SOD1 Cancer Research Results

SOD1, superoxide dismutase 1: Click to Expand ⟱

Source:

Type:

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.

Pca, Prostate Cancer: Click to Expand ⟱

Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.

Scientific Papers found: Click to Expand⟱

265-

ALA,

Alpha-Lipoic Acid Reduces Cell Growth, Inhibits Autophagy, and Counteracts Prostate Cancer Cell Migration and Invasion: Evidence from In Vitro Studies

in-vitro,

Pca,

LNCaP

 ALA (25–1000 μM) for 48 h

in-vitro,

Pca,

DU145

ROS↓, SOD↓, GSTP1/GSTπ↓, NRF2↓, p62↓, p62↑, SOD↑, p‑mTOR↑, Beclin-1↓, ROS↑, SOD1↑,

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 ⓘ

GSTP1/GSTπ↓, 1, NRF2↓, 1, ROS↓, 1, ROS↑, 1, SOD↓, 1, SOD↑, 1, SOD1↑, 1,

Autophagy & Lysosomes ⓘ

Beclin-1↓, 1, p62↓, 1, p62↑, 1,

Proliferation, Differentiation & Cell State ⓘ

p‑mTOR↑, 1,
Total Targets: 11

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: SOD1, superoxide dismutase 1

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