MCU Cancer Research Results

MCU, mitochondrial calcium uniporter: Click to Expand ⟱
Source:
Type:
Mitochondrial calcium uniporter (MCU) is a highly selective channel complex located in the inner mitochondrial membrane.
-MCU facilitates the uptake of calcium (Ca²⁺) into the mitochondrial matrix, a process that is crucial for regulating mitochondrial metabolism, cell signaling, and apoptosis.
-Mitochondrial Ca²⁺ uptake via MCU plays a key role in stimulating metabolic enzymes in the tricarboxylic acid (TCA) cycle, thereby influencing energy production.

-Overexpression of MCU has been linked in some studies to enhanced Ca²⁺ uptake, metabolic changes, and increased tumor cell migration.
-In this context, higher MCU levels (or enhanced activity) have been associated with more aggressive tumor behavior and poorer outcomes, although findings may vary with tumor subtype.
Scientific Papers found: Click to Expand⟱
2684- BBR,    Berberine is a Novel Mitochondrial Calcium Uniporter Inhibitor that Disrupts MCU‐EMRE Assembly
- in-vivo, Nor, NA
*MCU↓, These findings establish Berberine as a potent MCU inhibitor, offering a safe therapeutic strategy for diseases associated with dysregulated mitochondrial calcium homeostasis.
*mt-Ca+2↓, Berberine pretreatment reduces mitochondrial Ca2+ overload and mitigates ischemia/reperfusion‐induced myocardial injury in mice.
*cardioP↑, Berberine significantly reduces mitochondrial Ca2+ overload, providing cardioprotection against I/R‐induced myocardial injury in mice.

2315- Citrate,    Why and how citrate may sensitize malignant tumors to immunotherapy
- Review, Var, NA
Bcl-2↓, SCT can induce silent apoptosis by reducing expression of key pro-apoptotic proteins (Bcl-2, surviving, MCL1), and promoting the activation of caspases-3 and −9 and −8, as showed in multiple cancer cell lines
Mcl-1↓,
survivin↓,
Casp3↑,
Casp9↑,
Ferroptosis↑, SCT can also trigger ferroptosis, an iron-dependent form of lytic cell death inducing lipid peroxidation (LPO)
lipid-P↑,
Ca+2↓, citrate lowers mitochondrial Ca2+ concentration by chelation
Akt↓, by chelating cytosolic Ca2+, citrate inhibits the Ca2+/CAMKK2/AKT/mTOR signaling pathway, thereby suppressing HIF1-α dependent glycolysis
mTOR↓,
Hif1a↓,
MCU↓, reduces the activity of the mitochondrial calcium uniporter (MCU), resulting in decreasing ATP production, increasing ROS production
ATP↓,
ROS↑,
eff↑, Of note, ferroptosis can enhance the effectiveness of immunotherapy, as showed in glioma models


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   lipid-P↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,  

Core Metabolism/Glycolysis ⓘ

MCU↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp9↑, 1,   Ferroptosis↑, 1,   Mcl-1↓, 1,   survivin↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,  

Migration ⓘ

Ca+2↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  
Total Targets: 16

Pathway results for Effect on Normal Cells:


Core Metabolism/Glycolysis ⓘ

MCU↓, 1,  

Migration ⓘ

mt-Ca+2↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,  
Total Targets: 3

Scientific Paper Hit Count for: MCU, mitochondrial calcium uniporter
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#:1292  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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