PDE3B Cancer Research Results

PDE3B, Phosphodiesterase 3B: Click to Expand ⟱
Source:
Type:

Phosphodiesterase 3B (PDE3B) is a cyclic-nucleotide phosphodiesterase that hydrolyzes cAMP and cGMP, with a major physiological role in insulin-regulated metabolism, lipolysis, glucose homeostasis, and cellular signalling. By reducing intracellular cAMP, PDE3B can suppress cAMP/PKA-dependent signalling. In cancer, PDE3B expression or activity is context-dependent; PDE3B ↑ may support tumour-cell survival, metabolic adaptation, proliferation, or stem-like properties in selected cancers by lowering cAMP signalling, whereas PDE3B inhibition or activity ↓ may increase cAMP and produce antiproliferative or pro-apoptotic effects in susceptible models. Gene reference; PDE3 review.
-Typical cancer interpretation: PDE3B ↑ is potentially tumour-promoting in some cancers



Scientific Papers found: Click to Expand⟱
6984- Form,    Formononetin suppresses colitis-associated colon cancer by targeting lipid synthesis and mTORC2/Akt signaling
- in-vitro, Colon, HCT116 - Review, IBD, RAW264.7
*Inflam↓, Modern research highlights Formononetin (FN) for its significant anti-inflammatory and extensively studied anti-cancer properties;
AntiCan↑,
*NF-kB↓, FN can inhibit the activation of the NF-κB/MAPK signaling pathways in LPS-induced RAW264.7 cells, thereby exerting its anti-inflammatory effects.
*MAPK↓,
*colonLen↑, FN significantly enhanced the colon length and DAI score in mice, notably suppressed the production of inflammatory cytokines, and inhibited the NF-κB/MAPK signaling pathway, leading to an improvement in DSS-induced colitis.
TumCG↓, FN significantly inhibited CT-26 and HCT116 cell growth, reduced tumor growth rate, improved pathological damage in CAC mice, and inhibited inflammatory factor production, enhancing intestinal mucosa protection.
Apoptosis↑, FN promoted apoptosis of colon cancer cells by increasing autophagy proteins (LC3, Beclin-1) and apoptosis proteins (CL-Caspase3, Bax), while reducing Bcl-2 expression.
LC3II↑,
Beclin-1↑,
cl‑Casp3↑,
BAX↑,
Bcl-2↓,
IGF-1↓, FN reduced IGF-1, ACLY, A-CoA, FAS, HSL, ATGL, and FFA levels, and increased GSK-3 levels
ACLY↓,
Acetyl-CoA↓,
Fas↓,
HSL/LIPE↓,
ATGL/PNPLA2↓,
FFA/NEFA↓,
GSK‐3β↑,
p‑mTOR↓, FN also inhibited the expression of P-mTOR, Rictor, P-Akt, ACLY, PDE3B, P-PKA, and P-HSL
Rictor↓,
p‑Akt↓,
PDE3B↓,
p‑PKA↓,
p‑HSL/LIPE↑,
TumAuto↑, FN significantly inhibits colon cancer cell growth and exerts anti-CAC effects by activating autophagy and apoptosis pathways and regulating lipid metabolism.


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:


NA, unassigned(tgid=0) ⓘ

ATGL/PNPLA2↓, 1,   FFA/NEFA↓, 1,   HSL/LIPE↓, 1,   p‑HSL/LIPE↑, 1,   PDE3B↓, 1,   Rictor↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

Acetyl-CoA↓, 1,   ACLY↓, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   cl‑Casp3↑, 1,   Fas↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1,   LC3II↑, 1,   TumAuto↑, 1,  

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

GSK‐3β↑, 1,   IGF-1↓, 1,   p‑mTOR↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

p‑PKA↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,  
Total Targets: 23

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

colonLen↑, 1,  

Cell Death(tgid=5) ⓘ

MAPK↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,   NF-kB↓, 1,  
Total Targets: 4

Scientific Paper Hit Count for: PDE3B, Phosphodiesterase 3B
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#:1553  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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