Sulfasalazine / Iron 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)


Iron, Iron: Click to Expand ⟱
Source:
Type:
Iron is an essential nutrient that is crucial for various cellular processes, including DNA synthesis, cell proliferation, and oxygen transport.
Cancer cells often have increased iron requirements due to their rapid growth and proliferation. Some tumors can acquire iron through various mechanisms, including upregulating iron transport proteins. This can support their growth and survival.
Excess iron can lead to the production of reactive oxygen species (ROS) through Fenton reactions, which can cause oxidative damage to DNA, proteins, and lipids. This oxidative stress can contribute to cancer development and progression.
Scientific Papers found: Click to Expand⟱
5139- SAS,    Sulfasalazine induces ferroptosis in osteosarcomas by regulating Nrf2/SLC7A11/GPX4 signaling axis
- in-vitro, OS, MG63 - in-vitro, OS, U2OS
*Inflam↓, TumCP↓, TumCMig↓, Apoptosis↑, Ferroptosis↑, Iron↑, MDA↑, ROS↑, GSH↓, SOD↓, MMP↓, NRF2↓, xCT↓, GPx4↓, FTH1↓,

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,   GSH↓, 1,   Iron↑, 1,   MDA↑, 1,   NRF2↓, 1,   ROS↑, 1,   SOD↓, 1,   xCT↓, 1,  

Metal & Cofactor Biology ⓘ

FTH1↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   Ferroptosis↑, 1,  

Migration ⓘ

TumCMig↓, 1,   TumCP↓, 1,  
Total Targets: 15

Pathway results for Effect on Normal Cells:


Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  
Total Targets: 1

Scientific Paper Hit Count for: Iron, Iron
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#:160  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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