ATF2 Cancer Research Results

ATF2, Activating Transcription Factor 2: Click to Expand ⟱
Source:
Type:
ATF2 (Activating Transcription Factor 2)
-ATF2 is a member of the ATF/CREB (cyclic AMP response element‐binding protein) family of transcription factors.
-It functions by binding to specific DNA sequences to regulate the transcription of a variety of target genes involved in cell proliferation, stress response, apoptosis, and differentiation.
-ATF2 activity is regulated through phosphorylation by stress-activated protein kinases such as JNK, p38, and ERK, integrating signals from various cellular stressors.

-Increased ATF2 activity in certain lung cancer subtypes has been linked with increased invasiveness and metastatic potential.
Scientific Papers found: Click to Expand⟱
5463- AF,    Will Auranofin Become a Golden New Treatment Against COVID-19?
- Review, Covid, NA
IL6↓, This gold(I) compound has anti-inflammatory properties because it reduces IL-6 expression via inhibition of the NF-κB-IL-6-STAT3 signaling pathway.
NF-kB↓,
ATF2↓,
TrxR↓, by inhibiting redox enzymes such as thioredoxin reductase, auranofin increases cellular oxidative stress and promotes apoptosis.
ROS↑,
Apoptosis↑,
IL6↓, Recently, it was reported that auranofin reduced by 95% SARS-CoV-2 RNA in infected human cells in vitro and decreased SARS-CoV-2-induced cytokine expression, including IL-6.
Dose↑, After 14 days of treatment with 21 mg/day auranofin, plasma gold concentration reached 1.18 µM to 2.21 µM ‘auranofin equivalent’

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.

2922- LT,    Combination of transcriptomic and proteomic approaches helps unravel the mechanisms of luteolin in inducing liver cancer cell death via targeting AKT1 and SRC
- in-vitro, Liver, HUH7
Half-Life↝, However, after oral administration, luteolin showed relatively rapid absorption and slow elimination in rats, with a tmax (time to reach peak plasma level) of approximately 1.02 h and a t1/2 (elimination half-life) of 4.94 h, indicating that luteolin
TumCCA↑, luteolin could promote cell cycle arrest and apoptosis in HuH-7 cells
AKT1↓, Dramatic downregulation of components downstream of the AKT1-ASK2-ATF2 pathway (CycD, BCL2, CycA, etc.), the AKT1-NF-κB pathway (BCL-XL and MIP2) and the AKT1-GSK3β-β-catenin pathway (c-Myc and CCND1)
ATF2↓,
NF-kB↓,
GSK‐3β↓,
cMyc↓,
GSTs↓, expression change of NQO-1, GSTs, and TRXR1 indicated the increase in ROS
TrxR1↓,
ROS↑,

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↓,

2355- SK,    Pharmacological properties and derivatives of shikonin-A review in recent years
- Review, Var, NA
AntiCan↑, anticancer effects on various types of cancer by inhibiting cell proliferation and migration, inducing apoptosis, autophagy, and necroptosis.
TumCP↓,
TumCMig↓,
Apoptosis↑,
TumAuto↑,
Necroptosis↑,
ROS↑, Shikonin also triggers Reactive Oxygen Species (ROS) generation
TrxR1↓, inhibiting the activation of TrxR1, PKM2, RIP1/3, Src, and FAK
PKM2↓,
RIP1↓,
RIP3↓,
Src↓,
FAK↓,
PI3K↓, modulating the PI3K/AKT/mTOR and MAPKs signaling;
Akt↓, shikonin induced a dose-dependent reduction of miR-19a to inhibit the activity of PI3K/AKT/mTOR pathway
mTOR↓,
GRP58↓, shikonin induced apoptosis in human myeloid cell line HL-60 cells through downregulating the expression of ERS protein ERP57 (42).
MMPs↓, hikonin suppressed cell migration through inhibiting the NF-κB pathway and reducing the expression of MMP-2 and MMP-9
ATF2↓, shikonin inhibited cell proliferation and tumor growth through suppressing the ATF2 pathway
cl‑PARP↑, shikonin significantly upregulated the expression of apoptosis-related proteins cleaved PARP and caspase-3 and increased cell apoptosis through increasing the phosphorylation of p38 MAPK and JNK, and inhibiting the phosphorylation of ERK
Casp3↑,
p‑p38↑,
p‑JNK↑,
p‑ERK↓,


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:


Redox & Oxidative Stress ⓘ

GSTs↓, 1,   ROS↑, 3,   TrxR↓, 1,   TrxR1↓, 2,  

Core Metabolism/Glycolysis ⓘ

AKT1↓, 1,   cMyc↓, 1,   CREB↓, 3,   PKM2↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   ATF2↓, 6,   Casp3↑, 1,   GRP58↓, 1,   p‑JNK↑, 1,   Necroptosis↑, 1,   p‑p38↑, 1,   RIP1↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycA1/CCNA1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

cFos↓, 2,   p‑ERK↓, 1,   GSK‐3β↓, 1,   mTOR↓, 1,   PI3K↓, 1,   Src↓, 1,   TumCG↓, 2,   Wnt↓, 1,  

Migration ⓘ

FAK↓, 1,   MMPs↓, 2,   RIP3↓, 1,   TumCMig↓, 2,   TumCP↓, 2,   TumMeta↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   IL6↓, 2,   NF-kB↓, 5,   p50↓, 1,   p65↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose↑, 1,   Dose↝, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

IL6↓, 2,  

Functional Outcomes ⓘ

AntiCan↑, 2,   Remission↑, 1,   toxicity↓, 1,   toxicity↝, 1,  
Total Targets: 53

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

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

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 6

Scientific Paper Hit Count for: ATF2, Activating Transcription Factor 2
2 Piperine
1 Auranofin
1 Disulfiram
1 Copper and Cu NanoParticles
1 Zinc
1 Luteolin
1 Shikonin
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#:1295  State#:%  Dir#:1
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