MPT Cancer Research Results

MPT, mitochondrial permeability transition: Click to Expand ⟱
Source:
Type:
MPT refers to an alteration in the permeability of the inner mitochondrial membrane (IMM), Mitochondrial permeability transition (MPT) refers to a process involving the opening of the mitochondrial permeability transition pore (mPTP), which can lead to the loss of mitochondrial membrane potential, disruption of ATP synthesis, and release of pro-apoptotic factors into the cytosol. This process is critical in various physiological and pathological contexts, including cancer.

Mitochondrial permeability transition plays a significant role in cancer biology, with its dysregulation often associated with poor prognosis and protumorigenic effects. The specific roles of MPT can vary by cancer type and context.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
141- CUR,    Effect of curcumin on Bcl-2 and Bax expression in nude mice prostate cancer
- in-vivo, Pca, PC3
BAX↑, Bcl-2↓, TumCG↓, TumVol↓, TumW↓, Apoptosis↑, AR↓, Ca+2↑, MPT↑,
161- CUR,  MeSA,    Enhanced apoptotic effects by the combination of curcumin and methylseleninic acid: potential role of Mcl-1 and FAK
- in-vitro, BC, MDA-MB-231 - in-vitro, Pca, DU145
Mcl-1↑, Mcl-1↓, MPT↑, AIF↑, chemoPv↑, Apoptosis↑, ROS↑, FAK↓, STAT3↓, NF-kB↓,

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 ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   MPT↑, 2,  

Cell Death ⓘ

Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,   Mcl-1↓, 1,   Mcl-1↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

STAT3↓, 1,   TumCG↓, 1,  

Migration ⓘ

Ca+2↑, 1,   FAK↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 18

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: MPT, mitochondrial permeability transition
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:22  Cells:%  prod#:%  Target#:519  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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