Selenite (Sodium) / ROS Cancer Research Results

SSE, Selenite (Sodium): Click to Expand ⟱
Features:
Sodium Selenite - is inorganic selenium in the selenite oxidation state (Se⁴⁺)
Sodium selenite is produced industrially from selenium metal, which itself is obtained as a by-product of copper refining.
Mechanistic distinction from Selenium:
-Selenite reacts with GSH → GS–Se–SG intermediates
-Generates superoxide, H₂O₂
-Exploits cancer cells’ elevated basal oxidative stress
-Normal cells neutralize it more effectively (higher redox reserve)

Both the uptake and processing of selenium has recently shown to be upregulated in subsets of cancer cells
 due to their increased expression of xCT transporter
The more a tumor depends on xCT, the more toxic selenite becomes. High xCT Also Increases SSE Toxicity. High xCT increases intracellular thiols, which increases SSE chemical trapping, redox cycling, and cytotoxic impact.

Sodium selenite might protect against toxicity of AgNPs. also here


SSE and cancer
Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 Redox cycling with thiols (superoxide generation) ↑ O2•− / ↑ ROS Acute oxidative stress Defines sodium selenite anticancer mechanism in many models: early superoxide rise precedes mitochondrial apoptotic events (ref)
2 Glutathione buffering (GSH pool) ↓ GSH Loss of redox buffering Work in hepatoma models demonstrates GSH’s key role in selenite-driven oxidative stress and apoptosis (ref)
3 Mitochondrial integrity (ΔΨm) ↓ ΔΨm Mitochondrial dysfunction Sequential mechanism shown: superoxide rise → mitochondrial depolarization (ref)
4 Intrinsic apoptosis (cytochrome c → Caspase-9/3) ↑ cytochrome c release / ↑ Caspase-9/3 Programmed cell death Same sequential model shows cytochrome c release followed by caspase-9 and caspase-3 activation (ref)
5 ER stress / UPR (PERK → eIF2α → ATF4) ↑ PERK/eIF2α/ATF4 Proteotoxic stress signaling ER-stress module is shown as a core driver in selenite-induced autophagy→apoptosis progression (ref)
6 Stress MAPK (p38) as switch control ↑ p38 activation Signal switching (autophagy → apoptosis) Mechanistic evidence for p38 participating in the selenite-driven transition toward apoptosis (ref)
7 p53 activation (stress response) ↑ p53 phosphorylation (Ser15) Facilitates apoptosis programs NB4 leukemia model: selenite induces p53 Ser15 phosphorylation via p38/ERK in the autophagy–apoptosis switch context (ref)
8 DNA damage response (ATM-dependent signaling) ↑ ATM-dependent DDR Checkpoint activation & death signaling Selenium compounds (including selenite contexts) activate ATM-dependent DNA damage response signaling in colorectal cancer models (ref)
9 PI3K–AKT axis linked to autophagy/apoptosis balance ↓ PI3K/Akt (functional axis) / ↓ protective autophagy Apoptosis sensitization NB4 leukemia: sodium selenite increases apoptosis by autophagy inhibition through PI3K/Akt (ref)
10 NF-κB signaling ↓ NF-κB Reduced anti-apoptotic transcription Mechanistic study: sodium selenite induces ROS-mediated inhibition of NF-κB with downstream shift toward apoptosis (ref)
11 Angiogenesis signaling (VEGF) ↓ VEGF expression Reduced vascular support signals Prostate cancer PC3 model: sodium selenite inhibits expression of VEGF (and related inflammatory/pro-growth factors) in the tested context (ref)
12 Ferroptosis (iron-dependent oxidative death) ↑ ferroptosis Non-apoptotic oxidative death modality Paper explicitly reports sodium selenite as an inducer of ferroptosis across multiple human cancer cell types (ref)

Table to compare Sodium Selenite to SeNPs
-Sodium selenite → chemical oxidant (thiol attack → ROS shock).
-SeNPs → engineered redox stressor (signaling-level control, broader window).
-Selenomethionine / Se-yeast → redox buffer & selenium storage form (often protective to cancer cells, especially when oxidative stress is a therapeutic goal).
Dimension Sodium Selenite (Na2SeO3) Selenium Nanoparticles (SeNPs) Selenomethionine / Se-Yeast
Primary mechanistic class Direct redox-disrupting agent Controlled redox modulator / signaling perturbator Nutritional selenium reservoir / selenoprotein precursor
Initial molecular interaction Rapid reaction with cellular thiols (GSH, Trx, protein –SH) Cellular uptake → gradual selenium release or surface redox effects Nonspecific incorporation into proteins in place of methionine
ROS generation ↑↑ acute, non-buffered ROS burst ↑ mild–moderate, sustained ROS ↓ or ↔ (antioxidant bias)
Glutathione (GSH) system ↓↓ GSH depletion ↔ or mild ↓ (context-dependent) ↑ GSH recycling via GPX support
Redox selectivity (cancer vs normal) Limited; toxicity threshold close to efficacy Improved tumor selectivity window Poor for cancer killing; favors normal-cell protection
Mitochondrial integrity (ΔΨm) ↓↓ rapid depolarization ↓ gradual, dose-dependent disruption ↔ or ↑ mitochondrial protection
Dominant cell-death pathways Intrinsic apoptosis ± necrosis (high dose) Apoptosis ± ferroptosis ± autophagy-related death None (cytoprotective)
ER stress / UPR (PERK–CHOP) ↑ strong, early activation ↑ moderate, delayed activation ↓ ER stress via antioxidant capacity
DNA damage response ↑ oxidative DNA lesions (ATM/ATR) ↑ low–moderate, secondary to ROS ↓ DNA damage; improved repair environment
PI3K–AKT survival signaling ↓ secondary to oxidative collapse ↓ reported in multiple tumor models ↔ or ↑ survival signaling
NF-κB / inflammatory signaling ↓ via redox inhibition ↓ selectively; anti-inflammatory bias ↓ chronic inflammation (protective)
Ferroptosis involvement Minor / indirect ↑ lipid peroxidation; GPX4 modulation ↓↓ ferroptosis risk (GPX4 support)
Autophagy ↑ early (protective) → collapse ↑ contributory to tumor suppression ↔ homeostatic maintenance
Angiogenesis (VEGF) ↓ at cytotoxic doses ↓ at lower, tolerated doses ↔ or mild ↓ (indirect)
Immune compatibility Poor at anticancer doses Moderate–good; often immune-supportive High; supports immune competence
Pharmacologic control Poor (steep dose–toxicity curve) High (size, coating, release tunable) Low (slow turnover, storage form)
Normal tissue tolerance Low Moderate–high High
Overall cancer relevance Potent but hazardous cytotoxic agent Balanced anticancer redox modulator Generally counterproductive for direct cancer killing
Overall therapeutic profile Potent but narrow safety margin Lower acute potency, broader usable window


ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
4434- AgNPs,  SSE,    Sodium Selenite Ameliorates Silver Nanoparticles Induced Vascular Endothelial Cytotoxic Injury by Antioxidative Properties and Suppressing Inflammation Through Activating the Nrf2 Signaling Pathway
- vitro+vivo, Nor, NA
*ROS↓, *Inflam↓, *NLRP3↓, *NF-kB↓, *NRF2↑, *HO-1↑, *toxicity↓,
4714- Se,  SSE,  SeNPs,    Selenium in cancer management: exploring the therapeutic potential
- Review, Var, NA
Risk↓, *BioAv↑, eff↝, *ROS↓, MMP↓, ROS↑, P53↑, *toxicity↓, TumCP↓, Casp↑, Apoptosis↑,
5082- SSE,    Rationale for the treatment of cancer with sodium selenite
- Review, Var, NA
Risk↑, antiOx↑, ROS↑, Imm↑, NK cell↑, angioG↓, toxicity↓,
5088- SSE,    Superoxide-mediated ferroptosis in human cancer cells induced by sodium selenite
- in-vitro, BC, MCF-7 - in-vitro, GBM, U87MG - in-vitro, Pca, PC3 - in-vitro, Cerv, HeLa - in-vitro, GBM, A172
Ferroptosis↑, ROS↑, Iron↑, xCT↓, GSH↓, GPx4↓, lipid-P↑, TumCP↓, selectivity↑,
5087- SSE,    Sodium Selenite Alleviates Breast Cancer-Related Lymphedema Independent of Antioxidant Defense System
- Trial, BC, NA
eff↑, Inflam↓, Imm↑, ROS↑, *NK cell↑,
5086- SSE,    Sodium Selenite Induces Superoxide-Mediated Mitochondrial Damage and Subsequent Autophagic Cell Death in Malignant Glioma Cells
- in-vitro, GBM, U87MG - in-vitro, GBM, T98G - in-vitro, GBM, A172
TumAuto↑, ROS↑, TumCD↑, tumCV↓, selectivity↑, MMP↓, eff↓, MitoP↑,
5085- SSE,    Intravenous Infusion of High Dose Selenite in End-Stage Cancer Patients: Analysis of Systemic Exposure to Selenite and Seleno-Metabolites
- Review, Var, NA
toxicity↝, Half-Life↝, ROS↑, Thiols↓, NADPH↓, toxicity↝, other↝,
5084- SSE,  GEM,    The Antitumor Activity of Sodium Selenite Alone and in Combination with Gemcitabine in Pancreatic Cancer: An In Vitro and In Vivo Study
- in-vitro, PC, PANC1 - vitro+vivo, PC, Panc02
tumCV↓, ChemoSen↑, TumCG↓, OS↑, MMP↓, AIF↑, GSH↓, Trx↓, ROS↑, AntiTum↑,
5083- SSE,    Sodium Selenite as an Anticancer Agent
- Review, Var, NA
AntiCan↑, ROS↑,
5090- SSE,    Sodium Selenite Induces Ferroptosis in Non-small Cell Lung Cancer A549 Cells Via Reactive Oxygen Species (ROS)/Glutathione (GSH)/Glutathione Peroxidase4 (GPx4) Axis
- NA, Lung, A549
TumCP↓, ROS↑, GSH↓, MMP↓, GPx4↓, Iron↑,
5081- SSE,    Application Notes and Protocols: Selenite as a Selenium Source in Cell Culture Media Supplementation
- Review, Var, NA
Dose↝, ROS↑, Akt↓, mTOR↓, TumCCA↑, Apoptosis↑,
5080- SSE,    Sodium Selenite Regulates the Proliferation and Apoptosis of Gastric Cancer Cells by Suppressing the Expression of LncRNA HOXB-AS1
- in-vitro, GC, HGC27 - in-vitro, GC, NCI-N87
AntiTum↑, HOXB-AS1↓, TumCP↓, TumCI↓, Apoptosis↑, BAD↓, Bcl-2↓, cl‑Casp3↑, MMP2↓, E-cadherin↑, N-cadherin↓, ROS↑, NF-kB↓,
5079- SSE,  Rad,    The solvent and treatment regimen of sodium selenite cause its effects to vary on the radiation response of human bronchial cells from tumour and normal tissues
- in-vitro, Lung, A549 - in-vitro, Nor, BEAS-2B
chemoP↑, eff↝, ROS↑, MMP↓, Cyt‑c↑, TumCG↓, RadioS↝, other↝,
5078- SSE,  Rad,    Results from a Phase 1 Study of Sodium Selenite in Combination with Palliative Radiation Therapy in Patients with Metastatic Cancer
- Trial, Pca, NA
Half-Life↝, OS↑, Pain↓, PSA↓, GSH↓, ROS↑, selectivity↑, TumCG↓, AR↓, Dose↑, ChemoSen↑, RadioS↑,
5075- SSE,    Sodium selenite inhibits proliferation and metastasis through ROS‐mediated NF‐κB signaling in renal cell carcinoma
- vitro+vivo, RCC, 786-O
TumCP↓, TumCMig↓, Apoptosis↑, ROS↑, NF-kB↓, eff↓, E-cadherin↑, cl‑Casp3↑, VEGF↓, MMP9↓, EMT↓, MMP↓, mtDam↑, BAX↑, Bcl-2↓,
5074- SSE,    Application of Sodium Selenite in the Prevention and Treatment of Cancers
- Review, Var, NA
Imm↑, angioG↑, DNArepair↑, NK cell↑, ROS↑, AntiCan↑, selectivity↑, ER Stress↑, TumAuto↑, necrosis↑, toxicity↝, Dose↑,
5111- SSE,    Sodium selenite induces apoptosis via ROS-mediated NF-κB signaling and activation of the Bax-caspase-9-caspase-3 axis in 4T1 cells
- in-vitro, BC, 4T1
ROS↑, NF-kB↓, p65↓, mtDam↑, Casp9↑, Casp3↑, Apoptosis↑, eff↓,
5109- SSE,    Selenium compounds activate ATM-dependent DNA damage response via the mismatch repair protein hMLH1 in colorectal cancer cells
- in-vitro, CRC, HCT116
ROS↑, DNAdam↓, ATM↑, eff↓, TumCCA↑,
5106- SSE,  GSH,    Dual role of glutathione in selenite-induced oxidative stress and apoptosis in human hepatoma cells
- in-vitro, Liver, HepG2
ROS↑, Apoptosis↑, eff↑, GSH↓,
5105- SSE,    Sodium selenite induces apoptosis by generation of superoxide via the mitochondrial-dependent pathway in human prostate cancer cells
- in-vitro, Pca, LNCaP
TumCD↑, Apoptosis↑, ROS↑, eff↓, MMP↓, Cyt‑c↑, Casp3↑, Casp9↑, ER Stress↑, TumAuto↑, necrosis↑, chemoPv↑,
5089- SSE,  Se,    Redox-mediated effects of selenium on apoptosis and cell cycle in the LNCaP human prostate cancer cell line
- in-vitro, Pca, LNCaP
ROS↑, mtDam↑, TumCD↑, Apoptosis↑, TumCCA↑, Trx↓, angioG↓, GSH⇅, NADPH↓, GPx↑,
5096- SSE,    Selenium Toxicity Accelerated by Out-of-Control Response of Nrf2-xCT Pathway
- in-vitro, BC, MCF-7
xCT↑, ROS↑, NRF2↑,
5095- SSE,    Extracellular thiol-assisted selenium uptake dependent on the xc− cystine transporter explains the cancer-specific cytotoxicity of selenite
- in-vitro, Lung, H157
toxicity↝, eff↓, other↝, ROS↑, mtDam↑,
5093- SSE,    Pharmacological mechanisms of the anticancer action of sodium selenite against peritoneal cancer in mice
- in-vivo, Var, NA
AntiCan↑, eff↑, selectivity↑, ROS↑, Dose↝, Trx↓, GSH↓,
5092- SSE,    Redox-Active Selenium Compounds—From Toxicity and Cell Death to Cancer Treatment
- Review, Var, NA
*antiOx↑, ROS↑, GSH↓, BioAv↓,
5091- SSE,    Superoxide-mediated ferroptosis in human cancer cells induced by sodium selenite
- in-vitro, GBM, U87MG - in-vitro, Cerv, HeLa - in-vitro, BC, MCF-7 - in-vitro, Pca, PC3 - in-vitro, CRC, HT-29 - in-vitro, Nor, SVGp12
Ferroptosis↑, xCT↓, GSH↓, GPx4↓, Iron↑, lipid-P↑, ROS↑, eff↓, TumCP↓, TumCD↑,
4498- SSE,    Selenium in Human Health and Gut Microflora: Bioavailability of Selenocompounds and Relationship With Diseases
- Review, Var, NA - Review, AD, NA - Review, IBD, NA
*Imm↑, *GutMicro↑, *BioAv↑, *Risk↓, *Dose↝, Risk↓, *CRP↓, *GPx↓, *Inflam↓, *selenoP↑, *Dose↝, *ROS↓, *MDA↓, *SOD↑, *GPx↑, *IL1↓, *MCP1↓, *IL6↓, *TNF-α↓, Risk↓, *neuroP↑, *memory↑,
4497- SSE,    Selenium and inflammatory bowel disease
- Review, Var, NA - Review, IBD, NA
*GutMicro↑, *selenoP↑, *Inflam↓, Risk↓, *NF-kB↓, *ROS↓,
4494- SSE,    Advances in the study of selenium and human intestinal bacteria
- Review, IBD, NA - Review, Var, NA
*Risk↓, OS↑, *CRP↓, *GPx↑, *Inflam↓, *ROS↓, *GutMicro↑, *selenoP↑, *other↓,
1018- SSE,    Selenite-induced autophagy antagonizes apoptosis in colorectal cancer cells in vitro and in vivo
- vitro+vivo, CRC, HCT116 - vitro+vivo, CRC, SW480
TumAuto↑, LC3s↑, TumW↓, Weight∅, Beclin-1↑, p62↓, ROS↑,
1017- SSE,    Selenite induces apoptosis in colorectal cancer cells via AKT-mediated inhibition of β-catenin survival axis
- vitro+vivo, CRC, NA
Akt↓, β-catenin/ZEB1↓, cycD1/CCND1↓, survivin↓, Apoptosis↑, ROS↑,
1002- SSE,  Osi,  Adag,    Selenite as a dual apoptotic and ferroptotic agent synergizes with EGFR and KRAS inhibitors with epigenetic interference
- in-vitro, Lung, H1975 - in-vitro, Lung, H385
Apoptosis↑, Ferroptosis↑, DNMT1↓, TET1↑, TumCCA↑, cl‑PARP↑, cl‑Casp3↑, Cyt‑c↑, BIM↑, NOXA↑, Apoptosis↑, ROS↑, ER Stress↑, UPR↑,
4742- SSE,    Antitumor Effects of Selenium
- Review, Var, NA - Review, Arthritis, NA - Review, Sepsis, NA
*antiOx↓, *Inflam↓, Risk↓, TumCI↓, TumMeta↓, radioP↑, chemoP↑, Apoptosis↑, ROS↑, DNAdam↑, Dose↑, selectivity↑, *other↓, *BioAv↑, ROS↑, MMP↓, Casp↑, *Imm↑, *Pain↓, Sepsis↓, MMP2↓, MMP9↓, *Half-Life↓,
4739- SSE,  Chemo,  Rad,    Therapeutic Benefits of Selenium in Hematological Malignancies
- Review, Var, NA
ChemoSen↑, radioP↑, QoL↑, Risk↓, *selenoP↑, TumCP↓, Inflam↓, ChemoSen↑, TumCCA↑, Apoptosis↑, angioG↓, Dose⇅, ROS↑, eff↑, Risk↓, eff∅, CSCs↓, ROS↑,
4614- SSE,  Rad,    Updates on clinical studies of selenium supplementation in radiotherapy
- Review, Nor, NA
*toxicity∅, Risk↓, *selenoP↑, *ROS↓, *DNAdam↓, *QoL↑, *radioP↑, *Dose↝,
4731- SSE,    Dietary selenium mitigates cadmium-induced apoptosis and inflammation in chicken testicles by inhibiting oxidative stress through the activation of the Nrf2/HO-1 signaling pathway
- in-vivo, Nor, NA
*ROS↓, *MDA↓, *H2O2↓, *Catalase↑, *GSH↑, *NRF2↑, *HO-1↑, *Bcl-2↑, *other↝,
4723- SSE,    Selenium Induces Ferroptosis in Colorectal Cancer Cells via Direct Interaction with Nrf2 and Gpx4
- in-vitro, CRC, HCT116
TumCP↓, Iron↑, MDA↑, ROS↑, MMP↓, NRF2↓, GPx4↓, Ferroptosis↑,
4718- SSE,    High-Dose Selenium Induces Ferroptotic Cell Death in Ovarian Cancer
- in-vitro, Ovarian, NA
TumCP↑, ROS↑, GPx↓, lipid-P↑, Ferroptosis↑, Dose↑,
4716- SSE,    Selenium Substitution During Radiotherapy of Solid Tumours – Laboratory Data from Two Observation Studies in Gynaecological and Head and Neck Cancer Patients
- in-vivo, HNSCC, NA
Dose↝, *GPx↑, *ROS↓,
4468- VitC,  SSE,    Selenium modulates cancer cell response to pharmacologic ascorbate
- in-vivo, GBM, U87MG - in-vitro, CRC, HCT116
eff↓, TumCD↑, ChemoSen↑, ROS⇅, DNAdam↑, PARP↑, NAD↓, Glycolysis↓, Fenton↑, lipid-P↑, eff↓, H2O2↑, other↝,

Showing Research Papers: 1 to 40 of 40

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 40

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Fenton↑, 1,   Ferroptosis↑, 5,   GPx↓, 1,   GPx↑, 1,   GPx4↓, 4,   GSH↓, 8,   GSH⇅, 1,   H2O2↑, 1,   Iron↑, 4,   lipid-P↑, 4,   MDA↑, 1,   NRF2↓, 1,   NRF2↑, 1,   ROS↑, 34,   ROS⇅, 1,   Thiols↓, 1,   Trx↓, 3,   xCT↓, 2,   xCT↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   MMP↓, 9,   mtDam↑, 4,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,   NAD↓, 1,   NADPH↓, 2,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 13,   BAD↓, 1,   BAX↑, 1,   Bcl-2↓, 2,   BIM↑, 1,   Casp↑, 2,   Casp3↑, 2,   cl‑Casp3↑, 3,   Casp9↑, 2,   Cyt‑c↑, 3,   Ferroptosis↑, 5,   necrosis↑, 2,   NOXA↑, 1,   survivin↓, 1,   TumCD↑, 5,  

Transcription & Epigenetics ⓘ

other↝, 4,   tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 3,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3s↑, 1,   MitoP↑, 1,   p62↓, 1,   TumAuto↑, 4,  

DNA Damage & Repair ⓘ

ATM↑, 1,   DNAdam↓, 1,   DNAdam↑, 2,   DNArepair↑, 1,   DNMT1↓, 1,   P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 1,   HOXB-AS1↓, 1,   mTOR↓, 1,   TumCG↓, 3,  

Migration ⓘ

E-cadherin↑, 2,   MMP2↓, 2,   MMP9↓, 2,   N-cadherin↓, 1,   TET1↑, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 8,   TumCP↑, 1,   TumMeta↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   angioG↑, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

Imm↑, 3,   Inflam↓, 2,   NF-kB↓, 3,   NK cell↑, 2,   p65↓, 1,   PSA↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 5,   Dose↑, 4,   Dose⇅, 1,   Dose↝, 3,   eff↓, 9,   eff↑, 4,   eff↝, 2,   eff∅, 1,   Half-Life↝, 2,   RadioS↑, 1,   RadioS↝, 1,   selectivity↑, 6,  

Clinical Biomarkers ⓘ

AR↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 3,   AntiTum↑, 2,   chemoP↑, 2,   chemoPv↑, 1,   OS↑, 3,   Pain↓, 1,   QoL↑, 1,   radioP↑, 2,   Risk↓, 8,   Risk↑, 1,   toxicity↓, 1,   toxicity↝, 4,   TumW↓, 1,   Weight∅, 1,  

Infection & Microbiome ⓘ

Sepsis↓, 1,  
Total Targets: 117

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 1,   Catalase↑, 1,   GPx↓, 1,   GPx↑, 3,   GSH↑, 1,   H2O2↓, 1,   HO-1↑, 2,   MDA↓, 2,   NRF2↑, 2,   ROS↓, 8,   selenoP↑, 5,   SOD↑, 1,  

Cell Death ⓘ

Bcl-2↑, 1,  

Transcription & Epigenetics ⓘ

other↓, 2,   other↝, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Immune & Inflammatory Signaling ⓘ

CRP↓, 2,   IL1↓, 1,   IL6↓, 1,   Imm↑, 2,   Inflam↓, 5,   MCP1↓, 1,   NF-kB↓, 2,   NK cell↑, 1,   TNF-α↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 3,   Dose↝, 3,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

CRP↓, 2,   GutMicro↑, 3,   IL6↓, 1,  

Functional Outcomes ⓘ

memory↑, 1,   neuroP↑, 1,   Pain↓, 1,   QoL↑, 1,   radioP↑, 1,   Risk↓, 2,   toxicity↓, 2,   toxicity∅, 1,  
Total Targets: 41

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
40 Selenite (Sodium)
4 Radiotherapy/Radiation
2 Selenium
1 Silver-NanoParticles
1 Selenium NanoParticles
1 Gemcitabine (Gemzar)
1 Glutathione
1 Osimertinib
1 Adagrasib
1 Chemotherapy
1 Vitamin C (Ascorbic Acid)
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#:148  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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