salinomycin / ATP Cancer Research Results

Sal, salinomycin: Click to Expand ⟱
Features:
Salinomycin is a polyether ionophore antibiotic that is produced by the bacterium Streptomyces albus. It was first isolated in 1979 and has been found to have a range of biological activities, including antibacterial, antifungal, and anticancer properties.
It has been shown to induce apoptosis (programmed cell death) in a range of cancer cell lines, including breast, lung, and colon cancer cells. Salinomycin has also been found to inhibit the growth of cancer stem cells.
Salinomycin, a widely used antibiotic in poultry farming
Actions:
-Strong activity against cancer stem cells
-Disrupts mitochondrial ion gradients → ROS
-Non-thiol, non-NRF2 dominant

Key pathways
-Mitochondrial K⁺ dysregulation
-ROS-mediated apoptosis
-Wnt/β-catenin inhibition

Chemo relevance
-Generally compatible or synergistic
-Not a redox buffer

Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 K+ ionophore activity / ionic homeostasis ↑ K+ transport (ionophore) / ↓ intracellular K+ homeostasis Electrochemical disruption Salinomycin is directly described as a potassium ionophore in mechanistic studies of its anticancer effects (ref)
2 Cancer stem cell (CSC) fraction / stemness programs ↓ CSC proportion / tumor-initiating capacity Selective CSC depletion Landmark study showing salinomycin strongly reduces CSC proportion (e.g., >100-fold vs paclitaxel in their assay context) and inhibits tumor growth in vivo (ref)
3 Wnt/β-catenin signaling ↓ Loss of self-renewal signaling Primary mechanistic paper identifying salinomycin as an inhibitor of the Wnt signaling cascade (ref)
4 Wnt co-receptor LRP6 (Wnt pathway control point) ↓ LRP6 / ↓ Wnt signaling Wnt pathway suppression Shows salinomycin suppresses LRP6 expression at concentrations relevant to growth inhibition, linking activity to Wnt/β-catenin suppression (ref)
5 Autophagic flux + lysosomal proteolysis ↓ autophagic flux (blocked) / ↓ lysosomal proteolytic activity Abortive autophagy / stress accumulation Demonstrates salinomycin blocks autophagic flux and lysosomal proteolytic activity in breast cancer CSC and non-CSC populations (ref)
6 ER stress / UPR (ATF4 → CHOP/DDIT3) ↑ ER stress / ↑ CHOP axis Proteotoxic stress signaling Shows salinomycin stimulates ER stress and mediates autophagy through the ATF4–CHOP–TRIB3 axis (ref)
7 AKT–mTOR survival signaling (via TRIB3) ↓ AKT / ↓ mTOR signaling Reduced survival + altered autophagy control Same mechanistic work links ER stress activation to TRIB3-mediated inhibition of AKT1–mTOR signaling after salinomycin exposure (ref)
8 ROS generation and ROS-linked lysosomal dysfunction ↑ ROS Oxidative stress amplification Demonstrates salinomycin-induced ROS and connects ROS to lysosomal membrane permeability and impaired autophagy flux (ref)
9 Mitochondrial apoptosis (caspase cascade) ↑ Caspase-9/3 activation Programmed cell death Shows salinomycin triggers caspase-dependent apoptosis involving caspases (including 9 and 3) in a salinomycin toxicity/mechanism study (demonstrates directionality for caspase activation) (ref)
10 EMT phenotype ↑ E-cadherin / ↓ vimentin (EMT suppressed) Reduced migration/invasion Reports salinomycin increases epithelial markers and decreases mesenchymal markers in a dose-dependent manner, with reduced migration/invasion (ref)
11 ABC transporter–mediated multidrug resistance ↓ functional MDR phenotype Overcomes drug resistance Directly reports salinomycin overcomes ABC transporter–mediated multidrug/apoptosis resistance in leukemia stem cell–like cells (ref)
12 Ferroptosis susceptibility (GPX4 axis) in CSC context ↑ ferroptosis (context-dependent) Non-apoptotic oxidative death modality Reports salinomycin induces ferroptosis in a CSC context via a pathway converging on GPX4/GPX activity regulation (directionality: ferroptosis induction by salinomycin in that model) (ref)


ATP, Adenosine triphosphate: Click to Expand ⟱
Source:
Type:
Adenosine triphosphate (ATP) is the source of energy for use and storage at the cellular level.
Cellular ATP levels are critical for cell survival, and several reports have shown that reductions in cellular ATP levels can lead to apoptosis and other types of cell death in cancer cells, depending on the level of depletion.
Adenosine triphosphate (ATP) is one of the main biochemical components of the tumor microenvironment (TME), where it can promote tumor progression or tumor suppression depending on its concentration and on the specific ecto-nucleotidases and receptors expressed by immune and cancer cells.

Cancer cells, unlike normal cells, derive as much as 60% of their ATP from glycolysis via the “Warburg effect”, and the remaining 40% is derived from mitochondrial oxidative phosphorylation.
Scientific Papers found: Click to Expand⟱
5125- Sal,    Salinomycin induced ROS results in abortive autophagy and leads to regulated necrosis in glioblastoma
- in-vitro, GBM, NA
ER Stress↑, UPR↑, autoF↓, lysosome↝, ROS↑, lipid-P↑, CSCs↓, necrosis↑, ATP↓, MMP↓, MOMP↑, DNAdam↑, AIF↑, lysoMP↑, MitoP↑, Ca+2↑,
4898- Sal,    Salinomycin as a potent anticancer stem cell agent: State of the art and future directions
- Review, Var, NA
CSCs↓, AntiCan↑, ChemoSen↑, RadioS↑, Wnt↓, MAPK↓, TumAuto↑, ATP↓, ROS↑, DNAdam↑, ER Stress↑, CSCsMark↓, Iron↑, *toxicity↝,
4900- Sal,    Anticancer Mechanisms of Salinomycin in Breast Cancer and Its Clinical Applications
- Review, BC, NA
CSCs↓, Apoptosis↑, TumAuto↑, necrosis↑, TumCP↓, TumCI↓, TumCMig↓, TumCG↓, TumMeta↓, eff↑, Bcl-2↓, cMyc↓, Snail↓, ALDH↓, Myc↓, AR↓, ROS↑, NF-kB↓, PTCH1↓, Smo↓, Gli1↓, GLI2↓, Wnt↓, mTOR↓, GSK‐3β↓, cycD1/CCND1↓, survivin↓, P21↑, p27↑, CHOP↑, Ca+2↑, DNAdam↑, Hif1a↓, VEGF↓, angioG↓, MMP↓, ATP↓, p‑P53↑, γH2AX↑, ChemoSen↑,
4903- Sal,    Salinomycin: A new paradigm in cancer therapy
- Review, Var, NA
TumCG↓, ATP↓, CSCs↓, ROS↑, Casp↑, MMP↓, selectivity↑, OXPHOS↓, STAT3↓, P53↑, γH2AX↑, cycD1/CCND1↓, TumCCA↑, DNAdam↑, ChemoSen↑,
4909- Sal,    Salinomycin: Anti-tumor activity in a pre-clinical colorectal cancer model
- vitro+vivo, CRC, NA
AntiTum↑, Apoptosis↑, mtDam↑, ROS↑, SOD1↓, ChemoSen↑, CSCs↑, ALDH↓, TumCG↓, TumCP↓, TumCD↑, ATP↓,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Iron↑, 1,   lipid-P↑, 1,   OXPHOS↓, 1,   ROS↑, 5,   SOD1↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 5,   MMP↓, 3,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,  

Cell Death ⓘ

Apoptosis↑, 2,   Bcl-2↓, 1,   Casp↑, 1,   lysoMP↑, 1,   MAPK↓, 1,   MOMP↑, 1,   Myc↓, 1,   necrosis↑, 2,   p27↑, 1,   survivin↓, 1,   TumCD↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 2,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

autoF↓, 1,   lysosome↝, 1,   MitoP↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 4,   P53↑, 1,   p‑P53↑, 1,   γH2AX↑, 2,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 2,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 2,   CSCs↓, 4,   CSCs↑, 1,   CSCsMark↓, 1,   Gli1↓, 1,   GSK‐3β↓, 1,   mTOR↓, 1,   PTCH1↓, 1,   Smo↓, 1,   STAT3↓, 1,   TumCG↓, 3,   Wnt↓, 2,  

Migration ⓘ

Ca+2↑, 2,   GLI2↓, 1,   Snail↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 4,   eff↑, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   Myc↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,  
Total Targets: 67

Pathway results for Effect on Normal Cells:


Functional Outcomes ⓘ

toxicity↝, 1,  
Total Targets: 1

Scientific Paper Hit Count for: ATP, Adenosine triphosphate
5 salinomycin
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#:203  Target#:21  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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