OXPHOS Cancer Research Results

OXPHOS, Oxidative phosphorylation: Click to Expand ⟱
Source:
Type:
Oxidative phosphorylation (or phosphorylation) is the fourth and final step in cellular respiration.
Alterations in phosphorylation pathways result in serious outcomes in cancer. Many signalling pathways including Tyrosine kinase, MAP kinase, Cadherin-catenin complex, Cyclin-dependent kinase etc. are major players of the cell cycle and deregulation in their phosphorylation-dephosphorylation cascade has been shown to be manifested in the form of various types of cancers.
Many tumors exhibit a well-known metabolic shift known as the Warburg effect, where glycolysis is favored over OxPhos even in the presence of oxygen. However, this is not universal.
Many cancers, including certain subpopulations like cancer stem cells, still rely on OXPHOS for energy production, biosynthesis, and survival.

– In several cancers, especially during metastasis or in tumors with high metabolic plasticity, OxPhos can remain active or even be upregulated to meet energy demands.

In some cancers, high OxPhos activity correlates with aggressive features, resistance to standard therapies, and poor outcomes, particularly when tumor cells exploit mitochondrial metabolism for survival and metastasis.

– Conversely, low OxPhos activity can be associated with a reliance on glycolysis, which is also linked with rapid tumor growth and certain adverse prognostic features.

Inhibiting oxidative phosphorylation is not a universal strategy against all cancers. Targeting OXPHOS can potentially disrupt the metabolic flexibility of cancer cells, leading to their death or making them more susceptible to other treatments.
Since normal cells also rely on OXPHOS, inhibitors must be carefully targeted to avoid significant toxicity to healthy tissues.
Not all tumors are the same. Some may be more glycolytic, while others depend more on mitochondrial metabolism. Therefore, metabolic profiling of tumors is crucial before adopting this strategy. Inhibiting OXPHOS is being explored in combination with other treatments (such as chemo- or immunotherapies) to improve efficacy and overcome resistance.

In cancer cells, metabolic reprogramming is a hallmark where cells often rely on glycolysis (known as the Warburg effect); however, many cancer types also depend on OXPHOS for energy production and survival. Targeting OXPHOS(using inhibitor) to increase the production of reactive oxygen species (ROS) can selectively induce oxidative stress and cell death in cancer cells.

-One side effect of increased OXPHOS is the production of reactive oxygen species (ROS).
-Many cancer cells therefore simultaneously upregulate antioxidant systems to mitigate the damaging effects of elevated ROS.
-Increase in oxidative phosphorylation can inhibit cancer growth.
Scientific Papers found: Click to Expand⟱
3453- 5-ALA,    The heme precursor 5-aminolevulinic acid disrupts the Warburg effect in tumor cells and induces caspase-dependent apoptosis
- in-vitro, Lung, A549
OXPHOS↑, OCR↑, Warburg↓, ROS↑, SOD2↑, Catalase↑, HO-1↑, Casp3↑, Apoptosis↑,
5689- BJ,    Brucea javanica oil inhibited the proliferation, migration, and invasion of oral squamous carcinoma by regulated the MTFR2 pathway
- vitro+vivo, Oral, CAL27
TumCP↓, TumCMig↓, TumCI↓, SOD2↓, H2O2↓, OXPHOS↑, Glycolysis↓, ROS↑, RadioS↑, Hif1a↓, TumCG↓,
933- CUR,  EP,    Effective electrochemotherapy with curcumin in MDA-MB-231-human, triple negative breast cancer cells: A global proteomics study
- in-vitro, BC, NA
Apoptosis↑, ALDOA↓, ENO2↓, LDHA↓, LDHB↓, PFKP↓, PGK1↓, PGM1↓, PGAM1↓, OXPHOS↑, TCA↑,
1875- DCA,    Dichloroacetate inhibits neuroblastoma growth by specifically acting against malignant undifferentiated cells
- in-vitro, neuroblastoma, NA - in-vivo, NA, NA
selectivity↑, AntiCan↑, TumVol↓, PDKs↓, mt-OXPHOS↑, MMP↓, Glycolysis↓, toxicity↓, Warburg↓, ROS↑, eff↑,
5196- DCA,    Dichloroacetate induces apoptosis in endometrial cancer cells
- in-vitro, Var, NA
selectivity↑, MMP↓, survivin↓, Ca+2↓, P53↑, PDK1↓, PDH↑, Glycolysis↓, OXPHOS↑, ROS↑, Cyt‑c↑, Apoptosis↑, Casp↑, tumCV↓, PUMA↑,
4901- DCA,  Sal,    Dichloroacetate and Salinomycin as Therapeutic Agents in Cancer
- Review, NSCLC, NA
Glycolysis↓, OXPHOS↑, PDKs↓, ROS↑, Apoptosis↑, GlucoseCon↓, lactateProd↓, RadioS↑, TumAuto↑, mTOR↓, LC3s↓, p62↑, TumCG↓, OS↑, toxicity↝, ChemoSen↑, eff↑, eff↑, Ferritin↓, CSCs↓, EMT↓, ROS↑, Cyt‑c↑, Casp3↑, ER Stress↑, selectivity↑, eff↑, TumCG↓,
1863- dietFMD,  Chemo,    Effect of fasting on cancer: A narrative review of scientific evidence
- Review, Var, NA
eff↑, ChemoSideEff↓, ChemoSen↑, Insulin↓, HDAC↓, IGF-1↓, STAT5↓, BG↓, MAPK↓, HO-1↓, ATG3↑, Beclin-1↑, p62↑, SIRT1↑, LAMP2↑, OXPHOS↑, ROS↑, P53↑, DNAdam↑, TumCD↑, ATP↑, Treg lymp↓, M2 MC↓, CD8+↑, Glycolysis↓, GutMicro↑, GutMicro↑, Warburg↓, Dose↝,
1853- dietFMD,    Impact of Fasting on Patients With Cancer: An Integrative Review
- Review, Var, NA
*toxicity∅, QoL∅, eff↑, eff↝, ChemoSideEff↓, TumCG↓, Dose↑, toxicity↝, eff↑, IGF-1↑, *OXPHOS↑, BG↓, Insulin↓, RadioS↑,
5069- dietSTF,    The Role of Intermittent Fasting in the Activation of Autophagy Processes in the Context of Cancer Diseases
- Review, Var, NA
Risk↓, ChemoSen↑, RadioS↑, *Dose↝, *Dose↝, *Dose↝, *LDL↓, *CRP↓, *TNF-α↓, TumAuto↓, GLUT1↓, GLUT2↓, glucose↓, IGF-1↓, Insulin↓, mTOR↓, mTORC1↓, AMPK↑, Warburg↓, OXPHOS↑, ROS↑, DNAdam↑, JAK1↓, STAT↓, TumCP↓, QoL↑,
2512- H2,    Hydrogen Attenuates Allergic Inflammation by Reversing Energy Metabolic Pathway Switch
- in-vivo, asthmatic, NA
selectivity↑, lactateProd↓, ATP↑, HK2↓, PFK↓, Hif1a↓, PGC-1α↑, Glycolysis↓, OXPHOS↑, Dose↝,
2887- HNK,    Honokiol Restores Microglial Phagocytosis by Reversing Metabolic Reprogramming
- in-vitro, AD, BV2
*Glycolysis↑, *ATP↑, *ROS↓, *MMP↑, *OXPHOS↑, *PPARα↑, *PGC-1α↑,
2543- M-Blu,    The use of methylene blue to control the tumor oxygenation level
- in-vivo, Lung, NA
OCR↑, OXPHOS↑, Half-Life↝, AntiTum↑,
2541- M-Blu,    Spectroscopic Study of Methylene Blue Interaction with Coenzymes and its Effect on Tumor Metabolism
- in-vivo, Var, NA
TumCG↓, Glycolysis↓, OXPHOS↑, ROS↑, OCR↑, GlucoseCon↑, lactateProd↓,
2540- M-Blu,    Alternative mitochondrial electron transfer for the treatment of neurodegenerative diseases and cancers: Methylene blue connects the dots
- Review, Var, NA - Review, AD, NA
*OCR↑, *Glycolysis↓, *GlucoseCon↑, neuroP↑, Warburg↓, mt-OXPHOS↑, TumCCA↑, TumCP↓, ROS⇅, *cognitive↑, *mTOR↓, *mt-antiOx↑, *memory↑, *BBB↑, *eff↝, *ECAR↓, eff↑, lactateProd↓, NADPH↓, OXPHOS↑, AMPK↑, selectivity↑,
2384- MET,    Integration of metabolomics and transcriptomics reveals metformin suppresses thyroid cancer progression via inhibiting glycolysis and restraining DNA replication
- in-vitro, Thyroid, BCPAP - in-vivo, NA, NA - in-vitro, Thyroid, TPC-1
Glycolysis↓, OXPHOS↑, tumCV↓, TumCI↓, TumCMig↓, EMT↓, Apoptosis↑, TumCCA↑, LDHA↓, PKM2↓, IDH1↑, TumCG↓,
2242- MF,    Electromagnetic stimulation increases mitochondrial function in osteogenic cells and promotes bone fracture repair
- in-vitro, Nor, NA
*MMP↑, *Diff↑, *OXPHOS↑, *BMD↑, ATP∅,
2241- MF,    Pulsed electromagnetic therapy in cancer treatment: Progress and outlook
- Review, Var, NA
other↝, p‑ERK↝, P53↝, Cyt‑c↝, OXPHOS↑, Apoptosis↑, ROS↑,
2247- MF,    Effects of Pulsed Electromagnetic Field Treatment on Skeletal Muscle Tissue Recovery in a Rat Model of Collagenase-Induced Tendinopathy: Results from a Proteome Analysis
- in-vivo, Nor, NA
*Glycolysis↓, *LDHB↑, *NAD↑, *ATP↑, *antiOx↑, *ROS↑, *YAP/TEAD↑, *PGC-1α↑, *TCA↑, *FAO↑, *OXPHOS↑,
2260- MF,    Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- in-vitro, GBM, U87MG - in-vitro, GBM, LN229 - in-vivo, NA, NA
TumCP↓, TumCG↓, OS↑, ROS↑, SOD2↑, eff↓, ECAR↓, OCR↑, selectivity↑, *toxicity∅, TumVol↓, PGC-1α↑, OXPHOS↑, Glycolysis↓, PKM2↓,
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↓, Ca+2↑, COX2↓, ATP↑, MMP↑, ROS↑, OXPHOS↑, mitResp↑,
2396- PACs,    PKM2 is the target of proanthocyanidin B2 during the inhibition of hepatocellular carcinoma
- in-vitro, HCC, HCCLM3 - in-vitro, HCC, SMMC-7721 cell - in-vitro, HCC, Bel-7402 - in-vitro, HCC, HUH7 - in-vitro, HCC, HepG2 - in-vitro, Nor, L02
TumCP↓, TumCCA↓, Apoptosis↑, GlucoseCon↓, lactateProd↓, PKM2↓, Glycolysis↓, HK2↓, PFK↓, OXPHOS↑, ChemoSen↑, HSP90↓, Hif1a↓,
993- RES,    Resveratrol reverses the Warburg effect by targeting the pyruvate dehydrogenase complex in colon cancer cells
- in-vitro, CRC, Caco-2 - in-vivo, Nor, HCEC 1CT
TumCG↓, Glycolysis↓, PPP↓, ATP↑, PDH↑, Ca+2↝, TumCP↓, lactateProd↓, OCR↑, ECAR↓, *ECAR∅, *other?, cycE/CCNE↑, cycA1/CCNA1↑, TumCCA↑, cycD1/CCND1↑, OXPHOS↑,
3935- RT,    Sodium rutin ameliorates Alzheimer's disease-like pathology by enhancing microglial amyloid-β clearance
- in-vivo, AD, NA
*Aβ↓, *Glycolysis↓, *OXPHOS↑, *memory↑, *BioAv↓, *BioAv↑, *cognitive↑, *Inflam↓,
3194- SFN,    Sulforaphane impedes mitochondrial reprogramming and histone acetylation in polarizing M1 (LPS) macrophages
- in-vitro, Nor, NA
*OXPHOS↑, *M1↓, *IL1β↓, *IL6↓, *NOS2↓, *TNF-α↓, *ROS↓, *NO↓, *ACC↑,
1001- SIL,    Silibinin down-regulates PD-L1 expression in nasopharyngeal carcinoma by interfering with tumor cell glycolytic metabolism
- in-vitro, NA, NA
TumCG↓, Glycolysis↓, OXPHOS↑, LDHA↓, lactateProd↓, i-citrate↑, Hif1a↓, PD-L1↓,
2413- TTT,    Tumor treating fields (TTFields) impairs aberrant glycolysis in glioblastoma as evaluated by [18F]DASA-23, a non-invasive probe of pyruvate kinase M2 (PKM2) expression
- in-vitro, GBM, U87MG
PKM2↓, Glycolysis↓, OXPHOS↑,

Showing Research Papers: 1 to 26 of 26

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 26

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   H2O2↓, 1,   HO-1↓, 1,   HO-1↑, 1,   OXPHOS↑, 19,   mt-OXPHOS↑, 2,   ROS↑, 12,   ROS⇅, 1,   SOD2↓, 1,   SOD2↑, 2,  

Metal & Cofactor Biology ⓘ

Ferritin↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 4,   ATP∅, 1,   Insulin↓, 3,   mitResp↑, 1,   MMP↓, 2,   MMP↑, 1,   OCR↑, 5,   PGC-1α↑, 2,  

Core Metabolism/Glycolysis ⓘ

ALDOA↓, 1,   AMPK↑, 2,   i-citrate↑, 1,   ECAR↓, 2,   ENO2↓, 1,   glucose↓, 1,   GlucoseCon↓, 2,   GlucoseCon↑, 1,   GLUT2↓, 1,   Glycolysis↓, 13,   HK2↓, 2,   IDH1↑, 1,   lactateProd↓, 7,   LDHA↓, 3,   LDHB↓, 1,   NADPH↓, 1,   PDH↑, 2,   PDK1↓, 1,   PDKs↓, 2,   PFK↓, 2,   PFKP↓, 1,   PGAM1↓, 1,   PGK1↓, 1,   PGM1↓, 1,   PKM2↓, 4,   PPP↓, 1,   SIRT1↑, 1,   TCA↑, 1,   Warburg↓, 5,  

Cell Death ⓘ

Apoptosis↑, 7,   Casp↑, 1,   Casp3↑, 2,   Cyt‑c↑, 2,   Cyt‑c↝, 1,   MAPK↓, 1,   PUMA↑, 1,   survivin↓, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,   tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   HSP90↓, 1,  

Autophagy & Lysosomes ⓘ

ATG3↑, 1,   Beclin-1↑, 1,   LAMP2↑, 1,   LC3s↓, 1,   p62↑, 2,   TumAuto↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 2,   P53↝, 1,  

Cell Cycle & Senescence ⓘ

cycA1/CCNA1↑, 1,   cycD1/CCND1↑, 1,   cycE/CCNE↑, 1,   TumCCA↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 2,   p‑ERK↝, 1,   HDAC↓, 1,   IGF-1↓, 2,   IGF-1↑, 1,   mTOR↓, 2,   mTORC1↓, 1,   STAT↓, 1,   STAT5↓, 1,   TumCG↓, 10,  

Migration ⓘ

Ca+2↓, 1,   Ca+2↑, 1,   Ca+2↝, 1,   Treg lymp↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 6,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 4,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   JAK1↓, 1,   M2 MC↓, 1,   PD-L1↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 4,   Dose↑, 1,   Dose↝, 2,   eff↓, 1,   eff↑, 8,   eff↝, 1,   Half-Life↝, 1,   RadioS↑, 4,   selectivity↑, 6,  

Clinical Biomarkers ⓘ

BG↓, 2,   Ferritin↓, 1,   GutMicro↑, 2,   PD-L1↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   ChemoSideEff↓, 2,   neuroP↑, 1,   OS↑, 2,   QoL↑, 1,   QoL∅, 1,   Risk↓, 1,   toxicity↓, 1,   toxicity↝, 2,   TumVol↓, 2,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 125

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   mt-antiOx↑, 1,   OXPHOS↑, 6,   ROS↓, 2,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 2,   MMP↑, 2,   OCR↑, 1,   PGC-1α↑, 2,  

Core Metabolism/Glycolysis ⓘ

ACC↑, 1,   ECAR↓, 1,   ECAR∅, 1,   FAO↑, 1,   GlucoseCon↑, 1,   Glycolysis↓, 3,   Glycolysis↑, 1,   LDHB↑, 1,   LDL↓, 1,   NAD↑, 1,   PPARα↑, 1,   TCA↑, 1,  

Cell Death ⓘ

YAP/TEAD↑, 1,  

Transcription & Epigenetics ⓘ

other?, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,   mTOR↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

CRP↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 1,   M1↓, 1,   TNF-α↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   Dose↝, 3,   eff↝, 1,  

Clinical Biomarkers ⓘ

BMD↑, 1,   CRP↓, 1,   IL6↓, 1,   NOS2↓, 1,  

Functional Outcomes ⓘ

cognitive↑, 2,   memory↑, 2,   toxicity∅, 2,  
Total Targets: 45

Scientific Paper Hit Count for: OXPHOS, Oxidative phosphorylation
5 Magnetic Fields
3 Dichloroacetate
3 Methylene blue
2 diet FMD Fasting Mimicking Diet
1 5-Aminolevulinic acid
1 Brucea javanica
1 Curcumin
1 Electrical Pulses
1 salinomycin
1 Chemotherapy
1 diet Short Term Fasting
1 Hydrogen Gas
1 Honokiol
1 Metformin
1 Proanthocyanidins
1 Resveratrol
1 Rutin
1 Sulforaphane (mainly Broccoli)
1 Silymarin (Milk Thistle) silibinin
1 Tumor Treating Fields
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#:230  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

Home Page