PI3K Cancer Research Results

PI3K, Phosphatidylinositide-3-Kinases: Click to Expand ⟱
Source: HalifaxProj(inhibit) CGL-CS
Type:
Phosphatidylinositol 3-kinase (PtdIns3K or PI3K) is a family of enzymes that play a crucial role in cell signaling pathways, particularly in the regulation of cell growth, survival, and metabolism. The PI3K pathway is one of the most frequently altered pathways in human cancer. Inhibition of the PI3K pathway has been explored as a therapeutic strategy for cancer treatment. Several PI3K inhibitors have been developed and are currently being tested in clinical trials. These inhibitors can target specific components of the pathway, such as PI3K, AKT, or mTOR.

Class I phosphoinositide 3-kinase (PI3K)
Class III PtdIns3K
In contrast to the class III PtdIns3K as a positive regulator of autophagy, class I PI3K-AKT signaling has an opposing effect on the initiation of autophagy.

PI3K inhibitors include:
-Idelalisib , Copanlisib, Alpelisib
-LY294002?
-Wortmannin: potent PI3K inhibitor, has some associated toxicity.
-Quercetin:
-Curcumin
-Resveratrol
-Epigallocatechin Gallate (EGCG)


NPC, Nasopharyngeal Carcinoma (NPC): Click to Expand ⟱
Nasopharyngeal carcinoma, or nasopharynx cancer, is the most common cancer originating in the nasopharynx, most commonly in the postero-lateral nasopharynx or pharyngeal recess, accounting for 50% of cases.
Nasopharyngeal carcinoma (NPC) is a type of cancer that originates in the epithelial cells lining the nasopharynx, which is the upper part of the throat located behind the nose and above the soft palate.
-(NPC) is a malignant tumor which is commonly found in East Asia and Africa.


Scientific Papers found: Click to Expand⟱
4820- ASTX,    Astaxanthin suppresses the malignant behaviors of nasopharyngeal carcinoma cells by blocking PI3K/AKT and NF-κB pathways via miR-29a-3p
- in-vitro, NPC, NA
TumCP↓, TumCI↓, Apoptosis↑, TumCCA↑, cycD1/CCND1↓, Bcl-2↓, P21↑, BAX↑, PI3K↓, Akt↓, NF-kB↓, miR-29b↑,
5838- CAP,    Capsaicin Induces Autophagy and Apoptosis in Human Nasopharyngeal Carcinoma Cells by Downregulating the PI3K/AKT/mTOR Pathway
- in-vitro, NPC, NA
TumCG↓, TumCCA↑, TumAuto↑, Casp3↑, Ca+2↑, ROS↑, MMP↓, LC3‑Ⅱ/LC3‑Ⅰ↑, ATG5↑, p62↓, Fap1↓, PI3K↓, DNAdam↑,
2360- SK,    Shikonin inhibits growth, invasion and glycolysis of nasopharyngeal carcinoma cells through inactivating the phosphatidylinositol 3 kinase/AKT signal pathway
- in-vitro, NPC, HONE1 - in-vitro, NPC, SUNE-1
TumCP↓, Apoptosis↑, TumCMig↓, TumCI↓, GlucoseCon↓, lactateProd↓, ATP↓, PKM2↓, PI3K↓, Akt↓, MMP3↓, MMP9↓, TIMP1↑,

Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

ROS↑, 1,  

Mitochondria & Bioenergetics

ATP↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis

GlucoseCon↓, 1,   lactateProd↓, 1,   PKM2↓, 1,  

Cell Death

Akt↓, 2,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Fap1↓, 1,  

Autophagy & Lysosomes

ATG5↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   p62↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair

DNAdam↑, 1,  

Cell Cycle & Senescence

cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State

PI3K↓, 3,   TumCG↓, 1,  

Migration

Ca+2↑, 1,   miR-29b↑, 1,   MMP3↓, 1,   MMP9↓, 1,   TIMP1↑, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 2,  

Immune & Inflammatory Signaling

NF-kB↓, 1,  
Total Targets: 31

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PI3K, Phosphatidylinositide-3-Kinases
1 Astaxanthin
1 Capsaicin
1 Shikonin
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:67  Cells:%  prod#:%  Target#:252  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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