PIK3CA Cancer Research Results

PIK3CA, phosphoinositide-3-kinase, catalytic, alpha polypeptide: Click to Expand ⟱
Source: CGL-Driver Genes
Type: Oncogene
Class III PtdIns3K (PIK3C3/Vps34)
Class I phosphoinositide 3-kinase (PI3K)
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.

PIK3CA is a gene that encodes the p110α catalytic subunit of phosphoinositide 3-kinase (PI3K), which is a key player in the PI3K/AKT signaling pathway. This pathway is crucial for various cellular processes, including growth, proliferation, survival, and metabolism.
PIK3CA is often overexpressed, which can lead to increased activity of the PI3K/AKT signaling pathway. This overexpression can contribute to tumor growth, survival, and metastasis.

Class III PtdIns3K (PIK3C3/Vps34) is central to autophagy regulation. In many tumor types, higher expression is thought to promote autophagy, which can help cancer cells survive under metabolic and therapeutic stress. This survival advantage is one reason why high PIK3C3 expression sometimes correlates with a more aggressive phenotype and poorer overall prognosis.
Scientific Papers found: Click to Expand⟱
1338- AG,    The Modulatory Properties of Astragalus membranaceus Treatment on Triple-Negative Breast Cancer: An Integrated Pharmacological Method
- in-vitro, BC, NA
TumCI↓,
Apoptosis↑,
Symptoms↓,
PIK3CA↓,
Akt↓,
Bcl-2↓,

5893- CAR,  TV,    Thymol and Carvacrol: Molecular Mechanisms, Therapeutic Potential, and Synergy With Conventional Therapies in Cancer Management
- Review, Var, NA
*Inflam↓, Monoterpenes like thymol and carvacrol are recognized for their anti‐inflammatory and anticancer properties,
AntiCan↑,
PI3K↓, Thymol derivatives, such as 1,2,3‐triazoles and carvacrol, effectively target breast cancer (BC) through PI3K/AKT/mTOR and NOTCH pathways and inhibit PIK3CA expression.
Akt↓,
mTOR↓,
NOTCH↓,
PIK3CA↓,
EGFR↓, thymol exhibits anti‐EGFR activity, while carvacrol modulates the HIF‐1α/VEGF pathway, making them potential candidates for colorectal cancer (CRC) management.
Hif1a↓,
VEGF↓,
ChemoSen↑, Their synergistic potential with chemotherapy, radiotherapy, and other bioactive compounds strengthens their therapeutic promise.
RadioS↑,
eff↝, challenges such as stability, bioavailability, and the need for clinical trials hinder their clinical application.
*cardioP↑, cardioprotective (Joshi et al. 2023), neuroprotective (Forqani et al. 2023) and hepato‐nephroprotective
*neuroP↑,
*hepatoP↑,
Apoptosis↑, Induction of Apoptosis
MMP↓, The apoptosis was due to ROS production, variations in the mitochondrial membrane, caspase‐3 activation, and DNA damage
Casp3↑,
ROS↑,
DNAdam↑,
eff↑, Thymol derivative, known as compound 10 (IC50 6.17 μM) exhibited 3.2‐fold more inhibition than 5‐fluorouracil (IC50 20.09 μM) against MCF‐7
BAX↑, Carvacrol (25, 50, 75, and 90 μM) enhanced the expression of Bax, Bad, Fas‐L, and cytochrome c, activated caspase‐9/3 and caspase‐8, induced cell cycle at G0/G1
BAD↑,
FasL↑,
Cyt‑c↑,
Casp9↑,
Casp8↑,
TumCCA↑,
P21↑, improved the expression of proteins (p21, cyclin D1, CDK4), and downregulated the SMO and GLI1 proteins expression in CC
Smo↓,
Gli1↓,
JNK↑, Moreover, thymol activated JNK and p38 MAPK while impeding the ERK pathway
ERK↓,
MAPK↓, Besides thymol, carvacrol has also been reported to inhibit MAPK or ERK pathways in previous studies.
TRPM7↓, inhibited TRPM7 expression in liver fibrotic C57BL/6J mice
Wnt/(β-catenin)↓, hymol inhibited HCT116 and LoVo cell line invasion via downregulating the Wnt/β‐catenin pathway and reducing c‐Myc and Cyclin D1 expression
BioAv↝, thymol and carvacrol are volatile, and their stability is influenced by these factors (temperature, light, oxygen, and pH)
BioAv↑, Ultrasonication is an effective technique to enhance the stability of thymol and other bioactive compounds. 400 watts of power elevated the performance of NC‐CH formulations, and NC‐CH‐400 displayed increased solubility.


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

PIK3CA↓, 2,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 2,   BAD↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   FasL↑, 1,   JNK↑, 1,   MAPK↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   Gli1↓, 1,   mTOR↓, 1,   NOTCH↓, 1,   PI3K↓, 1,   Smo↓, 1,   TRPM7↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

TumCI↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 1,   eff↑, 1,   eff↝, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   Symptoms↓, 1,  
Total Targets: 39

Pathway results for Effect on Normal Cells:


Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,  
Total Targets: 4

Scientific Paper Hit Count for: PIK3CA, phosphoinositide-3-kinase, catalytic, alpha polypeptide
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#:256  State#:%  Dir#:1
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