Thymol-Thymus vulgaris / P21 Cancer Research Results

TV, Thymol-Thymus vulgaris: Click to Expand ⟱
Features:
Thyme
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P21, P21/CDKN1A: Click to Expand ⟱
Source:
Type: Proapototic
cyclin-dependent kinase inhibitor p21 (also known as p21 WAF1/Cip1) promotes cell cycle arrest in response to many stimuli.
P21 is a cyclin-dependent kinase inhibitor that plays a crucial role in regulating the cell cycle. It is encoded by the CDKN1A gene and is a key player in the cellular response to stress, including DNA damage.
P21 is often considered a tumor suppressor because its expression is upregulated in response to p53 activation, a well-known tumor suppressor protein. When DNA damage occurs, p53 can activate the transcription of the CDKN1A gene, leading to increased levels of P21, which helps prevent the proliferation of damaged cells.
In many cancers, the p53 pathway is disrupted, leading to decreased levels of P21. p21 is a apoptotic marker protein.
Cell cycle arrest gene p21
Field Suggested Entry
Target CDKN1A / p21 / p21Cip1/Waf1
Full Name Cyclin-dependent kinase inhibitor 1A
Target Class CIP/KIP-family cyclin-dependent kinase inhibitor
Main Binding Partners CDK2, CDK1, CDK4/6, cyclin complexes, PCNA
Primary Biology p53-mediated cell-cycle arrest, DNA damage response, senescence, differentiation, CDK inhibition, RB/E2F pathway suppression, apoptosis regulation
Cancer Relevance High but context-dependent: p21 can suppress tumor growth through cell-cycle arrest and senescence, but can also support apoptosis resistance, senescent-cell survival, and therapy resistance in some tumors
AD Relevance Medium: indirect relevance through neuronal cell-cycle re-entry, senescence, p53 stress signaling, and aging-related cell-cycle dysregulation
Therapeutic Direction Context-dependent. Restore/activate p21 for tumor-suppressive arrest where appropriate; inhibit or bypass p21 where it promotes apoptosis resistance, senescent-cell survival, or treatment resistance.


Scientific Papers found: Click to Expand⟱
5887- CAR,  TV,    Antitumor Effects of Carvacrol and Thymol: A Systematic Review
- Review, Var, NA
Apoptosis↑, TumCCA↑, TumMeta↓, TumCP↓, MAPK↓, PI3K↓, Akt↓, mTOR↓, eff↑, *Inflam↓, *antiOx↑, AXL↓, MDA↑, Casp3↑, Bcl-2↓, MMP2↓, MMP9↓, p‑JNK↑, BAX↑, MDA↓, TRPM7↓, MMP↓, Cyt‑c↑, Casp↑, cl‑PARP↑, ROS↑, CDK4↓, P21↑, F-actin↓, GSH↓, *SOD↑, *Catalase↑, *GPx↑, *GSR↑, *GSH↑, *lipid-P↓, *AST↓, *ALAT↓, *ALP↓, *LDH↓, DNAdam↑, AFP↓, VEGF↓, Weight↑, *chemoP↑, ROS↑,
5893- CAR,  TV,    Thymol and Carvacrol: Molecular Mechanisms, Therapeutic Potential, and Synergy With Conventional Therapies in Cancer Management
- Review, Var, NA
*Inflam↓, AntiCan↑, PI3K↓, Akt↓, mTOR↓, NOTCH↓, PIK3CA↓, EGFR↓, Hif1a↓, VEGF↓, ChemoSen↑, RadioS↑, eff↝, *cardioP↑, *neuroP↑, *hepatoP↑, Apoptosis↑, MMP↓, Casp3↑, ROS↑, DNAdam↑, eff↑, BAX↑, BAD↑, FasL↑, Cyt‑c↑, Casp9↑, Casp8↑, TumCCA↑, P21↑, Smo↓, Gli1↓, JNK↑, ERK↓, MAPK↓, TRPM7↓, Wnt/(β-catenin)↓, BioAv↝, BioAv↑,

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 ⓘ

GSH↓, 1,   MDA↓, 1,   MDA↑, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,  

Core Metabolism/Glycolysis ⓘ

PIK3CA↓, 1,  

Cell Death ⓘ

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

DNA Damage & Repair ⓘ

DNAdam↑, 2,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   P21↑, 2,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   Gli1↓, 1,   mTOR↓, 2,   NOTCH↓, 1,   PI3K↓, 2,   Smo↓, 1,   TRPM7↓, 2,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

AXL↓, 1,   F-actin↓, 1,   MMP2↓, 1,   MMP9↓, 1,   TumCP↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 1,   eff↑, 2,   eff↝, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

AFP↓, 1,   EGFR↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   Weight↑, 1,  
Total Targets: 52

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   GSR↑, 1,   lipid-P↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   LDH↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,  
Total Targets: 18

Scientific Paper Hit Count for: P21, P21/CDKN1A
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#:161  Target#:234  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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