CBP Cancer Research Results

CBP, CREB-binding protein: Click to Expand ⟱
Source:
Type:
CBP is a transcriptional coactivator that plays a crucial role in regulating gene expression, and it has been implicated in various cellular processes, including cell growth, differentiation, and apoptosis.
CBP is of interest because it can influence the activity of oncogenes and tumor suppressor genes. CBP can act as an oncogene in certain contexts. Its ability to enhance the transcription of genes that promote cell proliferation and survival can contribute to tumorigenesis. Overexpression of CBP has been observed in various cancers, including breast, colon, and prostate cancers.
CBP may also function as a tumor suppressor. For instance, mutations or loss of CBP expression can lead to the activation of oncogenic pathways. This dual role can depend on the specific cellular context and the presence of other signaling molecules.
CBP interacts with numerous transcription factors, including p53, which is a well-known tumor suppressor. The interaction between CBP and p53 is crucial for p53's role in regulating the cell cycle and apoptosis. Dysregulation of this interaction can lead to cancer development.
Overexpressed: breast,CRC, prostate, lung, HCC, ovrian, bladder, pancreatic, head and neck, AML.
Scientific Papers found: Click to Expand⟱
183- CUR,    Curcumin down-regulates AR gene expression and activation in prostate cancer cell lines
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
AR↓, Down-regulation of AR signal transduction.
AP-1↓, Down-regulation ofAP-1 and NF-KB signal transduction.
NF-kB↓, The results obtained here demonstrate that curcumin has a potential therapeutic effect on prostate cancer cells through down-regulation of AR and AR-related cofactors (AP-1, NF-kappaB and CBP).
CBP↓,

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↓,

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↓,


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

DDIT4↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   ROS↑, 1,   TrxR↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 3,   Apoptosis↑, 2,   mt-Apoptosis↑, 1,   Bcl-2↓, 1,   CBP↓, 5,   iNOS↓, 1,   JNK↑, 1,   MAPK↓, 1,   Mcl-1↓, 1,   survivin↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

EZH2↓, 1,   HATs↓, 4,   miR-218↑, 1,   PCAF↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   ER Stress↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

SESN2↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DFF45↓, 1,   DNAdam↑, 1,   P53↑, 1,   PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

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

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

CSCs↓, 1,   EMT↓, 1,   mTOR↓, 1,   NOTCH↓, 1,   p300↓, 4,   PI3K↓, 3,   STAT↓, 2,   STAT3↓, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   CDK4/6↓, 1,   Ki-67↓, 1,   MMP2↓, 1,   MMP3↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   SMAD2↓, 1,   SMAD3↓, 1,   TGF-β↓, 1,   TRIB3↑, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 3,   Twist↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

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

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 1,   eff↑, 1,   Half-Life↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

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

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   toxicity↓, 1,  
Total Targets: 79

Pathway results for Effect on Normal Cells:


Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,  
Total Targets: 1

Scientific Paper Hit Count for: CBP, CREB-binding protein
4 Garcinol
1 Curcumin
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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