p300 Cancer Research Results

p300, p300: Click to Expand ⟱
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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/PTGS2↓,
*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↓,

7087- GAR,    Garcinol as an Epigenetic Modulator: Mechanisms of Anti-Cancer Activity and Therapeutic Potential
- Review, Var, NA
HATs↓, Its activities include inhibition of histone acetyltransferases (HATs)
p300↓, By inhibiting HAT enzymes such as p300/CBP and PCAF, garcinol affects the acetylation status of multiple transcription factors and histones,
CBP↓,
NF-kB↓, including NF-κB, STAT3, PI3K/AKT, MAPK, and Wnt/β-catenin, resulting in the suppression of inflammation, angiogenesis, proliferation, and metastasis.
STAT3↓, inhibition of NF-kB, STAT 3, P13/Akt, COX-2, MAPK pathways
PI3K↓,
Akt↓,
MAPK↓,
Wnt↓,
β-catenin/ZEB1↓,
Inflam↓,
angioG↓,
TumCP↓,
TumMeta↓,
TumCCA↑, figure 3
EMT↓, inhibition of epithelial-to-mesenchymal transition (EMT), and cancer stem cell targeting.
CSCs↓,
P53↑, garcinol activates tumor-suppressor proteins such as p53 and inhibits thioredoxin reductase, resulting in elevated intracellular reactive oxygen species (ROS).
TrxR↓,
ROS↑,
JNK↑, The accumulation of ROS subsequently stimulates JNK activation and DNA damage signaling, reinforcing p53 function and promoting apoptosis rather than mere growth inhibition
DNAdam↑,
mt-Apoptosis↑, showing activation of mitochondrial apoptosis through the ROS/JNK/ATF-2/Bcl-2 axis
ER Stress↑, In rhabdomyosarcoma cells, garcinol was also shown to trigger endoplasmic reticulum (ER) stress, elevating the expression of stress-responsive genes such as DDIT3, DDIT4, TRIB3, and SESN2, which facilitate apoptosis under prolonged stress [
CHOP/DDIT3↑,
DDIT4↑,
TRIB3↑,
SESN2↑,
miR-218↑, garcinol upregulates let-c family miRNAs and miR-218 in breast cancer and NSCLC cells by the suppression of EMT and stemness
eff↑, When combined with HDAC inhibitors such as SAHA (Suberoylanilide Hydroxamic Acid), also known by its clinical name Vorinostat, garcinol provides complementary effects on maintaining histone acetylation balance,
ChemoSen↑, when used alongside chemotherapeutic agents such as doxorubicin or cisplatin, garcinol sensitizes resistant tumor cells by restoring apoptotic gene expression and overcoming drug resistance mechanisms
BioAv↓, garcinol suffers from poor aqueous solubility, rapid metabolism, and limited bioavailability,
Half-Life↓,
BioAv↑, These nanoformulations have demonstrated enhanced cellular uptake, prolonged plasma half-life, and superior cytotoxicity in breast, colon, and lung cancer models compared with free garcinol

7086- GAR,    Garcinol: An emerging epigenetic modifier with versatile anticancer properties
- Review, Var, NA
AntiCan↑, garcinol has demonstrated huge potential as an anti-cancer agent, inhibiting tumor growth, progression, and metastasis in various cancers, such as lung, liver, pancreas, prostate, breast, colon, and brain cancers.
TumCG↓,
TumMeta↓,
toxicity↓, garcinol offers a safer alternative with broad-spectrum activity and minimal adverse effects.
Apoptosis↑, anti-tumorigenic properties are linked to apoptosis induction, angiogenesis inhibition, and modulation of the tumor microenvironment
angioG↓,
*BioAv↝, nano-delivery systems have improved its bioavailability and therapeutic efficacy, overcoming challenges related to its solubility and stability.
HATs↓, Garcinol primarily targets histone acetyltransferases (HATs), particularly p300 and CBP (CREB-binding protein), leading to structural modifications in these proteins.
p300↓,
CBP↓,
PI3K↓, Garcinol exerts its anticancer effects primarily by modulating key signaling pathways, including the PI3K/AKT, NF-κB, JAK/STAT, and MAPK pathways.
Akt↓,
NF-kB↓,
STAT↓,
mTOR↓, figure 1
DFF45↓,
survivin↓,
N-cadherin↓,
Twist↓,
MMP2↓,
MMP3↓,
MMP9↓,
Mcl-1↓,
EZH2↓,
NOTCH↓,
CXCR4↓,
PGE2↓,
VEGF↓,
mPGES-1↓,
CycB/CCNB1↓,
CDK2↓,
CDK4/6↓,
iNOS↓,
COX2/PTGS2↓,
IL1↓,
TNF-α↓,
PARP↑,
Bcl-2↓,

7091- GAR,    Garcinol-A Natural Histone Acetyltransferase Inhibitor and New Anti-Cancer Epigenetic Drug
- Review, Var, NA
antiOx↑, Garcinol action in cancer cells is based on its antioxidant and anti-inflammatory properties, but also on its potency to inhibit histone acetyltransferases (HATs).
Inflam↓,
HATs↓,
p300↓, Elevated levels of P300/CBP and PCAF have been reported in many malignancies.
CBP↓,
PCAF↓,
cycD1/CCND1↓, Garcinol decreased cyclin D1 and cyclin D3 expression, decreased STAT expression, and caused inhibition of the PI3K/AKT pathway, which is crucial for proliferation, invasion, and metastasis
STAT↓,
PI3K↓,
Akt↓,
TumCP↓,
TumCI↓,
TumMeta↓,
TumCCA↑, garcinol application resulted in cell cycle arrest and a marked decrease in cyclin-dependent kinase 2 (CDK2) and cyclin-dependent kinase 4 (CDK4) expression
CDK2↓,
CDK4↓,

7092- GAR,    Garcinol and Its Role in Chronic Diseases
- Review, Var, NA
antiOx↑, demonstrated to be anti-oxidant, anti-inflammatory and anti-cancer in nature.
Inflam↓,
AntiCan↑,
NF-kB↓, Garcinia indica has been found to be an effective inhibitor of several key regulatory pathways (e.g., NF-kB, STAT3 etc.) in cancer cells, thereby being able to control malignant growth of solid tumours in vivo.
STAT3↓,
antiNeop↑, Despite its high potential as an anti-neoplastic modulator of several cancer types such as head and neck cancer, breast cancer, hepatocellular carcinoma, prostate cancer, colon cancer etc.
5LO↓, ability of garcinol to bind and inhibit 5-lipoxygenase (5-Lox),
eff↑, . The addition of 10 % FBS (fetal bovine serum) to medium leads to approximately 10-fold decrease in IC 50 value of garcinol for HCT116 cell growth.
HATs↓, Garcinol has been demonstrated to inhibit HATs such as p300 and PCAF both in vitro and in vivo
p300↓,
PCAF↓,
miR-200c↑, Garcinol treatment has been shown to cause upregulation of several tumor suppressor miRNAs, of which miR-200c was found to target and downregulate Notch1 in pancreatic CSCs
NOTCH1↓,
CSCs↓,
COX2/PTGS2↓, garcinol has been shown to cause significant reduction in expression level of cyclooxygenase-2 (COX-2), cyclin D1, and vascular endothelial growth factor
cycD1/CCND1↓,
VEGF↓,
PI3K↓, via inhibition of the extracellular signal-regulated protein kinase 1/2, PI3K/Akt and Wnt/b-catenin
Akt↓,
Wnt↑,
β-catenin/ZEB1↓,
ROS↑, It could lead to accumulation of reactive oxygen species (ROS), endoplasmic reticulum (ER) stress modulator GADD153
CHOP/DDIT3↑,
Bax:Bcl2↑, increased Bax2/Bcl-2 ratio, elevated tBid (truncated Bid), and caspase 8 in cancer cell.
Casp8↑,
FAK↓, garcinol can lead to inhibition of tyrosine phosphorylation of focal adhesion kinase (FAK),
*neuroP↑, garcinol being considered in development of therapeutics for neurodegenerative diseases such as Alzheimers’s, Parkinson’s to attenuate oxidative stress-induced neurotoxicity.
PCNA↓, Significant reduction in proliferating cell nuclear antigen (PCNA) index in ACF was also observed with gar- cinol treatment
*GSTs↑, Garcinol administration in such cases was also seen to enhance activities of liver glutathione S-transferase (GST) and quinone reductase (QR), which play an important role in detoxification process of body

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 10 of 10

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

DDIT4↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   ROS↑, 2,   TrxR↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

Elvol3↓, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 4,   Apoptosis↑, 3,   mt-Apoptosis↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Casp8↑, 1,   CBP↓, 4,   iNOS↓, 1,   JNK↑, 1,   MAPK↓, 1,   Mcl-1↓, 1,   survivin↓, 2,  

Transcription & Epigenetics(tgid=7) ⓘ

EZH2↓, 1,   HATs↓, 6,   miR-218↑, 1,   PCAF↓, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 2,   ER Stress↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

SESN2↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

BRCA1↑, 1,   DFF45↓, 1,   DNAdam↑, 1,   DNMTs↓, 2,   P53↑, 1,   PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 2,   CDK4↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 3,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CSCs↓, 2,   EMT↓, 2,   HDAC↓, 2,   HDAC1↓, 2,   HDAC3↓, 2,   HDAC8↓, 2,   mTOR↓, 1,   NOTCH↓, 1,   NOTCH1↓, 1,   p300↓, 9,   PI3K↓, 4,   STAT↓, 2,   STAT3↓, 2,   TOPflash↓, 1,   TumCG↓, 1,   Wnt↓, 1,   Wnt↑, 1,  

Migration(tgid=13) ⓘ

5LO↓, 1,   CDK4/6↓, 1,   E-cadherin↑, 1,   FAK↓, 1,   Ki-67↓, 1,   miR-200c↑, 1,   MMP2↓, 2,   MMP3↓, 1,   MMP9↓, 2,   N-cadherin↓, 2,   SMAD2↓, 1,   SMAD3↓, 1,   TGF-β↓, 1,   TRIB3↑, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumCP↓, 3,   TumMeta↓, 3,   Twist↓, 1,   Vim↓, 1,   Zeb1↓, 1,   ZO-1↑, 1,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,   VEGF↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2,   CXCR4↓, 1,   IL1↓, 1,   Inflam↓, 3,   mPGES-1↓, 1,   NF-kB↓, 5,   PGE2↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 2,   eff↑, 2,   Half-Life↓, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BRCA1↑, 1,   EZH2↓, 1,   Ki-67↓, 1,   TRIB3↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   antiNeop↑, 1,   chemoP↑, 1,   radioP↑, 1,   toxicity↓, 1,  
Total Targets: 103

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

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

Core Metabolism/Glycolysis(tgid=4) ⓘ

NADPH↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

p300↓, 1,   STAT3↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,  

Functional Outcomes(tgid=23) ⓘ

neuroP↑, 1,  
Total Targets: 13

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