Deguelin / Myc Cancer Research Results

Deg, Deguelin: Click to Expand ⟱
Features: Insect poisoning, anti-cancer
Deguelin is a natural compound of the flavonoid family of products isolated from several plant species, including Derris trifoliata Lour and Mundulea sericea (Leguminosae) (4)

Deguelin’s ability to modulate multiple signaling pathways—including PI3K/Akt, mTOR, NF-κB, HIF-1α, and MAPK
While preclinical studies have utilized dosages in the approximate range of 4–8 mg/kg in animal models, these figures are specific to the experimental conditions and species used in those studies.

Deguelin is a rotenoid (isoflavonoid-like botanical insecticide class) found in some Lonchocarpus / Derris species. In cancer literature it’s most often described as a mitochondrial Complex I inhibitor with downstream energy stress + survival pathway suppression (Akt/PI3K, NF-κB) and apoptosis/autophagy induction. A major caution is neurotoxicity signal: rotenoids (including deguelin) have been used in Parkinson’s disease animal models via Complex I inhibition.
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Active identity: Rotenoid (deguelin) — a potent mitochondrial Complex I inhibitor with downstream energy-stress signaling (AMPK/mTOR), survival pathway suppression (Akt, NF-κB), and apoptosis/autophagy induction in cancer models; higher caution category due to rotenoid neurotoxicity signals in animal models.



Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 Mitochondrial ETC Complex I inhibition (OXPHOS) Complex I ↓; ATP ↓; energetic stress ↑ (reported) Toxicity risk if exposure high/prolonged (mitochondrial inhibition) P, R Bioenergetic choke-point Deguelin is a rotenoid-class Complex I inhibitor; downstream effects often reflect energy stress + ROS/redox destabilization.
2 PI3K → AKT survival axis Akt signaling ↓ (reported; chemoprevention & tumor models) ↔ R, G Survival/growth suppression Deguelin is widely described as an Akt-pathway suppressor in cancer/chemoprevention literature.
3 AMPK → mTOR → survivin axis AMPK ↑; mTOR ↓; survivin ↓ (reported) ↔ R, G Energy-stress signaling → anti-growth Frequently presented as a mechanistic bridge between mitochondrial inhibition and reduced survival/proliferation programs.
4 NF-κB inflammatory / survival transcription IKK/IκB/NF-κB activity ↓ (reported) Inflammation tone ↓ (context) R, G Anti-inflammatory + anti-survival transcription Deguelin has been reported to suppress NF-κB signaling in multiple tumor systems.
5 Hsp90 client disruption (Akt, survivin, CDK4) (reported) Hsp90 client stability ↓; Akt/survivin/CDK4 ↓ (reported) ↔ R, G Multi-node pathway destabilization Some models report deguelin disrupts Hsp90-client interactions contributing to survival/proliferation collapse.
6 Intrinsic apoptosis (mitochondrial) ΔΨm ↓; cytochrome-c ↑; caspases ↑; cl-PARP ↑ (reported) ↔ / toxicity risk at higher exposure G Cell death execution Often downstream of energetic stress + survival pathway suppression.
7 Autophagy modulation Autophagy ↑ (reported; context-dependent; can be pro-death or adaptive) ↔ G Stress response / cell fate shift Autophagy is frequently reported alongside apoptosis; directionality and functional role vary by model.
8 Cell-cycle control Arrest ↑ (reported); cyclins/CDKs ↓ (context) ↔ G Cytostasis Often explained as downstream of Akt/mTOR and Hsp90-client disruption effects.
9 Angiogenesis / hypoxia programs (HIF-1α, VEGF) (reported) HIF-1α/VEGF outputs ↓ (reported in some models) ↔ R, G Anti-angiogenic support Anti-angiogenic effects are reported but are less “core” than the mitochondrial/Akt axes.
10 Safety constraint: rotenoid neurotoxicity signal — Parkinsonism-like syndrome reported in rat model with deguelin exposure — Translation constraint Deguelin (like rotenone) is a potent Complex I inhibitor; neurotoxicity signals exist in animal PD models, so long-term/high exposure should be treated as higher-risk than typical polyphenols.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (bioenergetic inhibition begins; early redox/kinase shifts)
  • R: 30 min–3 hr (AMPK/mTOR/NF-κB and stress pathway rewiring)
  • G: >3 hr (cell-cycle arrest, apoptosis/autophagy outcomes)
Myc, v-myc avian myelocytomatosis viral oncogene homolog: Click to Expand ⟱
Source: TCGA
Type:
Myc is a family of regulator genes and proteins that play a crucial role in cell cycle progression, apoptosis, and cellular transformation.
Myc is often found to be overexpressed or dysregulated in many types of tumors. This overexpression can lead to uncontrolled cell division and growth, contributing to the development and progression of cancer.
Myc is frequently overexpressed in various cancers, including hematological malignancies (like Burkitt lymphoma) and solid tumors (such as breast, lung, and colon cancers). This overexpression can result from genetic alterations, such as chromosomal translocations, amplifications, or mutations.

MYC is use as a clinical biomarker for risk biology-aggressiveness.
Scientific Papers found: Click to Expand⟱
1443- Deg,    Deguelin Action Involves c-Met and EGFR Signaling Pathways in Triple Negative Breast Cancer Cells
- vitro+vivo, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-435 - in-vitro, BC, BT549
EGFR↓, Akt↓, p‑ERK↓, NF-kB↓, p‑STAT3↓, survivin↓, Myc↓, TumCG↓, cMET↓,

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:


Cell Death ⓘ

Akt↓, 1,   Myc↓, 1,   survivin↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

cMET↓, 1,   p‑ERK↓, 1,   p‑STAT3↓, 1,   TumCG↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   Myc↓, 1,  
Total Targets: 11

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Myc, v-myc avian myelocytomatosis viral oncogene homolog
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#:69  Target#:210  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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