CREB Cancer Research Results

CREB, cAMP Response Element Binding Protein: Click to Expand ⟱
Source:
Type: transcription factor
CREB is a transcription factor that binds to specific DNA sequences, known as cAMP response elements (CRE), in the promoter regions of target genes.
CREB is activated by phosphorylation, which allows it to bind to CRE and recruit other transcriptional coactivators.
CREB regulates the expression of genes involved in various cellular processes, including:
    Cell growth and differentiation
    Apoptosis
    Metabolism
    Neurotransmission

CREB is also involved in the regulation of genes involved in cancer, including:
    Cell cycle progression
    Angiogenesis
    Invasion and metastasis

CREB is often overexpressed in cancer tissues.
High levels of CREB expression are associated with poor prognosis, increased tumor aggressiveness, and resistance to therapy. CREB can promote the expression of genes involved in cell survival and proliferation.
Scientific Papers found: Click to Expand⟱
279- ALA,    Lipoic acid-induced oxidative stress abrogates IGF-1R maturation by inhibiting the CREB/furin axis in breast cancer cell lines
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Furin↓,
IGF-1R↓,
ROS↑, LA (0.5 and 1 mM) exerts its anticancer effects in the context of ovarian cancer by inducing the generation of reactive oxygen species (ROS)
CREB↓, we then demonstrated that this oxidative stress induced by LA is essential to inhibit CREB expression
Furin↓, reduction of furin expression is the consequence of the downregulation of CREB
IGF-1R↓, All of these events contribute to an inhibition of IGF-1R maturation

573- ART/DHA,    Artesunate suppresses tumor growth and induces apoptosis through the modulation of multiple oncogenic cascades in a chronic myeloid leukemia xenograft mouse model
- vitro+vivo, NA, NA
p‑p38↓,
p‑ERK↓,
p‑CREB↓,
p‑Chk2↓,
p‑STAT5↓,
p‑RSK↓,
SOCS1↑,
Apoptosis↑,
Casp3↑,

5761- CAPE,    Caffeic acid phenethyl ester suppresses the proliferation of human prostate cancer cells through inhibition of AMPK and Akt signaling networks
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Pca, PC3
TumCP↓, We observed that CAPE dosage-dependently suppressed the proliferation of LNCaP, DU-145, and PC-3 human prostate cancer cells.
TumCG↓, Administration of CAPE by gavage significantly inhibited the tumor growth of LNCaP xenografts in nude mice.
TumCCA↑, CAPE caused retardation of xenograft growth and G1 cell cycle arrest in LNCaP cells
AMPK↓, ollowing CAPE treatment, AMPK, SGK1, and NF-κB pathways were down-regulated.
NF-kB↓,
β-catenin/ZEB1↓, This down-regulation likely resulted in the decrease of β-catenin and Creb signaling, cyclin D1 and cyclin E1 expression, Cdk2 and Cdk4 activity, as well as increase of p27Kip1 expression.
CREB↓,
cycD1/CCND1↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,

5013- DSF,  Cu,  Z,    Disulfiram inhibits activating transcription factor/cyclic AMP-responsive element binding protein and human melanoma growth in a metal-dependent manner in vitro, in mice and in a patient with metastatic disease
- vitro+vivo, Melanoma, NA - Case Report, Melanoma, NA
P-gp↓, disulfiram blocks the P-glycoprotein extrusion pump, inhibits the transcription factor nuclear factor-κB, sensitizes tumors to chemotherapy, reduces angiogenesis, and inhibits tumor growth in mice.
NF-kB↓,
ChemoSen↑,
angioG↓,
TumCG↓,
TumMeta↓, The combination of oral zinc gluconate and disulfiram at currently approved doses for alcoholism also induced >50% reduction in hepatic metastases and produced clinical remission in a patient with stage IV metastatic ocular melanoma, who has continu
Remission↑,
toxicity↓, who has continued on oral zinc gluconate and disulfiram therapy for 53 continuous months with negligible side effects.
ATF2↓, Disulfiram and Metals Inhibit ATF/CREB DNA Binding and Cyclin A Expression
CREB↓,
cycA1/CCNA1↓,
TumCG↓, Disulfiram and Zn2+ Inhibit Melanoma Growth and Angiogenesis in Mice
angioG↓,
Dose↝, 250 mg/d disulfiram with the largest meal of the day. This dose was increased to 500 mg/d after 1 month. Zinc gluconate (50 mg chelated elemental Zn2+, ) was also given thrice daily but not concurrent with disulfiram administration.
toxicity↝, On starting the protocol, the patient suffered grade 1 (National Cancer Institute Common Toxicity Criteria, version 2.0) diarrhea, nausea, depression, and malaise. Except for nausea, these side effects resolved within 2 months of continued treatment.

4003- Gins,    Neuroprotective Potentials of Panax Ginseng Against Alzheimer's Disease: A Review of Preclinical and Clinical Evidences
- Review, adrenal, NA
*neuroP↑, has neuroprotective effects against a series of pathological cascades in AD, including beta-amyloid formation, neuroinflammation, oxidative stress, and mitochondrial dysfunction.
*Inflam↓,
*ROS↓,
*BACE↓, Ginsenoside Re inhibits the activity of BACE1 by increasing PPARγ expression at the mRNA and protein levels in N2a/APP695 cells and thereby reduces the generation of Aβ1–40 and Aβ1–42
*PPARγ↑,
*Aβ↓, ginsenosides Rb1, Rd, Re, and Rg1 can inhibit Aβ aggregation to regulate the phosphorylation of tau protein in the prevention and treatment of AD.
*p‑tau↓, inhibiting tau phosphorylation
*NF-kB↓, Rd pretreatment at 10 mg/kg significantly suppresses the NF-κB pathway activity, reducing the generation of pro-inflammatory cytokines, such as interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor-α (TNF-α)
*IL1β↓,
*IL6↓,
*TNF-α↓,
*ROS↓, Ginsenoside Rg1 can reduce the NADPH oxidase 2 (NOX2)–mediated ROS production and neuronal apoptosis
*CREB↓, Ginsenoside F1 can decrease phosphorylated cAMP-response element binding protein (CREB) and increase cortical BDNF levels in the hippocampus, reducing Aβ plaques and improving memory function of APP/PS1 double-transgenic AD mice
*BDNF↑,
*memory↑,

5210- PI,    Piperine is a potent inhibitor of nuclear factor-kappaB (NF-kappaB), c-Fos, CREB, ATF-2 and proinflammatory cytokine gene expression in B16F-10 melanoma cells
- in-vitro, Melanoma, B16-BL6
IL1β↓, IL-1beta, IL-6, TNF-alpha and GM-CSF. Piperine treatment significantly reduced the above proinflammatory cytokines.
TNF-α↓,
MMPs↓, Piperine could inhibit the matrix metalloproteinase production
p65↓, p65, p50, c-Rel subunits of NF-kappaB and other transcription factors such as ATF-2, c-Fos and CREB were inhibited by the treatment of piperine.
p50↓,
NF-kB↓,
ATF2↓,
cFos↓,
CREB↓,

1016- PI,    Piperine suppresses the Wnt/β-catenin pathway and has anti-cancer effects on colorectal cancer cells
- in-vitro, CRC, HCT116 - in-vitro, CRC, SW480 - in-vitro, CRC, DLD1
β-catenin/ZEB1↓,
Wnt↓, piperine inhibits the canonical Wnt pathway induced by overexpression of β-catenin
TumCP↓, piperine impairs cell proliferation and migration in HCT116, SW480 and DLD-1 colorectal tumor cell line
TumCMig↓,
*antiOx↑, Studies have shown that piperine has diverse pharmacological properties, including anticonvulsive activity22, antioxidant activity23, anti-inflammatory24,25, liver protective26, neuroprotective27 and acts as an antimicrobial agent28.
*Inflam↓,
*hepatoP↑,
*neuroP↑,
*Bacteria↓,
*memory↑, exhibits potential to treat depressive disorders and to enhance memory in animal models29,30. In addition to all these properties, piperine also exerts an anticancer effect31.
AntiCan↑,
NF-kB↓, In melanoma cells, piperine inhibitis NF-κβ, c-Fos, ATF-2 and CREB
cFos↓,
ATF2↓,
CREB↓,


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↓, 1,   CREB↓, 5,   p‑CREB↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   ATF2↓, 3,   Casp3↑, 1,   p‑Chk2↓, 1,   p‑p38↓, 1,   p‑RSK↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycA1/CCNA1↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

cFos↓, 2,   p‑ERK↓, 1,   IGF-1R↓, 2,   p‑STAT5↓, 1,   TumCG↓, 3,   Wnt↓, 1,  

Migration ⓘ

Furin↓, 2,   MMPs↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   NF-kB↓, 4,   p50↓, 1,   p65↓, 1,   SOCS1↑, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose↝, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   Remission↑, 1,   toxicity↓, 1,   toxicity↝, 1,  
Total Targets: 42

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS↓, 2,  

Core Metabolism/Glycolysis ⓘ

CREB↓, 1,   PPARγ↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   IL6↓, 1,   Inflam↓, 2,   NF-kB↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,   p‑tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,   BACE↓, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,   memory↑, 2,   neuroP↑, 2,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 18

Scientific Paper Hit Count for: CREB, cAMP Response Element Binding Protein
2 Piperine
1 Alpha-Lipoic-Acid
1 Artemisinin
1 Caffeic Acid Phenethyl Ester (CAPE)
1 Disulfiram
1 Copper and Cu NanoParticles
1 Zinc
1 Ginseng
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#:%  Target#:798  State#:%  Dir#:1
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