mitResp Cancer Research Results

mitResp, mitochondrial respiration: Click to Expand ⟱

Source:

Type:

Mitochondrial respiration plays a crucial role in the development and progression of cancer. Cancer cells often exhibit altered metabolic profiles, including changes in mitochondrial respiration, to support their rapid growth and proliferation.

In cancer cells, mitochondrial respiration is often downregulated, and instead, they rely on glycolysis for energy production, even in the presence of oxygen. This phenomenon is known as the "Warburg effect."

There are several key players involved in the regulation of mitochondrial respiration in cancer cells, including:

Pyruvate dehydrogenase (PDH): a critical enzyme that converts pyruvate into acetyl-CoA, which is then fed into the citric acid cycle.
Citrate synthase: an enzyme that catalyzes the first step of the citric acid cycle.
Succinate dehydrogenase (SDH): an enzyme that participates in both the citric acid cycle and the electron transport chain.
Cytochrome c oxidase (COX): the final enzyme in the electron transport chain, responsible for generating ATP.
Alterations in the expression and activity of these enzymes can impact mitochondrial respiration in cancer cells. For example, increased expression of PDH and citrate synthase can enhance mitochondrial respiration, while decreased expression of SDH and COX can impair it.

Additionally, various transcription factors and signaling pathways regulate mitochondrial respiration in cancer cells, including:

HIF-1α (hypoxia-inducible factor 1 alpha): a transcription factor that promotes glycolysis and suppresses mitochondrial respiration in response to hypoxia.
c-Myc: a transcription factor that regulates the expression of genes involved in mitochondrial respiration and biogenesis.
PI3K/Akt/mTOR: a signaling pathway that promotes cell growth and proliferation, in part by regulating mitochondrial respiration.

Scientific Papers found: Click to Expand⟱

2348-

CAP,

Recent advances in analysis of capsaicin and its effects on metabolic pathways by mass spectrometry

Analysis,

Nor,

Warburg↓, Capsaicin inhibits the Warburg effect by binding directly to Cys424 residue and LDHA of pyruvate kinase isoenzyme type M2 (PKM2).
*PKM2↓,
*COX2↓, capsaicin targets COX-2 and down-regulates its expression, which results in the further inhibition of inflammation
*Inflam↓,
*Sepsis↓, capsaicin may be used as a new active ingredient to treat sepsis and inflammation
*AMPK↑, capsaicin activates adenylate-activated protein kinase (AMPK) and protein kinase A (PKA), in turn enhancing the activity of the mitochondrial respiratory chain and promoting fatty acid oxidation
*PKA↑,
*mitResp↑,
*FAO↑,
*FASN↓, capsaicin can inhibit the activity of fatty acid synthetase
*PGM1?,
*ATP↑, treatment resulted in increased intracellular ATP levels (the end product of glycolysis)
*ROS↓, Capsaicin can mitigate the negative effects of oxidative stress on human health by scavenging these free radicals and reducing the oxidative stress response.

5954-

CEL,

The molecular mechanisms of celecoxib in tumor development

Review,

Var,

TumCP↓, Celecoxib mainly regulates the proliferation, migration, and invasion of tumor cells by inhibiting the cyclooxygenases-2/prostaglandin E2 signal axis
TumCMig↓,
TumCI↓,
COX2↓,
p‑NF-kB↓, thereby inhibiting the phosphorylation of nuclear factor-κ-gene binding, Akt, signal transducer and activator of transcription and the expression of matrix metalloproteinase 2 and matrix metalloproteinase 9.
Akt↓,
MMP2↓,
MMP9↓,
Apoptosis↑, celecoxib could promote the apoptosis of tumor cells by enhancing mitochondrial oxidation, activating mitochondrial apoptosis process, promoting endoplasmic reticulum stress process, and autophagy.
mitResp↑,
ER Stress↑,
TumAuto↑,
ChemoSen↑, Celecoxib can also reduce the occurrence of drug resistance by increasing the sensitivity of cancer cells to chemotherapy drugs.
Inflam↓, NSAIDs achieve anti-inflammatory effects by inhibiting the activity of the inflammatory factor COX-2 and the synthesis of PGE2.
PGE2↓,
chemoPv↑, Numerous studies have confirmed that NSAIDs also have chemopreventive effects on tumors.
toxicity↓, Compared with other NSAIDs, celecoxib shows lower toxicity side effects (such as the most common gastrointestinal bleeding and gastric ulcer).[
Risk↓, Early studies have shown that celecoxib can effectively reduce the incidence of colorectal cancer, especially inhibiting the development of familial adenomatous polyposis to colorectal cancer.
PI3K↓, celecoxib can promote cancer cell apoptosis by inhibiting the signal pathway of 3-phosphoinositide-dependent kinase-1 and downstream protein kinase B (Akt) in human colon cancer cells.
RadioS↑, celecoxib enhances the sensitivity of cancer cells to radiation therapy
TumCMig↓, inhibits cancer cell migration and invasion by inhibiting the activity of C-Jun amino-terminal kinase and downregulating the expression of specific protein 1.
TumCI↓,
cJun↓,
Sp1/3/4↓,
ROS↑, Celecoxib targets mitochondria and promotes the release of ROS by significantly increased oxidative stress.
MMP↓, lead to the decrease of cell consumption and mitochondrial transmembrane potential (△ ψ m), increasing mitochondrial membrane permeability to promote the release of ROS
MPT↑,
Ca+2↑, promote Ca2+ influx, produce a higher pro-oxidation state, increase the accumulation of ROS in cancer cell mitochondria,
Glycolysis↓, inhibits the glycolysis process, ATP synthesis is significantly reduced, leading to cancer cell death.[
ATP↓,
CSCs↓, In addition to cancer cells, celecoxib can also inhibit CSCs.
Wnt/(β-catenin)↓, celecoxib can inhibit the transduction of Wnt/β-catenin signaling pathway
EMT↓, celecoxib can inhibit the process of EMT
toxicity↝, ong-term use increases the risk of hypertension among participants who already have cardiovascular risk factors.[

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↑,

1876-

DCA,

Chemo,

In vitro cytotoxicity of novel platinum-based drugs and dichloroacetate against lung carcinoid cell lines

in-vivo,

Lung,

H727

eff↑, DCA (10 mM) inhibited the growth of UMC- 11 cells by 22% and sensitised these highly resistant cells to carboplatin, satraplatin and JM118 1.4-2.4-fold.
TumCG↓,
Glycolysis↓, DCA that promotes mitochondrial respiration over aerobic glycolysis
mitResp↑,

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

2901-

HNK,

doxoR,

Honokiol protects against doxorubicin cardiotoxicity via improving mitochondrial function in mouse hearts

in-vivo,

Nor,

mice

*mitResp↑, mice treated with Honokiol showed enhanced mitochondrial respiration
*PPARγ↑, Honokiol modestly increased PPARγ transcriptional activities in cultured embryonic rat cardiomyocytes
*Inflam↓, Honokiol repressed cardiac inflammatory responses and oxidative stress in mice subjected to Dox treatment.
*ROS↓,
*cardioP↑, We conclude that Honokiol protects the heart from Dox-cardiotoxicity
*SOD2↑, Both SOD2 and CD36 were upregulated in the heart of Honokiol treated mice
*LDH↓, Furthermore, Honokiol treatment reduced the Dox-induced elevation of lactate dehydrogenase (LDH) activity (Fig. 6D) in mice subjected to acute Dox treatment.

2893-

HNK,

doxoR,

Honokiol protects against doxorubicin cardiotoxicity via improving mitochondrial function in mouse hearts

in-vivo,

Nor,

rat

*mitResp↑, Oxygen consumption in freshly isolated mitochondria from mice treated with Honokiol showed enhanced mitochondrial respiration.
*PPARγ↑, Honokiol modestly increased PPARγ transcriptional activities in cultured embryonic rat
*cardioP↑, Honokiol alleviated Dox-cardiotoxicity with improved cardiac function and reduced cardiomyocyte apoptosis
*SIRT3↑, recent study reported that Honokiol blocks and reverses cardiac hypertrophy in mice by activating mitochondrial SIRT3
*ROS↓, Honokiol treatment depressed total ROS levels, which illustrated by the less pronounced decreased ratio of GSH/GSSG in mice
*GSH↑,
*SOD2↑, Both SOD2 and CD36 were upregulated in the heart of Honokiol treated mice

1780-

MEL,

Utilizing Melatonin to Alleviate Side Effects of Chemotherapy: A Potentially Good Partner for Treating Cancer with Ageing

Review,

Var,

*antiOx↑, Melatonin is a potent antioxidant and antiageing molecule, is nontoxic, and enhances the efficacy and reduces the side effects of chemotherapy.
*toxicity↓,
ChemoSen↑,
*eff↑, melatonin was superior in preventing free radical destruction compared to other antioxidants, vitamin E, β-carotene, vitamin C, and garlic oil
*mitResp↑, increasing the expression and activity of the mitochondrial respiration chain complexes
*ATP↑, increasing the expression and activity of the mitochondrial respiration chain complexes
*ROS↓, most attractive property of melatonin is that its metabolites also regulate the mitochondrial redox status by scavenging ROS and RNS
*CardioT↓, melatonin has a protective effect on the heart without affecting DOX's antitumor activity,
*GSH↑, improving the de novo synthesis of glutathione (GSH) by promoting the activity of gamma-glutamylcysteine synthetase
*NOS2↓, melatonin inhibits the production of nitric oxide synthase (NOS)
*lipid-P↓, lipid peroxidation was reduced after melatonin treatment (role in induces organ failure)
eff↑, but it also enhances its antitumor activity more than vitamin E
*HO-1↑, melatonin upregulates heme oxygenase-1 (HO-1) (role in induces organ failure)
*NRF2↑, decreased bladder injury and apoptosis due to the upregulation of Nrf2 and nuclear transcription factor NF-κB expression
*NF-kB↑,
TumCP↓, significantly reduced cell proliferation
eff↑, Pretreatment with melatonin effectively preserved the ovaries from cisplatin-induced injury
neuroP↑, Melatonin has neuroprotective roles in oxaliplatin-induced peripheral neuropathy

1778-

MEL,

Melatonin: a well-documented antioxidant with conditional pro-oxidant actions

Review,

Var,

Review,

AD,

*ROS↓, melatonin and its metabolic derivatives possess strong free radical scavenging properties.
*antiOx↓, potent antioxidants against both ROS (reactive oxygen species) and RNS (reactive nitrogen species). reduce oxidative damage to lipids, proteins and DNA under a very wide set of conditions where toxic derivatives of oxygen are known to be produced.
ROS↑, a few studies using cultured cells found that melatonin promoted the generation of ROS at pharmacological concentrations (μm to mm range) in several tumor and nontumor cells; thus, melatonin functioned as a conditional pro-oxidant.
selectivity↑, melatonin functions as a prooxidant in cancer cells where it aids in the killing of tumor cells
Dose↑, Melatonin levels in the nucleus and mitochondria reached saturation with a lower dose of 40 mg/kg body weight, with no further accumulation under higher doses of injected melatonin
*mitResp↑, improves mitochondrial respiration and ATP production, thereby reducing electron leakage and ROS generation
*ATP↑,
*ROS↓,
eff↑, melatonin protects mitochondrial function in the brain of Alzheimer's patients through both MT1/MT2 dependent and independent mechanisms
ROS↑, Cytochrome P450 utilizes melatonin as a substrate to generate ROS in mitochondria (melatonin concentration ranges from 0.1 to 10 uM)
Dose↑, melatonin at high concentrations (10-1000uM ) was able to promote ROS generation and lead to Fas-induced apoptosis in human leukemic Jurkat cells. Concentrations of <10uM , melatonin did not induce significant ROS generation in these cancer cells
*toxicity∅, High levels of melatonin (uM to mM) did not cause cytotoxicity in several types of nontumor cells
ROS↑, lower concentrations of melatonin (0.1-10uM ), which exhibited antioxidant action in HepG2 cells within 24 hr, became pro-oxidant after 96 hr of treatment, as indicated by the increase of GSH with 24hr and depletion after 96 hr.
eff↓, Finally, a compound, chlorpromazine, which specifically interrupts the binding of melatonin to calmodulin [188], prevented melatonin-induced AA release and ROS generation;
ROS↝, It remains unknown whether the pro-oxidant action exists in vivo. the vast majority of evidence indicates that melatonin is a potent antioxidant in vivo even at pharmacological concentrations
Dose↑, decline of melatonin production with age may render it more beneficial to supplement melatonin to the aging population to improve health by reducing free radical damage
other↑, melatonin intake has the potential to improve cardiac function, inhibit cataract formation, maintain brain health, alleviate metabolic syndrome, obesity and diabetes,reduce tumorigenesis, protect tissues against ischemia

538-

MF,

The extremely low frequency electromagnetic stimulation selective for cancer cells elicits growth arrest through a metabolic shift

in-vitro,

BC,

MDA-MB-231

in-vitro,

Melanoma,

MSTO-211H

TumCG↓, did not affect the non-malignant counterpart.
Ca+2↑,
COX2↓,
ATP↑, (ATP5B) and mitochondrial transcription (MT-ATP6)
MMP↑, significant enhancement of mitochondrial membrane potential (ΔΨm)
ROS↑, demonstrated for the first time the association of ROS production with the stimulation of the mitochondrial metabolism triggered by the electromagnetic field
OXPHOS↑,
mitResp↑, Mitochondrial respiration is increased by ELF-EMF exposure

4899-

Sal,

Anticancer activity of salinomycin quaternary phosphonium salts

in-vitro,

Var,

eff↑, The effects of TPP + conjugates on mitochondria were stronger than that of salinomycin
selectivity↑, Significant selectivity of action of salinomcyin – TPP+ conjugates is proved. Compound 3b showed low toxic effects on both tested non-tumour cell lines as compared to that shown towards cancer cells (SI values ranged from 1.2 to 8.6).
CSCs↓, specific toxicity towards epithelial cancer stem cells (CSCs) in breast cancer.
TumCCA↑, compound 3a an increase in the percentage of cells in G0/G1 phase was noted
MMP↓, treatment with SAL and its derivatives resulted in the loss of MMP
ROS↑, results obtained in the present study showed that the ROS level was around 2-fold elevated after treatment with compounds 3a and 3f of both cancer cell lines as compared to the control.
mitResp↑, 2.5 times increase in the mitochondria respiration rate when applied in a concentration of 1 μM.

4891-

Sper,

Spermidine as a promising anticancer agent: Recent advances and newer insights on its molecular mechanisms

Review,

Var,

Review,

AD,

TumCCA↑, Spermidine specifically interferes with the tumour cell cycle, resulting in the inhibition of tumor cell proliferation and suppression of tumor growth.
TumCP↓,
TumCG↓,
*Inflam↓, health improving effects, that includes remarkable anti-inflammatory effects
*antiOx↑, It is also a potent antioxidant, and reportedly improves the respiratory function
*neuroP↑, Dietary intake of spermidine reduces the risk of neurodegeneration, metabolic diseases, heart ailments, and cancer.
*cognitive↑, spermidine-induced autophagy slows the rate of cognitive decline due to its ability to clear amyloid-beta plaques in the brain
*Aβ↓,
*mitResp↑, Spermidine supplementation also enhances mitochondrial metabolism, and translational activity.
AntiCan↑, anticancer properties of spermidine are of particular interest as it is known to reduce the cancer-related mortality in humans
TumCD↑, in addition to impacting their discourse with the immune effectors that result in expediting the identification of tumor-associated antigens and eventually cancer cell death
TumAuto↑, Inhibition of acetyltransferase EP300 by spermidine is known to induce autophagy, which is one of the desirable approaches in the treatment of cancer.
*AntiAge↑, Lifelong oral spermidine administration is reported to extend the lifespan in mice by 25%, as evidenced by genetic investigations.
LC3B-II↑, Western blotting experiments have showed a surge in the levels of LC3 II/LC3 I, Atg5, and Beclin 1 proteins in spermidine administered HeLa cells.
ATG5↑,
Beclin-1↑,
mt-ROS↑, Spermidine induces mitochondrial reactive oxygen species (mtROS) mediated M2-polarization by producing a surge in the levels of H2O2 and mitochondrial peroxide in the presence of spermidine.
H2O2↑,
Apoptosis↑, Spermine is known to induce apoptosis in primary human cells as well as the malignant tumor cells by producing a surge in the intracellular level of reactive oxygen species (ROS)
*ROS↑,
ChemoSen↑, A combination of 5-fluorouracil and spermine analogues N 1 , N 11 -diethylnorspermine (DENSPM) (6, Figure 5) at concentrations 1.25, 2.5, 5, and 10 μM or α-difluoromethylornithine (DFMO) led to a synergistic killing of HCT116 colon carcinoma cells
MMP↓, and loss of membrane potential of mitochondria followed by a subsequent release of cytochrome c
Cyt‑c↑,

1003-

SSE,

Sodium selenite inhibits proliferation of lung cancer cells by inhibiting NF-κB nuclear translocation and down-regulating PDK1 expression which is a key enzyme in energy metabolism expression

vitro+vivo,

Lung,

NF-kB↓,
PDK1↓,
p‑p65↑,
p‑IκB↑,
BAX↑,
lactateProd↓,
MMP↓,
Cyt‑c↑, release of Cytochrome C
mitResp↑,
Apoptosis↑,

4874-

Uro,

EGCG,

A Combination Therapy of Urolithin A+EGCG Has Stronger Protective Effects than Single Drug Urolithin A in a Humanized Amyloid Beta Knockin Mice for Late-Onset Alzheimer's Disease

in-vivo,

AD,

humanized homozygous amyloid beta knockin (hAbKI) mice of late-onset Alzheimer’s disease

*motorD↑, increased positive effects of urolithin A and a combination treatment of urolithin A+EGCG in hAbKI mice for phenotypic behavioral changes including motor coordination, locomotion/exploratory activity, spatial learning and working memory
*memory↑,
*MitoP↑, mitophagy and autophagy genes were upregulated
*Aβ↓, The levels of amyloid beta (Aβ) 40 and Aβ42 are reduced in both treatments, however, the reduction is higher for combined treatment
*mitResp↑, Mitochondrial respiration is stronger for urolithin A compared to EGCG, indicating that mitophagy enhancer, urolithin A is a better and more promising molecule to enhance mitophagy activity.
*Nrf1↑, table4
*PINK1↑,
*PARK2↑,
*ATG5↑,
*Bcl-2↑,
*H2O2↓, we found hydrogen peroxide levels were reduced in urolithin A (p = 0.0008) and urolithin A+EGCG (p = 0.0004) treated hAbKI mice relative to untreated mice.
*ROS↓, urolithin A and EGCG act as free radical scavengers in hAbKI mice
*lipid-P↓, (lipid peroxidation) were also significantly reduced in urolithin A (p = 0.0003) and urolithin A+EGCG (p = 0.0002) treated hAbKI mice relative to untreated hAbKI mice
*mt-ATP↑, mitochondrial ATP levels were increased in urolithin A (p = 0.007) and urolithin A+EGCG (p = 0.0002) treated hAbKI mice relative to hAbKI untreated mice.

Showing Research Papers: 1 to 14 of 14

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↓, 1, antiOx↑, 2, GSH↑, 2, H2O2↓, 1, HO-1↑, 1, lipid-P↓, 2, Nrf1↑, 1, NRF2↑, 1, PARK2↑, 1, ROS↓, 7, ROS↑, 1, SIRT3↑, 1, SOD2↑, 2,

Mitochondria & Bioenergetics ⓘ

ATP↑, 3, mt-ATP↑, 1, mitResp↑, 7, PINK1↑, 1,

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1, FAO↑, 1, FASN↓, 1, LDH↓, 1, PGM1?, 1, PKM2↓, 1, PPARγ↑, 2,

Cell Death ⓘ

Bcl-2↑, 1,

Autophagy & Lysosomes ⓘ

ATG5↑, 1, MitoP↑, 1,

Migration ⓘ

PKA↑, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, Inflam↓, 3, NF-kB↑, 1,

Protein Aggregation ⓘ

Aβ↓, 2,

Drug Metabolism & Resistance ⓘ

eff↑, 1,

Clinical Biomarkers ⓘ

LDH↓, 1, NOS2↓, 1,

Functional Outcomes ⓘ

AntiAge↑, 1, cardioP↑, 2, CardioT↓, 1, cognitive↑, 1, memory↑, 1, motorD↑, 1, neuroP↑, 1, toxicity↓, 1, toxicity∅, 1,

Infection & Microbiome ⓘ

Sepsis↓, 1,
Total Targets: 45

Scientific Paper Hit Count for: mitResp, mitochondrial respiration

3 Dichloroacetate
2 Honokiol
2 doxorubicin
2 Melatonin
1 Capsaicin
1 Celecoxib
1 5-fluorouracil
1 Chemotherapy
1 Magnetic Fields
1 salinomycin
1 Spermidine
1 Selenite (Sodium)
1 Urolithin
1 EGCG (Epigallocatechin Gallate)

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#:952  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

mitResp Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Autophagy & Lysosomes ⓘ

Migration ⓘ

Immune & Inflammatory Signaling ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Home Page