RAGE Cancer Research Results

RAGE, Receptor for advanced glycation end-product: Click to Expand ⟱
Source:
Type:
RAGE (receptor for advanced glycation end-product) is thought to be associated with metastasis and poor prognosis of various types of cancer.
Cancer — Chronic Inflammation, Metastatic Signaling, and Therapy Resistance

Frequently upregulated (expression and/or activity) in tumors and surrounding stroma.
Core Oncogenic Programs Driven by RAGE
a. Chronic inflammation
-Sustained NF-κB activation
-Autocrine loops that perpetuate cytokine and chemokine production

b. Proliferation and survival
-Activation of MAPK/ERK and PI3K–AKT pathways
-Resistance to apoptosis under stress

c. Invasion and metastasis
-Induction of EMT-associated programs
-Matrix remodeling and enhanced motility

d. Angiogenesis
-Upregulation of pro-angiogenic factors in hypoxic niches

Therapeutic Implications
-Direct targeting: blocking RAGE or key ligand interactions can dampen chronic inflammation and invasion (conceptually attractive; clinical translation ongoing).
-Combination logic: RAGE pathway inhibition may sensitize tumors to chemotherapy, radiation, or immunotherapy by reducing stress-adaptive signaling.
-Biomarker role: elevated RAGE/ligand signatures can indicate inflammation-driven disease states.

RAGE is used as a clinical biomarker for inflammation state.


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⟱
63- QC,    Quercetin facilitates cell death and chemosensitivity through RAGE/PI3K/AKT/mTOR axis in human pancreatic cancer cells
- in-vitro, Pca, NA
RAGE↓, PI3K↓, mTOR↓, Akt↓, Apoptosis↑, TumAuto↑, ChemoSen↑,

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:


Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,   PI3K↓, 1,  

Migration ⓘ

RAGE↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,  

Clinical Biomarkers ⓘ

RAGE↓, 1,  
Total Targets: 8

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: RAGE, Receptor for advanced glycation end-product
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#:383  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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