PLA2 Cancer Research Results

PLA2, Phospholipase A2: Click to Expand ⟱
Source:
Type:

PLA2 - Phospholipase A2

Abbreviation: PLA2

Type: Phospholipase / lipid-metabolizing enzyme family

Function: Hydrolyzes the sn-2 fatty-acid bond of membrane phospholipids, releasing free fatty acids such as arachidonic acid and lysophospholipids. PLA2 activity regulates eicosanoid production, inflammation, membrane remodeling, cell signaling, proliferation, and oxidative responses.

Cancer: ↑ Generally increased/pro-tumorigenic for several important PLA2 isoforms, particularly cPLA2α (PLA2G4A) and selected secreted PLA2 enzymes. Increased PLA2 signaling can promote arachidonic-acid/eicosanoid production, inflammation, angiogenesis, tumor growth, invasion, metastasis, and tumor-microenvironment signaling.

Alzheimer's Disease: ↑ Increased or overactivated cPLA2/arachidonic-acid signaling has been associated with Aβ-induced neurotoxicity, neuroinflammation, synaptic dysfunction, and cognitive impairment.
Scientific Papers found: Click to Expand⟱
7260- Gink,    Ginkgetin: A natural biflavone with versatile pharmacological activities
- Review, Var, NA - Review, Stroke, NA - Review, AD, NA
*AntiCan↑, Ginkgetin (GK), a natural non-toxic biflavone, has been shown to exhibit anti-cancer, anti-inflammatory, anti-microbial, anti-adipogenic, and neuroprotective activities.
*Inflam↓,
*AntiBio↑,
*neuroP↑,
*TumCCA↑, GK combats cancer progression by arresting cell cycle, inducing apoptosis, stimulating autophagy, and targeting many deregulated signaling pathways such as JAK/STAT and MAPKs.
Apoptosis↑,
TumAuto↑,
iNOS↓, GKhalts inflammation mediators like interleukins, iNOS, COX-2, PGE2, NF-κB, and acts as an inhibitor of PLA2
COX2↓,
PGE2↓,
NF-kB↓,
PLA2↓,
*neuroP↑, GK shows strong neuroprotection against oxidative stress-promoted cell death, inhibits cerebral micro-hemorrhage, decreases neurologic deficits, and halts apoptosis of neurons
*Stroke↓, in cerebral ischemia rat model, GK significantly improved I/R-stimulated neurological deficit scores
*AntiFungal↓, GK also acts as anti-fungal, anti-viral, anti-bacterial, leishmanicidal and anti-plasmodial agent.
*Bacteria↓,
Bcl-xL↓, steosarcoma cells, GK significantly suppressed the levels of B-cell lymphoma-extra-large (Bcl-xL) and B-cell lymphoma 2 (Bcl-2) proteins while significantly elevated levels of caspase-9 and -3 along with cleaved poly ADP ribose polymerase (PARP)
Bcl-2↓,
Casp9↑,
Casp3↑,
cl‑PARP↑,
IL6↓, GK selectively repressed the proliferation of prostate tumor via repressing interleukin 6 (IL-6)-induced as well as constitutive activation of STAT3
STAT3↓,
JAK1↓, GK abrogated the constitutive activation of both Src and JAK1 kinases which in turn halted STAT3 activation in FaDu and A549 cells.
survivin↓, suppressed its target genes including survivin, cyclooxygenase-2 (COX-2), inhibitor of apoptosis protein-1 (IAP-1), Bcl-xL, Bcl-2, matrix metalloproteinase 2 and 9 (MMP-2 and -9)
COX2↓,
IAP1↓,
MMP2↓,
MMP9↓,
PTEN↑, GK prompted the mRNA and protein expression of phosphatase and tensin homolog (PTEN) and SHP-1 which also paly role in STAT3 activation
SHP1↑,
eff↑, When GK is applied in combination with resveratrol, they synergistically act to suppress endothelial cell proliferation, migration, and reactive oxygen species (ROS) production as compared to mono drug
TumVol↓, GK decreased the weight and volume of tumor by 67.4% and 65.6%, respectively in the DU-145 xenografted mice model as compared to control and no toxic effect towards normal cells had been observed
TumW↓,
*toxicity↓,
*ROS↓, mediated neuronal cell damage in vitro by reducing intracellular ROS and maintaining MMP


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:


NA, unassigned(tgid=0) ⓘ

PLA2↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp3↑, 1,   Casp9↑, 1,   IAP1↓, 1,   iNOS↓, 1,   survivin↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

PTEN↑, 1,   SHP1↑, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

MMP2↓, 1,   MMP9↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 2,   IL6↓, 1,   JAK1↓, 1,   NF-kB↓, 1,   PGE2↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

TumVol↓, 1,   TumW↓, 1,  
Total Targets: 25

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1,   Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   neuroP↑, 2,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↓, 1,   Bacteria↓, 1,  
Total Targets: 10

Scientific Paper Hit Count for: PLA2, Phospholipase A2
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#:%  Target#:1615  State#:%  Dir#:1
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