PERK Cancer Research Results

PERK, protein kinase-like ER kinase: Click to Expand ⟱
Source:
Type:
PERK is a type of kinase that is activated in response to endoplasmic reticulum (ER) stress, which occurs when the ER is overwhelmed with unfolded or misfolded proteins. Once activated, PERK phosphorylates and activates the eukaryotic translation initiation factor 2 alpha (eIF2α), leading to the attenuation of global protein synthesis and the induction of specific genes involved in the UPR.
PERK is overexpressed in various types of cancer, including breast, lung, and colon cancer, and that its expression is often associated with poor prognosis.
PERK has been shown to have both tumor-suppressive and tumor-promoting roles, depending on the context.
-PERK, as the sensor of ER stress.
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⟱
3033- RosA,    Rosemary (Rosmarinus officinalis) Extract Modulates CHOP/GADD153 to Promote Androgen Receptor Degradation and Decreases Xenograft Tumor Growth
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, LNCaP - vitro+vivo, NA, NA
ER Stress↑, selectivity↑, AR↓, TumCG↓, TumCCA↑, CHOP↑, PERK↓, GRP78/BiP↑, PSA↓,

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:


Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   PERK↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Immune & Inflammatory Signaling ⓘ

PSA↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   PSA↓, 1,  
Total Targets: 11

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PERK, protein kinase-like ER kinase
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#:617  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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