VDAC1 Cancer Research Results

VDAC1, Voltage-Dependent Anion Channel 1: Click to Expand ⟱
Source:
Type:
VDAC1 is a pore-forming protein in the outer mitochondrial membrane that regulates metabolite flux (ATP/ADP, ions), mitochondrial–cytosolic communication, and apoptosis signaling. In Alzheimer’s disease, VDAC1 sits at a convergence point between mitochondrial dysfunction, oxidative stress, and neuronal death, all core features of AD pathophysiology.
-Upregulated VDAC1 detected in AD post-mortem cortex and hippocampus.
Scientific Papers found: Click to Expand⟱
7982- itraC,    Simultaneous Targeting of NPC1 and VDAC1 by Itraconazole Leads to Synergistic Inhibition of mTOR Signaling and Angiogenesis
- in-vitro, Nor, HUVECs - in-vitro, Lung, A549 - in-vitro, Cerv, HeLa - in-vitro, Nor, HEK293
angioG↓, The antifungal drug itraconazole was recently found to exhibit potent antiangiogenic activity and has since been repurposed as an investigational anticancer agent.
mTOR↓, through inhibition of the mTOR signaling pathway
NPC1L1↓, we demonstrate that cholesterol trafficking inhibition by itraconazole is due to direct inhibition of the lysosomal protein NPC1
AMPK↑, These results strongly suggested a causal relationship between AMPK activation and mTOR inhibition by itraconazole.
VDAC1↓, novel antiangiogenic mechanism of action of itraconazole, whereby direct inhibition of both VDAC1 and NPC1 lead to mTOR inhibition

7983- itraC,    Antifungal drug itraconazole targets VDAC1 to modulate the AMPK/mTOR signaling axis in endothelial cells
- in-vitro, Nor, HUVECs
angioG↓, angiogenesis inhibitor itraconazole,
VDAC1↓, VDAC1 inhibition perturbs mitochondrial ATP production, leading to activation of the AMP-activated protein kinase pathway and subsequent inhibition of mechanistic target of rapamycin, a regulator of EC proliferation.
mt-ATP↓,
AMPK↑, Itraconazole Activates AMPK in HUVEC
mTOR↓,
TumCP↓,

8089- KAE,    Kaempferol impairs aerobic glycolysis against melanoma metastasis via inhibiting the mitochondrial binding of HK2 and VDAC1
- in-vitro, Melanoma, A375 - in-vitro, Melanoma, B16-F10
TumCMig↓, KAM inhibited the migration and invasion of A375 and B16F10 cells, and reduced the lung metastasis of melanoma cells.
TumCI↓,
TumMeta↓,
ECAR↓, Extracellular acidification rates (ECAR) and glucose consumption were obviously suppressed by KAM, as well as the production of ATP, pyruvate and lactate.
GlucoseCon↓,
ATP↓,
Pyruv↓,
lactateProd↓,
HK2↓, Mechanistically, the activity of hexokinase (HK), the first key kinase of aerobic glycolysis, was significantly inhibited by KAM.
VDAC1↓, voltage-dependent anion channel 1 (VDAC1) on mitochondria was inhibited by KAM through AKT/GSK-3β signal pathway.
Akt↓,
GSK‐3β↝,
Glycolysis↓, In conclusion, KAM inhibits melanoma metastasis via blocking aerobic glycolysis of melanoma cells, in which the binding of HK2 and VDAC1 on mitochondria was broken.

4862- Uro,    Neuroprotective effect of Urolithin A via downregulating VDAC1-mediated autophagy in Alzheimer's disease
- in-vivo, AD, NA - in-vitro, Nor, PC12
*cognitive↑, UA improved cognitive dysfunction and reduced Aβ deposition in APP/PS1 mice
*p‑PI3K↓, UA down-regulated the phosphorylation level of PI3K/AKT/mTOR and up-regulated the phosphorylation level of AMPK
*p‑Akt↓,
*AMPK↑,
*VDAC1↓, UA down-regulated VDAC1
*neuroP↑, These findings demonstrated that UA down-regulated VDAC1 played a key neuroprotective role on AD by inhibiting the PI3K/AKT/mTOR pathway and activating the AMPK pathway to promote autophagy.
*PARK2↑, Mechanistically, UA may increase the expression of Parkin (Parkinson’s disease related-1) and PINK1 (PTEN induced kinase 1), and the LC3BII/I
*PTEN↑,
*LC3‑Ⅱ/LC3‑Ⅰ↑,
*p62↓, by inhibiting VDAC1, and reduce the expression level of p62, activating autophagy.
*Aβ↓, UA treatment significantly decreased the number of Aβ plaques in the hippocampus of APP/PS1 mice compared with APP/PS1 mice
*Apoptosis↓, UA inhibits Aβ-induced apoptosis and promotes autophagy


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

VDAC1↓, 3,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   mt-ATP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 2,   ECAR↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,   NPC1L1↓, 1,   Pyruv↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,  

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

GSK‐3β↝, 1,   mTOR↓, 2,  

Migration(tgid=13) ⓘ

TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,  
Total Targets: 19

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

PARK2↑, 1,   VDAC1↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↓, 1,   Apoptosis↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   p62↓, 1,  

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

p‑PI3K↓, 1,   PTEN↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 1,   neuroP↑, 1,  
Total Targets: 12

Scientific Paper Hit Count for: VDAC1, Voltage-Dependent Anion Channel 1
2 itraconazole
1 Kaempferol
1 Urolithin
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#:1405  State#:%  Dir#:1
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