Necroptosis Cancer Research Results

Necroptosis, Necroptosis: Click to Expand ⟱
Source:
Type: type of cell death
Necroptosis, is a form of programmed cell death that is regulated by the cell's own mechanisms. It is a form of cell death that is mediated by specific signaling pathways, including the RIP1-RIP3-MLKL pathway. Necroptosis is characterized by the activation of specific enzymes, such as RIP1 and RIP3, which lead to the formation of a necroptotic complex that ultimately causes cell death.

Necroptosis expression can be elevated in certain types of cancer, it can also be reduced in other types of cancer.
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⟱
1563- Api,  MET,    Metformin-induced ROS upregulation as amplified by apigenin causes profound anticancer activity while sparing normal cells
- in-vitro, Nor, HDFa - in-vitro, PC, AsPC-1 - in-vitro, PC, MIA PaCa-2 - in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP - in-vivo, NA, NA
selectivity↑, selectivity↑, selectivity↓, ROS↑, eff↑, tumCV↓, MMP↓, Dose∅, eff↓, DNAdam↑, Apoptosis↑, TumAuto↑, Necroptosis↑, p‑P53↑, BIM↑, BAX↑, p‑PARP↑, Casp3↑, Casp8↑, Casp9↑, Cyt‑c↑, Bcl-2↓, AIF↑, p62↑, LC3B↑, MLKL↑, p‑MLKL↓, RIP3↑, p‑RIP3↑, TumCG↑, TumW↓,

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:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   MMP↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   BIM↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   MLKL↑, 1,   p‑MLKL↓, 1,   Necroptosis↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Autophagy & Lysosomes ⓘ

LC3B↑, 1,   p62↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   p‑P53↑, 1,   p‑PARP↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↑, 1,  

Migration ⓘ

RIP3↑, 1,   p‑RIP3↑, 1,  

Drug Metabolism & Resistance ⓘ

Dose∅, 1,   eff↓, 1,   eff↑, 1,   selectivity↓, 1,   selectivity↑, 2,  

Functional Outcomes ⓘ

TumW↓, 1,  
Total Targets: 30

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Necroptosis, Necroptosis
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#:944  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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