P53 Cancer Research Results

P53, P53-Guardian of the Genome: Click to Expand ⟱
Source: TCGA
Type: Proapototic
TP53 is the most commonly mutated gene in human cancer. TP53 is a gene that encodes for the p53 tumor suppressor protein ; TP73 (Chr.1p36.33) and TP63 (Chr.3q28) genes that encode transcription factors p73 and p63, respectively, are TP53 homologous structures.
p53 is a crucial tumor suppressor protein that plays a significant role in regulating the cell cycle, maintaining genomic stability, and preventing tumor formation. It is often referred to as the "guardian of the genome" due to its role in protecting cells from DNA damage and stress.
TP53 gene, which encodes the p53 protein, is one of the most frequently mutated genes in human cancers.
Overexpression of MDM2, an inhibitor of p53, can lead to decreased p53 activity even in the presence of wild-type p53.
In some cancers, particularly those with mutant p53, there may be an overexpression of the p53 protein.
Cancers with overexpression: Breast, lung, colorectal, overian, head and neck, Esophageal, bladder, pancreatic, and liver.
Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


Scientific Papers found: Click to Expand⟱
2640- Api,    Apigenin: A Promising Molecule for Cancer Prevention
- Review, Var, NA
chemoPv↑, ITGB4↓, TumCI↓, TumMeta↓, Akt↓, ERK↓, p‑JNK↓, *Inflam↓, *PKCδ↓, *MAPK↓, EGFR↓, CK2↓, TumCCA↑, CDK1↓, P53↓, P21↑, Bax:Bcl2↑, Cyt‑c↑, APAF1↑, Casp↑, cl‑PARP↑, VEGF↓, Hif1a↓, IGF-1↓, IGFBP3↑, E-cadherin↑, β-catenin/ZEB1↓, HSPs↓, Telomerase↓, FASN↓, MMPs↓, HER2/EBBR2↓, CK2↓, eff↑, AntiAg↑, eff↑, FAK↓, ROS↑, Bcl-2↓, Cyt‑c↑, cl‑Casp3↑, cl‑Casp7↑, cl‑Casp8↑, cl‑Casp9↑, cl‑IAP2↑, AR↓, PSA↓, p‑pRB↓, p‑GSK‐3β↓, CDK4↓, ChemoSen↑, Ca+2↑, cal2↑,
557- ART/DHA,    Artemisinin and Its Derivatives in Cancer Care
- Review, Var, NA
*BioAv↓, *BioAv↑, Apoptosis↑, EGFR↓, CD31↓, Ki-67↓, P53↓, TfR1/CD71↑, P-gp↓, PD-1↝,
5690- BJ,  BRU,    Brusatol: A potential sensitizing agent for cancer therapy from Brucea javanica
- Review, Var, NA
NRF2↓, TumCG↓, ChemoSen↑, ROS↑, NF-kB↓, Akt↓, mTOR↓, TumCCA↑, Apoptosis↑, PARP↑, Casp↑, P53↓, Bcl-2↓, PI3K↓, JAK2↓, EMT↓, p27↑, ROCK1↓, MMP2↓, MMP9↓, NRF2↓, AntiTum↑, HO-1↓, NQO1↓, VEGF↓, MRP1↓, RadioS↑, PhotoS↑, toxicity↝,
2828- FIS,    Fisetin, a Potent Anticancer Flavonol Exhibiting Cytotoxic Activity against Neoplastic Malignant Cells and Cancerous Conditions: A Scoping, Comprehensive Review
- Review, Var, NA
*neuroP↑, *antiOx↑, *Inflam↓, RenoP↑, COX2↓, Wnt↓, EGFR↓, NF-kB↓, Casp3↑, Ca+2↑, Casp8↑, TumCCA↑, CDK1↓, PI3K↓, Akt↓, mTOR↓, MAPK↓, *P53↓, *P21↓, *p16↓, mTORC1↓, mTORC2↓, P53↑, P21↑, cycD1/CCND1↓, cycA1/CCNA1↓, CDK2↓, CDK4↓, BAX↑, Bcl-2↓, PCNA↓, HER2/EBBR2↓, Cyt‑c↑, MMP↓, cl‑Casp9↑, MMP2↓, MMP9↓, cl‑PARP↑, uPA↓, DR4↑, DR5↑, ROS↓, AIF↑, CDC25↓, Dose↑, CHOP↑, ROS↑, cMyc↓, cardioP↑,
3277- Lyco,    Recent trends and advances in the epidemiology, synergism, and delivery system of lycopene as an anti-cancer agent
- Review, Var, NA
antiOx↑, TumCP↓, Apoptosis↑, TumMeta↑, ChemoSen↑, BioAv↓, Dose↝, BioAv↓, BioAv↑, SOD↑, Catalase↑, GPx↑, IL2↑, IL4↑, IL1↑, TNF-α↑, GSH↑, GPx↑, GSTA1↑, GSR↑, PPARγ↑, Casp3↑, NF-kB↓, COX2↓, Bcl-2↑, BAX↓, P53↓, CHK1↓, Chk2↓, γH2AX↓, DNAdam↓, ROS↓, P21↑, PCNA↓, β-catenin/ZEB1↓, PGE2↓, ERK↓, cMyc↓, cycE/CCNE↓, JAK1↓, STAT3↓, SIRT1↑, cl‑PARP↑, cycD1/CCND1↓, TNF-α↓, IL6↓, p65↓, MMP2↓, MMP9↓, Wnt↓,
198- MFrot,  MF,    Biological effects of rotating magnetic field: A review from 1969 to 2021
- Review, Var, NA
AntiCan↑, breath↑, Pain↓, Appetite↑, Strength↑, BowelM↑, TumMeta↓, TumCCA↑, ETC↓, MMP↓, TumCD↑, selectivity↑, ROS↑, Casp3↑, TumCG↓, TumCCA↑, ChrMod↑, TumMeta↓, Imm↑, DCells↑, Akt↓, OS⇅, toxicity↓, QoL↑, hepatoP↑, Pain↓, Weight↑, Strength↑, Sleep↑, IL6↓, CD4+↑, CD8+↑, Ca+2↑, radioP↑, chemoP↑, *BMD↑, *AntiAge↑, *AMPK↑, *P21↓, *P53↓, *mTOR↓, *OS↑, *β-Endo↑, *5HT↓,
4919- PEITC,    Natural compound PEITC inhibits gain of function of p53 mutants in cancer cells by switching YAP-binding partners between p53 and p73
- in-vitro, Var, NA
Apoptosis↑, TumCCA↑, P53↓,
3352- QC,    A review of quercetin: Antioxidant and anticancer properties
- Review, Var, NA
*antiOx↑, *lipid-P↓, *TNF-α↓, *NF-kB↓, *COX2↓, *IronCh↑, P53↓, TumCCA↑, HSPs↓, P21↓, RAS↓, ER(estro)↑, OS?,

Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 2,   GSH↑, 1,   GSR↑, 1,   GSTA1↑, 1,   HO-1↓, 1,   NQO1↓, 1,   NRF2↓, 2,   ROS↓, 2,   ROS↑, 4,   SOD↑, 1,  

Metal & Cofactor Biology ⓘ

TfR1/CD71↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   CDC25↓, 1,   ETC↓, 1,   MMP↓, 2,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 2,   FASN↓, 1,   PPARγ↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 4,   APAF1↑, 1,   Apoptosis↑, 4,   BAX↓, 1,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   Bcl-2↑, 1,   Casp↑, 2,   Casp3↑, 3,   cl‑Casp3↑, 1,   cl‑Casp7↑, 1,   Casp8↑, 1,   cl‑Casp8↑, 1,   cl‑Casp9↑, 2,   Chk2↓, 1,   CK2↓, 2,   Cyt‑c↑, 3,   DR4↑, 1,   DR5↑, 1,   cl‑IAP2↑, 1,   p‑JNK↓, 1,   MAPK↓, 1,   p27↑, 1,   Telomerase↓, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 2,  

Transcription & Epigenetics ⓘ

BowelM↑, 1,   ChrMod↑, 1,   PhotoS↑, 1,   p‑pRB↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   HSPs↓, 2,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   DNAdam↓, 1,   P53↓, 6,   P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 3,   PCNA↓, 2,   γH2AX↓, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 2,   CDK2↓, 1,   CDK4↓, 2,   cycA1/CCNA1↓, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   P21↓, 1,   P21↑, 3,   TumCCA↑, 7,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   ERK↓, 2,   p‑GSK‐3β↓, 1,   IGF-1↓, 1,   IGFBP3↑, 1,   mTOR↓, 2,   mTORC1↓, 1,   mTORC2↓, 1,   PI3K↓, 2,   RAS↓, 1,   STAT3↓, 1,   TumCG↓, 2,   Wnt↓, 2,  

Migration ⓘ

AntiAg↑, 1,   Ca+2↑, 3,   cal2↑, 1,   CD31↓, 1,   E-cadherin↑, 1,   FAK↓, 1,   ITGB4↓, 1,   Ki-67↓, 1,   MMP2↓, 3,   MMP9↓, 3,   MMPs↓, 1,   ROCK1↓, 1,   TumCI↓, 1,   TumCP↓, 1,   TumMeta↓, 3,   TumMeta↑, 1,   uPA↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 3,   Hif1a↓, 1,   VEGF↓, 2,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   COX2↓, 2,   DCells↑, 1,   IL1↑, 1,   IL2↑, 1,   IL4↑, 1,   IL6↓, 2,   Imm↑, 1,   JAK1↓, 1,   JAK2↓, 1,   NF-kB↓, 3,   p65↓, 1,   PD-1↝, 1,   PGE2↓, 1,   PSA↓, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   ER(estro)↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 1,   ChemoSen↑, 3,   Dose↑, 1,   Dose↝, 1,   eff↑, 2,   MRP1↓, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 3,   HER2/EBBR2↓, 2,   IL6↓, 2,   Ki-67↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   Appetite↑, 1,   breath↑, 1,   cardioP↑, 1,   chemoP↑, 1,   chemoPv↑, 1,   hepatoP↑, 1,   OS?, 1,   OS⇅, 1,   Pain↓, 2,   QoL↑, 1,   radioP↑, 1,   RenoP↑, 1,   Sleep↑, 1,   Strength↑, 2,   toxicity↓, 1,   toxicity↝, 1,   Weight↑, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 160

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   lipid-P↓, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,  

Cell Death ⓘ

MAPK↓, 1,  

DNA Damage & Repair ⓘ

p16↓, 1,   P53↓, 2,  

Cell Cycle & Senescence ⓘ

P21↓, 2,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,  

Migration ⓘ

PKCδ↓, 1,   β-Endo↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 2,   NF-kB↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

5HT↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,  

Clinical Biomarkers ⓘ

BMD↑, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   neuroP↑, 1,   OS↑, 1,  
Total Targets: 22

Scientific Paper Hit Count for: P53, P53-Guardian of the Genome
1 Apigenin (mainly Parsley)
1 Artemisinin
1 Brucea javanica
1 brusatol
1 Fisetin
1 Lycopene
1 Magnetic Field Rotating
1 Magnetic Fields
1 Phenethyl isothiocyanate
1 Quercetin
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:26  Cells:%  prod#:%  Target#:236  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

Home Page