SOD1 Cancer Research Results

SOD1, superoxide dismutase 1: Click to Expand ⟱
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SOD1 (superoxide dismutase 1) is a key antioxidant enzyme that catalyzes the dismutation of superoxide radicals into oxygen and hydrogen peroxide.

In several cancers including breast, lung, HCC, and others, alterations in SOD1 expression have been observed, reflecting its role in managing oxidative stress.
• Elevated SOD1 levels are sometimes associated with aggressive tumor behavior, therapy resistance, or decreased apoptosis due to enhanced ROS detoxification.
• Conversely, the protective role of antioxidants can also mitigate oxidative mutation loads, leading to context-dependent and occasionally favorable outcomes.

In non-small cell lung cancer (NSCLC), increased SOD1 levels have been reported in some cohorts, potentially as a mechanism to cope with high reactive oxygen species (ROS) levels.
Scientific Papers found: Click to Expand⟱
2612- Ba,  MF,    The effect of a static magnetic field and baicalin or baicalein interactions on amelanotic melanoma cell cultures (C32)
- in-vitro, Melanoma, NA
SOD1↑, Baicalein ONLY: increase in the expression of the SOD1 , SOD2 and GPX1 genes compared to the nontreated cell cultures
SOD2↑,
GPx1↑,
Dose?, A chamber with a field induction of 0.7 T was used for the tests
eff↝, There was no significant difference in the expression of the SOD1, SOD2 or GPX1 genes in the melanoma cell cultures that had only been exposed to a static magnetic field (0.7 T)
SOD1↓, Baicalein + 0.7T MF: decreases SOD1 , SOD2 and GPX1
SOD2↓,
GPx1↓,

2654- CUR,    Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence
- Review, Var, NA
ROS↑, ROS induction has been implicated as one of the mechanisms of the anticancer activity of curcumin and its derivatives in various cancers
Catalase↓, Curcumin induces ROS by inhibiting the activity of various ROS-related metabolic enzymes, such as CAT, SOD1, glyoxalase 1, and NAD(P)H dehydrogenase [quinone] 1 [146,149]
SOD1↓,
GLO-I↓,
NADPH↓,
TumCCA↑, ROS accumulation further mediates G1 or G2/M cell cycle arrest [146,147,150,154], senescence [146], and apoptosis.
Apoptosis↑,
Akt↓, downregulation of AKT phosphorylation [145
ER Stress↑, endoplasmic reticulum stress (namely through the PERK–ATF4–CHOP axis)
JNK↑, activation of the JNK pathway [151],
STAT3↓, and inhibition of STAT3 [155].
BioAv↑, Additionally, the combination of curcumin and piperine, a pro-oxidative phytochemical that drastically increases the bioavailability of curcumin in humans

5012- DSF,  Cu,    Advancing Cancer Therapy with Copper/Disulfiram Nanomedicines and Drug Delivery Systems
ROS↑, DSF’s anticancer mechanism is primarily due to its generating reactive oxygen species, inhibiting aldehyde dehydrogenase (ALDH) activity inhibition, and decreasing the levels of transcriptional proteins
ALDH↓,
TumCP↓, DSF also shows inhibitory effects in cancer cell proliferation, the self-renewal of cancer stem cells (CSCs), angiogenesis, drug resistance, and suppresses cancer cell metastasis.
CSCs↓,
angioG↓,
TumMeta↓,
DNAdam↑, anti-cancer mechanism of DSF/Cu (II) may be mediated by the regulation of reactive oxygen species (ROS), enzyme activity regulation, induction of DNA damage, proteasome inhibition, and transcription factors
Proteasome↓,
SOD1↓, The complex of DSF and Cu (II)has been reported to inhibit the enzyme superoxide dismutase 1 (SOD1), one of the major enzymesthat mitigates oxidative damage in melanoma cells
GSR↓, The inhibition of Glutathione reductase (GSR) inhibition by DSF disrupts glutathione GSH redox cycling, producing an accumulation of oxidized glutathione (GSSG) and a lower GSH/GSSG ratio, producing an increase in ROS level
ox-GSSG↑,
GSH/GSSG↓,
MMP↓, DSF induces the disruption of the mitochondrial membrane potential and cause apoptosis in human melanoma cell lines
Akt↓, induced the apoptosis of erbB2-positive breast cancer cells by inhibiting AKT, cyclin D1, and NFκB signaling
cycD1/CCND1↓,
NF-kB↓,
CSCs↓, In hepatocellular carcinoma, DSF decreases CSCs by inhibiting the p38 mitogen-activated protein kinase (MAPK) pathway [118].
MAPK↓,
angioG↓, Thus, the inhibition of DSF/Cu (II) in CSCs decrease angiogenesis.
DrugR↓, DSF/Cu (II) overcomes drug resistance via targeting the proteasome, epithelial–mesenchymal transition (EMT), P-gp, CSC activity
EMT↓,
Vim↓, By downregulating associated proteins such as Vimentin, DSF/Cu (II) inhibits the EMT, which consequently overcomes the paclitaxel resistance of prostate and lung cancer
BioAv↑, The use of these nanoparticle-based formulations can increase the accumulation of DSF at the target site, thereby reducing the toxic effects on healthy tissues and improving the therapeutic index.
eff↑, In clinical trials, DSF is provided orally, but Cu (II) is critical for the efficacy of DSF

3212- EGCG,    EGCG maintained Nrf2-mediated redox homeostasis and minimized etoposide resistance in lung cancer cells
- in-vitro, Lung, A549 - in-vivo, Lung, NCIH23
NRF2⇅, In A549, EGCG downregulated nuclear Nrf2 by upregulating the nuclear localization of Keap1 whereas in NCIH23, EGCG augmented Nrf2 by reducing Keap1.
eff↑, Though the direction of Nrf2 regulation was opposite in two cell lines, optimum level of Nrf2 was maintained which increased responsiveness towards etoposide. EGCG sensitized/potentiated lung adenocarcinoma cells towards chemotherapy by inducing G2/
SOD1↑, n NCIH23, the downstream targets of Nrf2, NQO1 and MRP1 did not show any significant alteration in expression with respect to control, with an exception of SOD1(upregulated by 1.28 times)
SOD1↓, EGCG showed exactly opposite effect in A549. It again effectively fitted in a U-shaped hormetic downregulation for all three downstream targets. EGCG (0.5 μM/12 h) most effectively downregulated SOD-1, NQO1 and MRP1expression
MMP2⇅, However, EGCG (0.5 μM) itself increased the activity of MMP-2 and MMP-9. The lowest dose of EGCG required to inhibit MMP-2 and MMP-9 was reported, 8–13 μM in different cancer cell lines
MMP9⇅,

5050- HPT,    Reactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review
- Review, Nor, NA
*ROS↑, Heat stress was suggested to be an environmental factor responsible for stimulating ROS production because of similarities in responses observed following heat stress compared with that occurring following exposure to oxidative stress.
*SOD1↓, Heat stress was also shown to decrease superoxide dismutase 1 (SOD-1) mRNA levels, cytoplasmic SOD protein and enzyme activity, leading to the increase of ROS generation
*GSH↓, Furthermore, several studies demonstrated that heat stress results in a dramatic decrease in glutathione (GSH) levels.
other↑, Nowadays, a variety of diseases and degenerative processes such as cancer, Alzheimer’s and autoimmune diseases are mediated by oxidative stress.
HIF-1↑, heat stress activates hypoxia-inducible factor 1 (HIF-1) through ERK-NADPH oxidase-mediated ROS production, and this enhances tumour oxygenation by up-regulating HIF-1 target gene
ROS↑,

4909- Sal,    Salinomycin: Anti-tumor activity in a pre-clinical colorectal cancer model
- vitro+vivo, CRC, NA
AntiTum↑, salinomycin alone or in combination with FOLFOX exerts superior antitumor activity compared to FOLFOX therapy in a patient-derived mouse xenograft model of colorectal cancer
Apoptosis↑, Salinomycin induces apoptosis of human colorectal cancer cells, accompanied by accumulation of dysfunctional mitochondria and reactive oxygen species
mtDam↑,
ROS↑, Accumulation of dysfunctional mitochondria and increased production of reactive oxygen species upon salinomycin treatment
SOD1↓, These effects are associated with expressional down-regulation of superoxide dismutase-1 (SOD1) in response to salinomycin treatment.
ChemoSen↑, salinomycin alone or in combination with 5-fluorouracil and oxaliplatin exerts increased antitumoral activity compared to common chemotherapy.
CSCs↑, Anti-stem cell activity of salinomycin in TIC cultures
ALDH↓, Strikingly, exposure to 5-FU and oxaliplatin resulted in a more pronounced reduction of the ALDH1+ population compared to salinomycin treatment
TumCG↓, Salinomycin inhibits tumor growth in a patient-derived xenograft model
TumCP↓, Salinomycin inhibits proliferation, induces cell death and abolishes ATP production of human colorectal cancer cells
TumCD↑,
ATP↓,

3296- SIL,    Silibinin induces oral cancer cell apoptosis and reactive oxygen species generation by activating the JNK/c-Jun pathway
- in-vitro, Oral, Ca9-22 - in-vivo, Oral, YD10B
TumCP↓, Silibinin effectively suppressed YD10B and Ca9-22 cell proliferation and colony formation in a dose-dependent manner.
TumCCA↑, Moreover, it induced cell cycle arrest in the G0/G1 phase, apoptosis, and ROS generation in these cells.
ROS↑,
SOD1↓, silibinin downregulated SOD1 and SOD2 and triggered the JNK/c-Jun pathway in oral cancer cells.
SOD2↓,
*JNK↑, inducing apoptosis, G0/G1 arrest, ROS generation, and activation of the JNK/c-Jun pathway.
toxicity?, Silibinin significantly inhibited xenograft tumor growth in nude mice, with no obvious toxicity.
TumCMig↓, Silibinin inhibits oral cancer cell migration and invasion
TumCI↓,
N-cadherin↓, silibinin downregulated N-cadherin and vimentin expression and upregulated E-cadherin expression in YD10B and Ca9-22 cells
Vim↓,
E-cadherin↑,
EMT↓, Together, these results indicate that silibinin inhibits the migration and invasion of oral cancer cells by suppressing the EMT.
P53↑, silibinin significantly induced the expression of p53, cleaved caspase-3, cleaved PARP, and Bax, and downregulated the expression of the anti-apoptotic marker protein Bcl-2
cl‑Casp3↑,
cl‑PARP↑,
BAX↑,
Bcl-2↓,
SOD↓, silibinin inhibits SOD expression, induces ROS production, and activates the JNK/c-Jun pathway in oral cancer cells.


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   GPx1↓, 1,   GPx1↑, 1,   GSH/GSSG↓, 1,   GSR↓, 1,   ox-GSSG↑, 1,   NRF2⇅, 1,   ROS↑, 5,   SOD↓, 1,   SOD1↓, 6,   SOD1↑, 2,   SOD2↓, 2,   SOD2↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

GLO-I↓, 1,   NADPH↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,   cl‑Casp3↑, 1,   JNK↑, 1,   MAPK↓, 1,   Proteasome↓, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

other↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 2,   CSCs↓, 2,   CSCs↑, 1,   EMT↓, 2,   STAT3↓, 1,   TumCG↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   MMP2⇅, 1,   MMP9⇅, 1,   N-cadherin↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 3,   TumMeta↓, 1,   Vim↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   HIF-1↑, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   ChemoSen↑, 1,   Dose?, 1,   DrugR↓, 1,   eff↑, 2,   eff↝, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,   toxicity?, 1,  
Total Targets: 60

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   ROS↑, 1,   SOD1↓, 1,  

Cell Death ⓘ

JNK↑, 1,  
Total Targets: 4

Scientific Paper Hit Count for: SOD1, superoxide dismutase 1
1 Baicalein
1 Magnetic Fields
1 Curcumin
1 Disulfiram
1 Copper and Cu NanoParticles
1 EGCG (Epigallocatechin Gallate)
1 Hyperthermia
1 salinomycin
1 Silymarin (Milk Thistle) silibinin
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

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