Database Query Results : Selenite (Sodium), ,

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


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↑,
4459- SeNPs,  VitC,  SSE,    Nano and mesosized selenium and its synthesis using the ascorbic acid route
*eff↑, *Dose↝, *Dose↝,
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↑,
5077- SSE,    Antitumor effects of sodium selenite on acute lymphocytic leukemia
- in-vitro, AML, NA
TumCD↑, Apoptosis↑,
5076- SSE,    Sodium selenite inhibits the growth of cervical cancer cells through the PI3K/AKT pathway
- in-vivo, Cerv, HeLa - in-vivo, Cerv, SiHa
TumCG↓, toxicity↓, tumCV↓, Apoptosis↑, p‑PI3K↓, p‑Akt↓, eff↑,
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↑,
5073- SSE,    Pharmacokinetics and Toxicity of Sodium Selenite in the Treatment of Patients with Carcinoma in a Phase I Clinical Trial: The SECAR Study
- Trial, Var, NA
AntiTum↑, ChemoSen↑, Dose↑, Half-Life↝, toxicity↝, toxicity↝,
5097- SSE,    Examining xCT-mediated selenium uptake and selenoprotein production capacity in cells
- in-vitro, Var, NA
other↝,
5112- SSE,    https://pubmed.ncbi.nlm.nih.gov/19811770/
- in-vitro, Pca, PC3
VEGF↓, IL6↓, NF-kB↓, p65↓,
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↓,
5110- SSE,    Autophagy inhibition through PI3K/Akt increases apoptosis by sodium selenite in NB4 cells
- in-vitro, AML, APL NB4
Apoptosis↑, selectivity↑, TumAuto↓, PI3K↓, Akt↓,
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↑,
5108- SSE,    Activation of p53 by sodium selenite switched human leukemia NB4 cells from autophagy to apoptosis
- in-vitro, AML, U937
p‑P53↑, Beclin-1↓, LC3I↓, Apoptosis↑, Casp↑,
5107- SSE,    Involvement of p38 in signal switching from autophagy to apoptosis via the PERK/eIF2α/ATF4 axis in selenite-treated NB4 cells
- vitro+vivo, AML, APL NB4
PERK↑, eIF2α↑, ATF4↑, Apoptosis↑, AntiTum↑, ER Stress↑, p38↑,
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↑,
5094- SSE,    Sodium Selenite Prevents Matrine-Induced Nephrotoxicity by Suppressing Ferroptosis via the GSH-GPX4 Antioxidant System
- vitro+vivo, Nor, NRK52E
*GPx4↑, *xCT↑, *GSH↑, *RenoP↑,
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↑,
4748- SSE,  Chemo,  antiOx,    Efficacy and safety of intravenous administration of high-dose selenium for preventing chemotherapy-induced peripheral neuropathy in gastric cancer patients receiving adjuvant oxaliplatin and capecitabine after gastrectomy: a retrospective pilot study
- Trial, GC, NA
toxicity↓, chemoP∅, *neuroP↑, *Dose↝,
1697- SSE,  Calc,    Calcium intake may explain the reduction of colorectal cancer odds by dietary selenium - a case-control study in Poland
- Human, CRC, NA
Risk↓, Risk↓, Dose∅, AntiCan↑,
4753- SSE,  Chemo,    Selenium and Lung Cancer: A Systematic Review and Meta Analysis
- Review, Lung, NA
Risk⇅, chemoP↑, radioP↑,
4500- SSE,    Dietary selenium affects host selenoproteome expression by influencing the gut microbiota
- in-vivo, Nor, NA
*GutMicro↑, Risk↓, *GPx↑,
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↓,
4216- SSE,    Selenium ameliorates mercuric chloride-induced brain damage through activating BDNF/TrKB/PI3K/AKT and inhibiting NF-κB signaling pathways
- in-vitro, NA, NA
*BDNF↑, *TrkB↓, *PI3K↑, *Akt↑, *neuroP↑,
1707- SSE,    A Diet Lacking Selenium, but Not Zinc, Copper or Manganese, Induces Anticancer Activity in Mice with Metastatic Cancers
- in-vivo, Ovarian, NA - in-vivo, BC, NA
OS↓,
1706- SSE,    Selenium in Prostate Cancer: Prevention, Progression, and Treatment
- Review, Pca, NA
Risk∅, ChemoSen↑, Risk↓, toxicity↝, Risk↑, eff↑, *toxicity↑, RadioS↑, eff↓, eff↑, ChemoSen↑, ChemoSideEff↓,
4610- SSE,  Rad,    Protection during radiotherapy: selenium
- Review, Var, NA
*radioP↑, *antiOx↑, *Inflam↓, *DNAdam↓, *lipid-P↓, *selenoP↑, *GPx1↑, *BUN↓,
1688- SSE,    Potential Role of Selenium in the Treatment of Cancer and Viral Infections
- Review, Var, NA
IL2↑, INF-γ↑, Th1 response↑, Th2↑, Dose↑, AntiCan∅, Risk↑, chemoP↑, Hif1a↓, VEGF↓, selectivity↑, *GADD45A↑, NRF2↓, *NRF2↑, ChemoSen↑, angioG↓, PrxI↓, ChemoSideEff↓, eff↑,
1687- SSE,    Selenium for preventing cancer
- Analysis, Var, NA
eff∅, AntiCan∅,
1062- SSE,    Sodium Selenite Decreased HDAC Activity, Cell Proliferation and Induced Apoptosis in Three Human Glioblastoma Cells
- in-vitro, GBM, LN229 - in-vitro, GBM, T98G - in-vitro, GBM, U87MG
HDAC↓, TumCP↓, TumCCA↑, Apoptosis↑, Casp3↝, MMP2↓, *BioAv↝,
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↑,
1003- SSE,    Sodium selenite inhibits proliferation of lung cancer cells by inhibiting NF-κB nuclear translocation and down-regulating PDK1 expression which is a key enzyme in energy metabolism expression
- vitro+vivo, Lung, NA
NF-kB↓, PDK1↓, p‑p65↑, p‑IκB↑, BAX↑, lactateProd↓, MMP↓, Cyt‑c↑, mitResp↑, Apoptosis↑,
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↑,
4732- SSE,    Selenium inhibits ferroptosis and ameliorates autistic-like behaviors of BTBR mice by regulating the Nrf2/GPx4 pathway
- in-vivo, Autism, NA
*Ferroptosis↓, *NRF2↑, *GPx4↑, *other↝,
4750- SSE,  Rad,    Selenium in Radiation Oncology—15 Years of Experiences in Germany
- Review, Var, NA
RadioS∅, radioP↑, eff↑,
984- SSE,    Effects of selenite on estrogen receptor-alpha expression and activity in MCF-7 breast cancer cells
- in-vitro, BC, MCF-7
ERα/ESR1↓, PR↑, pS2/TFF1↑, Catalase↑,
4743- SSE,    Selenium for alleviating the side effects of chemotherapy, radiotherapy and surgery in cancer patients
- Review, Var, NA
eff↝, chemoP↝, radioP↝,
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↓,
4741- SSE,    Selenium in Oncological Intervention
- Review, Var, NA
Risk↓, *other↝, Risk↓, AntiTum↑, chemoR↓, chemoP↑,
4740- SSE,    Optimising Selenium for Modulation of Cancer Treatments
- Review, Var, NA
*selenoP↑, *Dose↓, Risk↓, *toxicity↝, Dose↑, chemoP↑, radioP↑,
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↑,
4733- SSE,    Selenium supplementation of lung epithelial cells enhances nuclear factor E2-related factor 2 (Nrf2) activation following thioredoxin reductase inhibition
- NA, Nor, NA
*selenoP↑, *Trx↑, *GPx↑, *NRF2↑,
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↝,
4728- SSE,    Selective Impact of Selenium Compounds on Two Cytokine Storm Players
- NA, Covid, NA
*IL6↓, *TNF-α↓, *NRF2↑, *other↑, *eff↑,
4727- SSE,    Selenium inhibits ferroptosis in ulcerative colitis through the induction of Nrf2/Gpx4
- in-vivo, Col, NA
*Ferroptosis↓, *NRF2↑, *GPx4↑, *eff↑, *other↓, *antiOx↑, *Inflam↓, AntiTum↑,
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↝,

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 71

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 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↓, 2,   NRF2↑, 1,   PrxI↓, 1,   ROS↑, 34,   ROS⇅, 1,   Thiols↓, 1,   Trx↓, 3,   xCT↓, 2,   xCT↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   mitResp↑, 1,   MMP↓, 10,   mtDam↑, 4,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,   lactateProd↓, 1,   NAD↓, 1,   NADPH↓, 2,   PDK1↓, 1,  

Cell Death ⓘ

Akt↓, 3,   p‑Akt↓, 1,   Apoptosis↑, 20,   BAD↓, 1,   BAX↑, 2,   Bcl-2↓, 2,   BIM↑, 1,   Casp↑, 3,   Casp3↑, 2,   Casp3↝, 1,   cl‑Casp3↑, 3,   Casp9↑, 2,   Cyt‑c↑, 4,   Ferroptosis↑, 5,   necrosis↑, 2,   NOXA↑, 1,   p38↑, 1,   pS2/TFF1↑, 1,   survivin↓, 1,   TumCD↑, 6,  

Transcription & Epigenetics ⓘ

other↝, 5,   tumCV↓, 3,  

Protein Folding & ER Stress ⓘ

eIF2α↑, 1,   ER Stress↑, 4,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↓, 1,   Beclin-1↑, 1,   LC3I↓, 1,   LC3s↑, 1,   MitoP↑, 1,   p62↓, 1,   TumAuto↓, 1,   TumAuto↑, 4,  

DNA Damage & Repair ⓘ

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

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 1,   HDAC↓, 1,   HOXB-AS1↓, 1,   mTOR↓, 1,   PI3K↓, 1,   p‑PI3K↓, 1,   PR↑, 1,   TumCG↓, 4,  

Migration ⓘ

E-cadherin↑, 2,   MMP2↓, 3,   MMP9↓, 2,   N-cadherin↓, 1,   TET1↑, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 9,   TumCP↑, 1,   TumMeta↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 4,   angioG↑, 1,   ATF4↑, 1,   Hif1a↓, 1,   VEGF↓, 3,  

Immune & Inflammatory Signaling ⓘ

IL2↑, 1,   IL6↓, 1,   Imm↑, 3,   INF-γ↑, 1,   Inflam↓, 2,   p‑IκB↑, 1,   NF-kB↓, 5,   NK cell↑, 2,   p65↓, 2,   p‑p65↑, 1,   PSA↓, 1,   Th1 response↑, 1,   Th2↑, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   ERα/ESR1↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   chemoR↓, 1,   ChemoSen↑, 9,   Dose↑, 7,   Dose⇅, 1,   Dose↝, 3,   Dose∅, 1,   eff↓, 10,   eff↑, 9,   eff↝, 3,   eff∅, 2,   Half-Life↝, 3,   RadioS↑, 2,   RadioS↝, 1,   RadioS∅, 1,   selectivity↑, 8,  

Clinical Biomarkers ⓘ

AR↓, 1,   ERα/ESR1↓, 1,   IL6↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 4,   AntiCan∅, 2,   AntiTum↑, 6,   chemoP↑, 6,   chemoP↝, 1,   chemoP∅, 1,   chemoPv↑, 1,   ChemoSideEff↓, 2,   OS↓, 1,   OS↑, 3,   Pain↓, 1,   QoL↑, 1,   radioP↑, 5,   radioP↝, 1,   Risk↓, 15,   Risk↑, 3,   Risk⇅, 1,   Risk∅, 1,   toxicity↓, 3,   toxicity↝, 7,   TumW↓, 1,   Weight∅, 1,  

Infection & Microbiome ⓘ

Sepsis↓, 1,  
Total Targets: 159

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 3,   Catalase↑, 1,   Ferroptosis↓, 2,   GPx↓, 1,   GPx↑, 5,   GPx1↑, 1,   GPx4↑, 3,   GSH↑, 2,   H2O2↓, 1,   HO-1↑, 2,   lipid-P↓, 1,   MDA↓, 2,   NRF2↑, 7,   ROS↓, 8,   selenoP↑, 8,   SOD↑, 1,   Trx↑, 1,   xCT↑, 1,  

Core Metabolism/Glycolysis ⓘ

BUN↓, 1,  

Cell Death ⓘ

Akt↑, 1,   Bcl-2↑, 1,   Ferroptosis↓, 2,  

Transcription & Epigenetics ⓘ

other↓, 3,   other↑, 1,   other↝, 3,  

DNA Damage & Repair ⓘ

DNAdam↓, 2,   GADD45A↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↑, 1,  

Immune & Inflammatory Signaling ⓘ

CRP↓, 2,   IL1↓, 1,   IL6↓, 2,   Imm↑, 2,   Inflam↓, 7,   MCP1↓, 1,   NF-kB↓, 2,   NK cell↑, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,   TrkB↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 3,   BioAv↝, 1,   Dose↓, 1,   Dose↝, 6,   eff↑, 3,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

CRP↓, 2,   GutMicro↑, 4,   IL6↓, 2,  

Functional Outcomes ⓘ

memory↑, 1,   neuroP↑, 3,   Pain↓, 1,   QoL↑, 1,   radioP↑, 2,   RenoP↑, 1,   Risk↓, 2,   toxicity↓, 2,   toxicity↑, 1,   toxicity↝, 1,   toxicity∅, 1,  
Total Targets: 61

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#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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