salinomycin / TumCP 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)


TumCP, Tumor Cell proliferation: Click to Expand ⟱
Source:
Type:
Tumor cell proliferation is a key characteristic of cancer. It refers to the rapid and uncontrolled growth of cells that can lead to the formation of tumors.
Scientific Papers found: Click to Expand⟱
4997- Sal,    Salinomycin Treatment Specifically Inhibits Cell Proliferation of Cancer Stem Cells Revealed by Longitudinal Single Cell Tracking in Combination with Fluorescence Microscopy
- in-vitro, BC, NA
CD24↓, TumCP↓, CSCs↓,
5127- Sal,    Salinomycin repressed the epithelial–mesenchymal transition of epithelial ovarian cancer cells via downregulating Wnt/β-catenin pathway
- in-vitro, Ovarian, NA
TumCI↓, E-cadherin↑, N-cadherin↓, Vim↓, Wnt↓, β-catenin/ZEB1↓, TumCP↓, TumCMig↓, EMT↓,
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↑,
4902- Sal,  OXA,    Salinomycin and oxaliplatin synergistically enhances cytotoxic effect on human colorectal cancer cells in vitro and in vivo
- vitro+vivo, CRC, NA
RadioS↑, ChemoSen↑, TumCP↓, Apoptosis↑, ROS↑, MMP↓, MAPK↑, eff↓, TumCG↓, TumCCA↑,
4908- Sal,    Salinomycin triggers prostate cancer cell apoptosis by inducing oxidative and endoplasmic reticulum stress via suppressing Nrf2 signaling
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145
tumCV↓, ROS↑, lipid-P↑, UPR↑, ER Stress↑, NRF2↓, NADPH↓, HO-1↓, SOD↓, Catalase↓, GPx↓, eff↓, TumCP↓,
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 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   GPx↓, 1,   HO-1↓, 1,   lipid-P↑, 1,   NRF2↓, 1,   ROS↑, 4,   SOD↓, 1,   SOD1↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 2,   MMP↓, 2,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   NADPH↓, 1,  

Cell Death ⓘ

Apoptosis↑, 3,   Bcl-2↓, 1,   MAPK↑, 1,   Myc↓, 1,   necrosis↑, 1,   p27↑, 1,   survivin↓, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

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

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

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

Cell Cycle & Senescence ⓘ

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

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 2,   CD24↓, 1,   CSCs↓, 2,   CSCs↑, 1,   EMT↓, 1,   Gli1↓, 1,   GSK‐3β↓, 1,   mTOR↓, 1,   PTCH1↓, 1,   Smo↓, 1,   TumCG↓, 3,   Wnt↓, 2,  

Migration ⓘ

Ca+2↑, 1,   E-cadherin↑, 1,   GLI2↓, 1,   N-cadherin↓, 1,   Snail↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 6,   TumMeta↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

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

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 3,   eff↓, 2,   eff↑, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   Myc↓, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,  
Total Targets: 67

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TumCP, Tumor Cell proliferation
6 salinomycin
1 Oxaliplatin
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#:327  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

Home Page