lipid-P Cancer Research Results

lipid-P, lipid peroxidation: Click to Expand ⟱
Source:
Type:
Lipid peroxidation is a chain reaction process in which free radicals (often reactive oxygen species, or ROS) attack lipids containing carbon-carbon double bonds, especially polyunsaturated fatty acids. This attack results in the formation of lipid radicals, peroxides, and subsequent breakdown products.
Lipid peroxidation can cause damage to cell membranes, leading to increased permeability and disruption of cellular functions. This damage can initiate a cascade of events that may contribute to carcinogenesis.
The byproducts of lipid peroxidation, such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), can form adducts with DNA, leading to mutations. These mutations can disrupt normal cellular processes and contribute to the development of cancer.
Lipid peroxidation damages cell membranes, disrupts cellular functions, and can trigger inflammatory responses. It is a marker of oxidative stress and is implicated in many chronic diseases.

Negative Prognostic Indicator: In many cancers, high levels of lipid phosphates, particularly S1P, are associated with poor prognosis, indicating a more aggressive tumor phenotype and potential resistance to therapy.
Mixed Evidence: The prognostic significance of lipid phosphates can vary by cancer type, with some studies showing that their expression may not always correlate with adverse outcomes.
GBM, Glioblastoma: Click to Expand ⟱
Glioblastoma is a fast-growing and aggressive brain tumor.
Scientific Papers found: Click to Expand⟱
3345- ART/DHA,    Dihydroartemisinin-induced unfolded protein response feedback attenuates ferroptosis via PERK/ATF4/HSPA5 pathway in glioma cells
- in-vitro, GBM, NA
ROS↑, Ferroptosis↑, lipid-P↑, HSP70/HSPA5↑, ER Stress↑, ATF4↑, GRP78/BiP↑, MDA↑, GSH↓, eff↑, GPx4↑,
5099- JG,    Juglone induces ferroptosis in glioblastoma cells by inhibiting the Nrf2-GPX4 axis through the phosphorylation of p38MAPK
- vitro+vivo, GBM, LN229 - vitro+vivo, GBM, T98G
Ferroptosis↑, p‑MAPK↑, NRF2↓, GPx4↓, TumPF↓, Apoptosis↑, ROS↑, GSH↓, lipid-P↑, Ki-67↓, TumCG↓,
5125- Sal,    Salinomycin induced ROS results in abortive autophagy and leads to regulated necrosis in glioblastoma
- in-vitro, GBM, NA
ER Stress↑, UPR↑, autoF↓, lysosome↝, ROS↑, lipid-P↑, CSCs↓, necrosis↑, ATP↓, MMP↓, MOMP↑, DNAdam↑, AIF↑, lysoMP↑, MitoP↑, Ca+2↑,
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↑,
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↑,
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 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Fenton↑, 1,   Ferroptosis↑, 4,   GPx4↓, 3,   GPx4↑, 1,   GSH↓, 4,   H2O2↑, 1,   Iron↑, 2,   lipid-P↑, 6,   MDA↑, 1,   NRF2↓, 1,   ROS↑, 5,   ROS⇅, 1,   xCT↓, 2,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,   NAD↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   Ferroptosis↑, 4,   lysoMP↑, 1,   p‑MAPK↑, 1,   MOMP↑, 1,   necrosis↑, 1,   TumCD↑, 2,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 2,   GRP78/BiP↑, 1,   HSP70/HSPA5↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

autoF↓, 1,   lysosome↝, 1,   MitoP↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   PARP↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   TumCG↓, 1,  

Migration ⓘ

Ca+2↑, 1,   Ki-67↓, 1,   TumCP↓, 2,   TumPF↓, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↓, 3,   eff↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,  
Total Targets: 47

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: lipid-P, lipid peroxidation
3 Selenite (Sodium)
1 Artemisinin
1 Juglone
1 salinomycin
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:27  Cells:%  prod#:%  Target#:453  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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