immunotherapy / OXPHOS Cancer Research Results

immuno, immunotherapy: Click to Expand ⟱
Features: 
Immunotherapy is not one drug class. It includes:
-Immune checkpoint inhibitors (PD-1, PD-L1, CTLA-4)
-CAR-T therapies
-Monoclonal antibodies
-Cytokine therapies (IL-2, IFN-α)
-Cancer vaccines
-Bispecific T-cell engagers
PD-1 blockade antibody therapy is one of the cornerstone approaches in modern cancer immunotherapy.
Under normal physiological conditions, when PD-1 binds to its ligands (PD-L1 or PD-L2) on other cells, it functions as a "checkpoint" to reduce overly active T cell responses and prevent autoimmunity.
PD-1 blockade therapies involve monoclonal antibodies that target either PD-1 or its ligand PD-L1.
• By blocking the interaction between PD-1 and its ligands, these antibodies effectively release the "brakes" on T cells.
• The re-activated T cells can then recognize and destroy cancer cells more efficiently.

Immunotherapy Class Example Agents Primary Target Core Mechanism Interaction Considerations Net Effect
PD-1 inhibitors Nivolumab, Pembrolizumab PD-1 receptor on T cells Blocks inhibitory PD-1 signaling → restores cytotoxic T-cell activity High-dose steroids or strong immunosuppressants may blunt effect; autoimmune risk ↑ Anti-tumor immune activation
PD-L1 inhibitors Atezolizumab, Durvalumab PD-L1 on tumor/immune cells Prevents PD-L1 from engaging PD-1 → enhances T-cell response Similar immune-related adverse event (irAE) profile as PD-1 inhibitors ↑ Immune activation
CTLA-4 inhibitors Ipilimumab CTLA-4 checkpoint Enhances early T-cell priming in lymph nodes Higher autoimmune toxicity risk vs PD-1 class ↑ T-cell priming
CAR-T therapy CD19 CAR-T products Tumor antigen (e.g., CD19) Genetically engineered T cells directly target tumor cells Risk of cytokine release syndrome (CRS) and neurotoxicity Direct immune-mediated tumor killing
Monoclonal antibodies (non-checkpoint) Trastuzumab, Rituximab Specific tumor antigens Antibody-dependent cellular cytotoxicity (ADCC) or receptor blockade Combination with chemo common; immune activation depends on Fc engagement Targeted immune-mediated killing
Cytokine therapy IL-2, IFN-α Immune activation pathways Stimulates T-cell and NK cell proliferation High systemic toxicity; rarely used now vs checkpoint inhibitors Broad immune stimulation
Cancer vaccines mRNA or peptide-based Tumor antigens Induces tumor-specific immune memory Often combined with checkpoint blockade Adaptive immune priming
Bispecific T-cell engagers Blinatumomab CD3 + tumor antigen Bridges T cells directly to tumor cells CRS risk; continuous infusion in some protocols Direct T-cell redirection


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⟱
6203- Cuc,  immuno,    Isocucurbitacin B targets STAT3 to induce ferroptosis and promote anti-PD1 immunotherapy responses in breast cancer
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549 - in-vivo, BC, 4T1
Ferroptosis↑, STAT3↓, GPx4↓, Imm↑, PD-L1↓, TumCG↓, ATP↓, OXPHOS↓,

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:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GPx4↓, 1,   OXPHOS↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,  

Cell Death ⓘ

Ferroptosis↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

STAT3↓, 1,   TumCG↓, 1,  

Immune & Inflammatory Signaling ⓘ

Imm↑, 1,   PD-L1↓, 1,  

Clinical Biomarkers ⓘ

PD-L1↓, 1,  
Total Targets: 10

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: OXPHOS, Oxidative phosphorylation
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#:207  Target#:230  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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