p300 Cancer Research Results

p300, p300: Click to Expand ⟱
Source:
Type:
p300 is a transcriptional coactivator protein that plays a crucial role in regulating gene expression, cell growth, and differentiation.
p300 has been shown to promote tumor initiation and progression by regulating the expression of genes involved in cell growth, survival, and metastasis.
p300 is overexpressed in various types of cancer, with poor prognosis.
Scientific Papers found: Click to Expand⟱
1485- CUR,  Chemo,  Rad,    Curcumin, the golden spice from Indian saffron, is a chemosensitizer and radiosensitizer for tumors and chemoprotector and radioprotector for normal organs
- Review, Var, NA
ChemoSen↑, Such effects of curcumin were due to its ability to sensitize cancer cells for increased production of ROS
NF-kB↓, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF-κB, STAT3, COX2, Akt
*STAT3↓, curcumin acts as a chemosensitizer and radiosensitizer has also been studied extensively. For example, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF-kB, STAT3, COX2, Akt,
*COX2↓,
*Akt↓,
*NRF2↑, The protective effects of curcumin appear to be mediated through its ability to induce the activation of NRF2 and induce the expression of antioxidant enzymes (e.g., hemeoxygenase-1, glutathione peroxidase
*HO-1↑,
*GPx↑,
*NADPH↑,
*GSH↑, increase glutathione (a product of the modulatory subunit of gamma-glutamyl-cysteine ligase)
*ROS↓, dietary curcumin can inhibit chemotherapy-induced apoptosis via inhibition of ROS generation and blocking JNK signaling
*p300↓, inhibit p300 HAT activity
radioP↑, radioprotector for normal organs
chemoP↑, curcumin has also been shown to protect normal organs such as liver, kidney, oral mucosa, and heart from chemotherapy and radiotherapy-induced toxicity.
RadioS↑,

1505- CUR,    Epigenetic targets of bioactive dietary components for cancer prevention and therapy
- Review, NA, NA
TumCCA↑,
Apoptosis↑,
DNMTs↓, curcumin also inhibits DNMT activities and histone modification such as HDAC inhibition in tumorigenesis
HDAC↓,
HATs↓, inhibitory activity against HDACs and HATs in several in vitro cancer models
TumCP↓,
p300↓, Significant decreases in the amounts of p300, HDAC1, HDAC3, and HDAC8
HDAC1↓,
HDAC3↓,
HDAC8↓,
NF-kB↓, inhibition of nuclear translocation of the NF-κB/p65 subunit

127- CUR,    The chromatin remodeling protein BRG1 links ELOVL3 trans-activation to prostate cancer metastasis
- in-vitro, Pca, DU145
Elvol3↓, Similar to p300 depletion, curcumin treatment assuaged Elovl3 induction
p300↓,

817- GAR,    Garcinol inhibits esophageal cancer metastasis by suppressing the p300 and TGF-β1 signaling pathways
- vitro+vivo, SCC, KYSE150 - vitro+vivo, SCC, KYSE450
HATs↓, Garcinol, a natural compound extracted from Gambogic genera, is a histone acetyltransferase (HAT) inhibitor
TumCCA↑,
Apoptosis↑,
TumCMig↓,
TumCI↓,
CBP↓,
p300↓,
TGF-β↓, suppressed TGF-β1-activated Smad and non-Smad pathway
Ki-67↓,
SMAD2↓,
SMAD3↓,

1506- RES,    Epigenetic targets of bioactive dietary components for cancer prevention and therapy
- Review, NA, NA
DNMTs↓, weaker DNMT inhibitory activity than other dietary bioactive components such as EGCG
BRCA1↑, resveratrol treatment, which was associated with BRAC-1 reactivation in MCF-7 cells
HDAC↓, resveratrol is associated with activation of the type III HDAC inhibitors, sirtuin 1 (SIRT1), and p300, in multiple in vitro and in vivo models
SIRT1↑,
p300↓, Significant decreases in the amounts of p300, HDAC1, HDAC3, and HDAC8
survivin↓,
HDAC1↓,
HDAC3↓,
HDAC8↓,

1820- VitK3,    Vitamin K3 (menadione) suppresses epithelial-mesenchymal-transition and Wnt signaling pathway in human colorectal cancer cells
- in-vitro, CRC, SW480 - in-vitro, CRC, SW-620
selectivity↑, Menadione showed cytotoxicity against human CRC cells (SW480 and SW620) and human primary colon cancer cells but was relatively ineffective against the cells from human normal colon (CRL-1790)
TumCI↓, Menadione suppressed invasion, migration and epithelial-mesenchymal transition in human CRC cells
TumCMig↓,
EMT↓,
E-cadherin↑, by upregulating the expression of E-cadherin (CDH1), ZO-1
ZO-1↑,
N-cadherin↓, and downregulating that of N-cadherin (CDH2), Vimentin (VIM), ZEB1, MMP2 and MMP9.
Vim↓,
Zeb1↓,
MMP2↓,
MMP9↓,
TOPflash↓, Menadione decreased TOPFlash/FOPFlash luciferase activity
β-catenin/ZEB1↓, β-catenin (CTNNB1), TCF7L2, Bcl9l, p300 (EP300) and cyclin D1 (CCND1) was suppressed
p300↓,
cycD1/CCND1↓,
TumCCA↑, SubG0 phase of cell cycle


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Core Metabolism/Glycolysis ⓘ

Elvol3↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Apoptosis↑, 2,   CBP↓, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

HATs↓, 2,  

DNA Damage & Repair ⓘ

BRCA1↑, 1,   DNMTs↓, 2,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   HDAC↓, 2,   HDAC1↓, 2,   HDAC3↓, 2,   HDAC8↓, 2,   p300↓, 5,   TOPflash↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   Ki-67↓, 1,   MMP2↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   SMAD2↓, 1,   SMAD3↓, 1,   TGF-β↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 1,   Vim↓, 1,   Zeb1↓, 1,   ZO-1↑, 1,   β-catenin/ZEB1↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 2,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

BRCA1↑, 1,   Ki-67↓, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   radioP↑, 1,  
Total Targets: 40

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GPx↑, 1,   GSH↑, 1,   HO-1↑, 1,   NRF2↑, 1,   ROS↓, 1,  

Core Metabolism/Glycolysis ⓘ

NADPH↑, 1,  

Cell Death ⓘ

Akt↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

p300↓, 1,   STAT3↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,  
Total Targets: 10

Scientific Paper Hit Count for: p300, p300
3 Curcumin
1 Chemotherapy
1 Radiotherapy/Radiation
1 Garcinol
1 Resveratrol
1 VitK3,menadione
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

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