophagy was found to be mediated by the generation of ROS, the inhibition of the mammalian targets of rapamycin (mTOR),
LC3s↓, Lu and colleagues found that LC3 decreased while p62 levels increased, both of which are hallmarks of autophagy inhibition
p62↑,
TumCG↓, In vivo studies have demonstrated that DCA inhibits the growth of A549 and H1975 tumor xenografts and enhances the survival of tumor-bearing nude mice
OS↑,
toxicity↝, the most clinically limiting side effect of DCA is peripheral neuropathy
ChemoSen↑, DCA exerts synergistic potential with the most widely used chemotherapy agent, paclitaxel, on NSCLC cells.
eff↑, DCA has also been shown to have anticancer synergies with various non-traditional agents, the most prominent of which is metformin.
eff↑, Another compound that DCA has been shown to have a strong synergism with is ivermectin.
Ferritin↓, SAL and its derivatives prevent the movement of iron from the lumen to the cytosol, triggering an iron-depletion reaction that is characterized by the rapid degradation of ferritin
CSCs↓, SAL has been shown to selectively target CSCs in vitro and in vivo, but its mode of action is not fully understood.
EMT↓, SAL has also been shown to suppress the epithelial–mesenchymal transition (EMT) as well as transforming growth factors (TGFs). EMT is a process that is pivotal to metastasis.
ROS↑, SAL triggers apoptosis by elevating intracellular ROS levels, leading to the translocation of Bax protein to the mitochondria, cytochrome c (Cytc) release, and the activation of caspase-3
Cyt‑c↑,
Casp3↑,
ER Stress↑, SAL was observed to upregulate ER stress-related proteins in a time-/dose-dependent manner
selectivity↑, SAL induced cell death in multiple apoptosis-resistant cancer cell lines, but not in normal healthy human cells
eff↑, Skeberdytė and colleagues were among the first to recognize that DCA had synergistic potential with SAL.
TumCG↓, DCA and SAL were found to significantly suppress tumor growth in vivo in the mice.

1628-

HCA,

ALA,

Addition of Hydroxy Citrate improves effect of ALA

Review,

Var,

ACLY↓, Hydroxycitrate is a known inhibitor of ATP citrate lyase ( also called ATP-citric synthase
other↓, Lipoic Acid Increases PDC (pyruvate dehydrogenase complex)
ROS↑, oxidative onslaught, making the cancer cell susceptible to oxidative therapies such as alpha lipoic acid.
eff↑, the addition of hydroxycitrate increases the effect of ALA.
PDKs↓, An inhibitory effect of lipoic acid on PDKs would result in… increased PDC pyruvate dehydrogenase complex (PDC) activity.

2044-

PB,

DCA,

Differential inhibition of PDKs by phenylbutyrate and enhancement of pyruvate dehydrogenase complex activity by combination with dichloroacetate

in-vivo,

NA,

mice

PDK1↓, We investigated the inhibitory activity of phenylbutyrate toward PDKs and found that PDK isoforms 1-to-3 are inhibited whereas PDK4 is unaffected.
PDKs↓,
eff↑, phenylbutyrate combined to DCA results in greater increase of PDHC activity compared to each drug alone.
PDH↑,

1888-

VitB1/Thiamine,

DCA,

High Dose Vitamin B1 Reduces Proliferation in Cancer Cell Lines Analogous to Dichloroacetate

in-vitro,

PC,

SK-N-BE

NA,

PC,

PANC1

p‑PDH↓, Both thiamine and DCA reduced the extent of PDH phosphorylation, reduced glucose consumption, lactate production, and mitochondrial membrane potential.
GlucoseCon↓, High dose thiamine reduces glucose consumption and lactate production
lactateProd↓,
MMP↓,
Casp3↑, High dose thiamine and DCA did not increase ROS but increased caspase-3 activity
eff↑, Our findings suggest that high dose thiamine reduces cancer cell proliferation by a mechanism similar to that described for dichloroacetate
PDKs↓,
selectivity↑, An advantage to targeting PDK activity is that overexpression of PDKs and extensive phosphorylation of PDH is found in cancer cells and not in normal tissue [14]. This may provide for selective targeting towards malignant tissue
TumCG↓, thiamine suppressed tumor growth at doses greater than 75 times the recommended daily intake
Dose∅, IC50 of thiamine was lower than DCA for both cell lines with values of 4.9 for SK-N-BE and 5.4 mM for Panc-1.
MMP↓, decrease in mitochondrial membrane potential
ROS∅, cells treated with thiamine or DCA were assayed for peroxide following 30 min, 1 h, and 2 h of treatment. No significant change in ROS was observed over all time
toxicity↑, Smithline et al. reported no adverse effects in healthy patients who were given 1.5g/day of thiamine [34]. Only minor side effects, such as nausea and indigestion were reported in patients given doses as high as 7.5 g/day
antiOx↑, Free thiamine has direct antioxidant properties

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 18

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, GSH↑, 1, HO-1↑, 1, lipidDe↓, 1, NRF2↑, 2, ROS↓, 1,

Metal & Cofactor Biology ⓘ

IronCh↑, 1,

Mitochondria & Bioenergetics ⓘ

OCR↓, 1,

Core Metabolism/Glycolysis ⓘ

ACC↓, 1, p‑ACC↑, 1, p‑AMPK↑, 1, ECAR↑, 1, FAO↑, 1, GlucoseCon↑, 1, Glycolysis↑, 1, HK2↑, 1, LDHA↑, 1, PDH↑, 1, PDKs↓, 2, PKM2↑, 1, SREBP1↓, 1,

Transcription & Epigenetics ⓘ

Ach↑, 1,

Migration ⓘ

Ca+2↓, 1, VCAM-1↓, 1,

Angiogenesis & Vasculature ⓘ

Hif1a↑, 1, VEGF↑, 1,

Barriers & Transport ⓘ

BBB↑, 1, GLUT3↑, 1, GLUT4↑, 1,

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,

Synaptic & Neurotransmission ⓘ

ChAT↑, 1, p‑tau↓, 1,

Protein Aggregation ⓘ

Aβ↓, 1,

Functional Outcomes ⓘ

cognitive↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 1, toxicity∅, 1,
Total Targets: 38

Scientific Paper Hit Count for: PDKs, pyruvate dehydrogenase kinase

15 Dichloroacetate
2 Alpha-Lipoic-Acid
2 salinomycin
1 Baicalin
1 5-fluorouracil
1 Metformin
1 Chemotherapy
1 HydroxyCitric Acid
1 Phenylbutyrate
1 Vitamin B1/Thiamine

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#:1201  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

Database Query Results : , , PDKs

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Barriers & Transport ⓘ

Cellular Microenvironment ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Transcription & Epigenetics ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Functional Outcomes ⓘ

Home Page