ICAD Cancer Research Results

ICAD, inhibitor of caspase-activated DNase: Click to Expand ⟱
Source:
Type:
ICAD (inhibitor of caspase-activated DNase, also known as DFFA)
ICAD is the physiological inhibitor of CAD, the nuclease responsible for executing DNA fragmentation during apoptosis.
• Caspase-mediated cleavage of ICAD is a key regulatory step that unleashes CAD activity during apoptosis.

Its dysregulation (either up‐ or down‐regulation) has been linked to altered apoptotic responses, genomic instability, and ultimately clinical outcomes.
Either overexpression or underexpression can disrupt this balance:
▪ Overexpression may blunt the full execution of apoptosis in response to stresses (e.g., chemotherapy).
▪ Underexpression may lead to unscheduled or incomplete apoptosis, which in some scenarios might paradoxically fuel genomic instability.
Scientific Papers found: Click to Expand⟱
3192- SFN,    Transcriptome analysis reveals a dynamic and differential transcriptional response to sulforaphane in normal and prostate cancer cells and suggests a role for Sp1 in chemoprevention
- in-vitro, Pca, PC3
Sp1/3/4↓, Sp1 protein was significantly decreased by SFN treatment in prostate cancer cells . Because SFN decreased the expression of Sp1, and to a lesser extent Sp3
selectivity↑, SFN alters gene expression differentially in normal and cancer cells with key targets in chemopreventive processes, making it a promising dietary anti-cancer agent.
NRF2↑, through the induction of phase 2 enzymes via Keap1-Nrf2 signaling
HDAC↓, SFN also inhibits the activity and/or expression of genes that regulate epigenetic mechanisms including histone deactylases (HDACs) and DNA methyltransferases (DNMTs) in cancer cells
DNMTs↓,
TumCCA↑, 15 μM SFN treatment induces cell cycle arrest at the G1 phase and only modestly increases apoptosis
selectivity↑, Normal prostate epithelial cells (PREC) do not undergo cell cycle arrest or apoptosis in response to this SFN treatment
HO-1↑, In all cell lines and time points, HO1 and NQO1 were identified as significantly upregulated by SFN
NQO1↑,
CDK2↓, MX non-receptor tyrosine kinase (BMX), cyclin-dependent kinase 2 (CDK2), and polo-like kinase 1 (PLK1) had decreased expression with SFN treatment
TumCP↓, suppression of Sp1 expression decreased prostate cancer cells proliferation.
BID↑, SFN treatment produced a significant increase in the expression of the apoptosis related genes Bid, Smac/Diablo, and ICAD only in PC-3 cells (
Smad1↑,
Diablo↑,
ICAD↑,
Cyt‑c↑, It also increased the expression of cytochrome c, c-IAP1, and HSP27 in PC-3 cells while it decreased expression in PREC cells.
IAP1↑,
HSP27↑,
*Cyt‑c↓,
*IAP1↓,
*HSP27↓,
survivin↓, In these studies, inhibition of Sp1 is associated with inhibition of the cancer promoting genes survivin, CDK4, VEGF and the androgen receptor.
CDK4↓,
VEGF↓,
AR↓,


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↑, 1,   NQO1↑, 1,   NRF2↑, 1,  

Cell Death ⓘ

BID↑, 1,   Cyt‑c↑, 1,   Diablo↑, 1,   IAP1↑, 1,   ICAD↑, 1,   survivin↓, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,  

Protein Folding & ER Stress ⓘ

HSP27↑, 1,  

DNA Damage & Repair ⓘ

DNMTs↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,  

Migration ⓘ

Smad1↑, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

selectivity↑, 2,  

Clinical Biomarkers ⓘ

AR↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Cell Death ⓘ

Cyt‑c↓, 1,   IAP1↓, 1,  

Protein Folding & ER Stress ⓘ

HSP27↓, 1,  
Total Targets: 3

Scientific Paper Hit Count for: ICAD, inhibitor of caspase-activated DNase
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#:877  State#:%  Dir#:2
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