Sulfasalazine / eff Cancer Research Results

SAS, Sulfasalazine: Click to Expand ⟱
Features:
Sulfasalazine is primarily known as an anti-inflammatory and disease‐modifying antirheumatic drug (DMARD), used for conditions such as rheumatoid arthritis and inflammatory bowel diseases (e.g., ulcerative colitis).

-Inhibit the nuclear factor kappa B (NF-κB) pathway.
-Sulfasalazine has been noted to interfere with the cystine/glutamate antiporter (system x_c⁻), which can reduce glutathione levels in cancer cells, potentially making them more susceptible to oxidative stress.

-Ability to inhibit anti-oxidant production (for ProOxidant effect).

Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 System xC− (xCT/SLC7A11 cystine–glutamate antiporter) ↓ cystine uptake Limits cystine supply Sulfasalazine is used as an xCT inhibitor; blocking cystine uptake is the core upstream action in cancer models (ref)
2 Glutathione biosynthesis / GSH pool ↓ GSH Loss of redox buffering In glioma cells, cystine uptake blockade by sulfasalazine leads to glutathione depletion (ref)
3 ROS accumulation ↑ ROS Oxidative stress amplification Glioma study: sulfasalazine increases ROS after GSH depletion (mechanistic sequence shown) (ref)
4 DNA damage (oxidative/genotoxic stress) ↑ DNA damage Checkpoint/death signaling Glioma study: sulfasalazine causes DNA damage as part of the ROS-driven cytotoxic cascade (ref)
5 Radiosensitization (oxidative vulnerability) ↑ radiation sensitivity Enhances radiotherapy effect Melanoma model: sulfasalazine decreases glutathione and synergistically enhances X-irradiation cytotoxicity (ref)
6 Ferroptosis (system xC− → GSH/GPX4 vulnerability) ↑ ferroptotic death Iron-dependent oxidative death Paclitaxel-resistant uterine serous carcinoma model: sulfasalazine (xCT inhibitor) induces ferroptotic cell death signatures (ref)
7 Mitochondrial apoptosis (caspase pathway) ↑ apoptosis Programmed cell death Osteosarcoma work: sulfasalazine blocks system xC− and induces cell death consistent with ferroptosis/apoptosis programs (apoptosis markers reported in the paper’s mechanism set) (ref)
8 NF-κB activation (IκBα degradation / IKK activity) ↓ NF-κB activation Reduced pro-survival/inflammatory transcription Mechanistic paper shows sulfasalazine blocks NF-κB activation by inhibiting IκBα degradation via IKK inhibition (ref)
9 NF-κB nuclear translocation ↓ nuclear NF-κB Transcriptional shutdown Colon cancer cells: sulfasalazine prevents TNFα-induced NF-κB nuclear translocation and NF-κB–dependent transcription (ref)
10 Chemo-sensitization via xCT inhibition ↑ chemo sensitivity (context-dependent) Combination benefit Mechanistic rationale: xCT inhibition lowers GSH and oxidative defense, increasing sensitivity to cytotoxic stress (glioma + radiation shown explicitly) (ref)
11 Tumor growth suppression in vivo (xCT-targeted stress) ↓ tumor growth Anti-tumor efficacy Glioma xenograft model: sulfasalazine plus radiosurgery improves survival compared to control/monotherapy (ref)
12 Resistance axis: xCT-high / antioxidant-high tumors ↑ vulnerability when xCT-high Targeted susceptibility Endometrial/USC model: sulfasalazine shows stronger cytotoxicity in resistant (stress-adapted) cells consistent with xCT dependence (ref)


eff, efficacy: Click to Expand ⟱
Source:
Type:
Power to enhance an anti cancer effect
Scientific Papers found: Click to Expand⟱
5042- SAS,    xCT: A Critical Molecule That Links Cancer Metabolism to Redox Signaling
- Review, Var, NA
xCT↓, GSH↓, TumCG↓, TumCI↓, ROS↑, RadioS↑, eff↓,
5138- SAS,  Rad,    Drug repurposing: sulfasalazine sensitizes gliomas to gamma knife radiosurgery by blocking cystine uptake through system Xc-, leading to glutathione depletion
- vitro+vivo, GBM, NA
cystine↓, GSH↓, ROS↑, RadioS↑, eff↓, DNAdam↑, OS↑,
5041- SAS,  Cisplatin,    Xc− inhibitor sulfasalazine sensitizes colorectal cancer to cisplatin by a GSH-dependent mechanism
- in-vitro, CRC, NA
xCT↓, Inflam↓, Apoptosis↓, GSH↓, ROS↑, TumCG↓, selectivity↑, eff↑, eff↓,

Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

cystine↓, 1,   GSH↓, 3,   ROS↑, 3,   xCT↓, 2,  

Cell Death ⓘ

Apoptosis↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 2,  

Migration ⓘ

TumCI↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

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

Functional Outcomes ⓘ

OS↑, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: eff, efficacy
3 Sulfasalazine
1 Radiotherapy/Radiation
1 Cisplatin
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#:286  Target#:961  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

Home Page