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.

Scientific Papers found: Click to Expand⟱

7521-

CA,

Protective effects of caffeic acid and caffeic acid phenethyl ester against acrolein-induced neurotoxicity in HT22 mouse hippocampal cells

in-vitro,

AD,

HT22

 HT22 mouse hippocampal cells

*neuroP↑, CA/CAPE significantly attenuated acrolein-induced neurotoxicity, ROS accumulation, and GSH depletion.
*ROS↓,
*GSH↑,
*Akt↑, CA/CAPE showed protective effects against acrolein by modulating MAPKs and Akt/GSK3β signaling pathways.
*GSK‐3β↑,
*BACE/β-secretase↓, CA/CAPE restored the changes of β-secretase (BACE-1) and/or activation of α-secretase (ADAM-10) induced by acrolein.
*p38↓, CA/CAPE inhibited the activation of p38 and JNK1 while promoted the activation of ERK and Akt/GSK3 caused by acrolein
*RAGE↓, In our study, ADAM-10 and LR-11 were decreased while BACE-1 and RAGE were increased after the exposure of acrolein for 24 h (Fig. 3). Of interest, these changes were almost restored by both CA and CAPE
*ADAM10↑,

5952-

Cela,

Celastrol attenuates Alzheimer’s disease-mediated learning and memory impairment by inhibiting endoplasmic reticulum stress-induced inflammation and oxidative stress

in-vivo,

AD,

AD mice

*memory↑, pre-treatment with celastrol could prevent learning and memory decline in AD mice by reducing inflammation and oxidative stress.
*Inflam↓,
*ROS↓,
*ER Stress↓, celastrol suppressed AD progression by targeting ER stress
*neuroP↑, celastrol treatment could be beneficial in addressing learning and memory deficits in AD, paving the way for potential neuroprotective treatments.
*Dose↝, administered celastrol intraperitoneally before the Aβ25-35 injection, while others received it after the injection. (1, 3, 6 mg/kg/day) for 2 days
*MDA↓, AD mouse group treated with celastrol showed lower levels of protein carbonyl and MDA and higher activity of CAT and SOD compared to the AD group
*SOD↑,
*Catalase↑,
*Aβ↓, Research has shown that celastrol can reduce cell death and Aβ production in cell experiments
BACE/β-secretase↓, celastrol treatment significantly restored the expression of BACE1, LRP1, NEP, and RAGE in the brain
LRP1↑, Activation of LRP1 by celastrol may lead to the attenuation of AD symptoms.
RAGE↓,

7012-

Fuc,

Fucoidan: A promising natural therapeutic agent for protecting human kidney health

Review,

EC,

*RenoP↑, Fucoidan exhibits significant anti-inflammatory effects in kidney protection.
*Inflam↓,
*antiOx↑, Antioxidant properties effectively reduce oxidative stress in renal tissues.
*ROS↓,
*BloodF↑, Enhances renal function by improving blood flow and diuresis.
*diuretic↑,
*BioAv↓, High-MW fucoidans often display stronger anticoagulant and viscosity-modulating effects. However, they may have limited oral bioavailability,
*BioAv↑, whereas low- to medium-MW fractions show improved tissue penetration, more favorable absorption, and can retain potent anti-inflammatory and anti-fibrotic activities, making them attractive for chronic kidney disease applications
*MAPK↓, (LMWF) has been reported in models of renal ischemia-reperfusion injury, where it inhibits the MAPK signaling pathway and subsequently reduces inflammation and fibrosis
*ERK↑, fucoidan can activate the ERK/MAPK signaling pathway, which plays a crucial role in preserving the endothelial glycocalyx in CKD
*NLRP3↓, fucoidan attenuates NLRP3 inflammasome activation and subsequent podocyte pyroptosis, ultimately leading to improved renal function and reduced inflammation in diabetic kidney disease (DKD)
*NRF2↑, By inhibiting ROS-generating systems (e.g., NADPH oxidase) and activating Nrf2-dependent transcription of antioxidant genes, fucoidan limits mitochondrial dysfunction and prevents oxidative injury to podocytes and tubular epithelial cells
*MDA↓, fucoidan nanoparticles significantly reduced levels of malondialdehyde (MDA), a marker of lipid peroxidation and oxidative stress, while simultaneously upregulating the levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx)
*SOD↑,
*GPx↑,
*Catalase↑, Altogether, fucoidan directly reduces renal oxidative stress by scavenging reactive oxygen species and upregulating endogenous antioxidant defenses (e.g., SOD, CAT, GPx) in tubular and glomerular cells, by suppressing upstream ROS generation
*lipid-P↓, fucoidan limits lipid peroxidation and DNA damage, thereby preserving podocyte integrity and tubular epithelial viability
*DNAdam↓,
*Fibrosis↓, Inhibition of fibrosis
*JAK2↓, fucoidan combats renal fibrosis is via the restriction of the JAK2/STAT3 signaling pathway.
*STAT3↓,
*uricA↓, By reducing serum uric acid levels, fucoidan significantly inhibits the activation of JAK2/STAT3, consequently decreasing the expression of key fibrotic markers such as collagen I and α-smooth muscle actin (α-SMA)
*COL1↓,
*α-SMA↓,
*SIRT1↑, fucoidan’s anti-fibrotic effects are further attributed to its activation of protective pathways such as Sirt-1, GLP-1R, and Nrf2/HO-1(
*HO-1↑,
*GLP-1R↑,
*HMGB1↓, Stimulating these protective pathways results in the inhibition of pro-fibrotic signaling cascades, including the HMGB1/RAGE/NF-κB/TGF-β1 pathway
*RAGE↓,
*NF-kB↓,
*TGF-β1↓,
*PI3K↓, Fucoidan also exhibits potential in curtailing the inflammatory processes associated with renal fibrosis through its inhibitory effects on the PI3K/Akt/NF-κB signaling cascade.
*Akt↓,
*GutMicro↑, research has elucidated the important role of gut microbiota in mediating the protective effects of fucoidan, suggesting that modulation of microbial communities may underlie its benefits in renal health
*SCFAs↑, Fucoidan’s positive impact on gut microbiota includes enhancing the production of short-chain fatty acids (SCFAs), especially butyrate, which are known to support gut integrity and overall health (
*Buty↑,
*IBI↑, Fucoidan's ability to enhance SCFA production has been linked to improved intestinal barrier integrity, a crucial factor in preventing the translocation of harmful substances into the bloodstream, which can exacerbate kidney injury
*TJ↑, Studies indicate that fucoidan can upregulate the expression of tight junction proteins, crucial for maintaining the integrity of the intestinal epithelium
*Dose↝, national approval in China for renal indications, indicate that fucoidan is generally safe at oral doses of 50–300 mg/day and up to 1–3 g/day in short‑ to mid‑term studies, with no major hematologic, hepatic, or renal toxicity reported.

7275-

GGB,

Protective Effect of Ginkgolide B against Cognitive Impairment in Mice via Regulation of Gut Microbiota

in-vivo,

AD,

Male mice were induced with d-galactose and aluminum chloride to establish an AD animal model

*cognitive↑, Our results showed that GB significantly alleviated cognitive dysfunction, neurodegeneration, and neuropathological changes in AD model mice
*neuroP↑,
*RAGE↓, Moreover, GB treatment remarkably reduced the levels of RAGE and Bax and increased the level of Bcl-2 in AD model mice.
*BAX↓,
*Bcl-2↑,
*GutMicro↑, GB treatment reversed the decreased abundance of Lactobacillus and the increased abundance of Bacteroidales, Muribaculaceae, and Alloprevotella, which led to reconstruction of gut microbiota.

7365-

HibSad,

Insight into the molecular evidence supporting the remarkable chemotherapeutic potential of Hibiscus sabdariffa L

Review,

Var,

chemoPv↑, Both crude extracts and pure compounds of the plant were reported to induce chemoprevention, selective cytotoxicity, cell cycle arrest, apoptosis, autophagy and anti-metastasis effects in varied types of human cancer cells.
selectivity↑,
TumCCA↑,
Apoptosis↑,
TumAuto↑,
TumMeta↓,
ATG5↑, figure 3
Beclin-1↑,
LC3II↑,
MMP2↓,
MMP9↓,
CD31/PECAM-1↓,
VEGF↓,
uPA↓,
TIMP2↑,
NF-kB↓,
p38↑,
P53↑,
Casp3↑,
Casp8↑,
Casp9↑,
Bcl-2↓,
BAX↑,
Cyt‑c↑,
TNF-α↑,
Fas↑,
FasL↑,
JNK↑,
cJun↑,
angioG↓,
VEGFR2/KDR/Flk1↓,
PCNA↓,
CCN2/CTGF↓,
RAGE↓,

3261-

Lyco,

Lycopene and Vascular Health

Review,

Stroke,

 endothelial cells

*Inflam↓, main activity profile of lycopene includes antiatherosclerotic, antioxidant, anti-inflammatory, antihypertensive, antiplatelet, anti-apoptotic, and protective endothelial effects, the ability to improve the metabolic profile, and reduce arterial stif
*antiOx↑, It is a much more potent antioxidant than alpha-tocopherol (10 × more potent) or beta-carotene (twice as potent)
*AntiAg↑, lycopene, protecting against myocardial infarction and stroke, is its antiplatelet activity
*cardioP↑, favorable effect in patients with subclinical atherosclerosis, metabolic syndrome, hypertension, peripheral vascular disease, stroke and several other cardiovascular disorders
*SOD↑, Lycopene modulates also the production of antioxidant enzymes, such as superoxide dismutase and catalase
*Catalase↑,
*ROS↓, By reducing oxidative stress and reactive oxygen species, lycopene increases the bioavailability of nitric oxide (NO), improves endothelium-dependent vasodilation and reduces protein, lipids, DNA, and mitochondrial damage (
*mtDam↓,
*cardioP↑, Lycopene exerts a cardioprotective effect against atrazine induced cardiac injury due to its anti-inflammatory effect, by blocking the NF-kappa B pathway and NO production
*NF-kB↓,
*NO↓,
*COX2/PTGS2↓, downregulation of cyclooxygenase 2,
*LDL↓, significant reductions in total and LDL cholesterol were revealed only at doses of, at least, 25 mg lycopene/day
*eff↑, It was noticed that lycopene can potentiate the antiplatelet effect of aspirin, which requires low lycopene diet
*ER Stress↓, Lycopene protects the cardiomyocytes by relieving ERS
*BioAv↑, Lycopene is very bioavailable in the presence of oil, especially in monounsaturated oils, other dietary fats and processed tomato products
*eff↑, Lycopene can increase the antioxidant properties of vitamin C, E, polyphenols and beta-carotene in a synergistic way
*MMPs↓, figure 3, secretion of MMPs
*COX2/PTGS2↓,
*RAGE↓,

63-

QC,

Quercetin facilitates cell death and chemosensitivity through RAGE/PI3K/AKT/mTOR axis in human pancreatic cancer cells

in-vitro,

Pca,

RAGE↓, Silencing RAGE expression by suppressing the PI3K/AKT/mTOR axis
PI3K↓,
mTOR↓,
Akt↓,
Apoptosis↑,
TumAuto↑,
ChemoSen↑, Quercetin facilitates cell death and chemosensitivity through RAGE/PI3K/AKT/mTOR axis in human pancreatic cancer cells

923-

QC,

Quercetin as an innovative therapeutic tool for cancer chemoprevention: Molecular mechanisms and implications in human health

Review,

Var,

ROS↑, decided by the availability of intracellular reduced glutathione (GSH),
GSH↓, extended exposure with high concentration of quercetin causes a substantial decline in GSH levels
Ca+2↝,
MMP↓,
Casp3↑, activation of caspase-3, -8, and -9
Casp8↑,
Casp9↑,
other↓, when p53 is inhibited, cancer cells become vulnerable to quercetin-induced apoptosis
*ROS↓, Quercetin (QC), a plant-derived bioflavonoid, is known for its ROS scavenging properties and was recently discovered to have various antitumor properties in a variety of solid tumors.
*NRF2↑, Moreover, the therapeutic efficacy of QC has also been defined in rat models through the activation of Nrf-2/HO-1 against high glucose-induced damage
HO-1↑,
TumCCA↑, QC increases cell cycle arrest via regulating p21WAF1, cyclin B, and p27KIP1
Inflam↓, QC-mediated anti-inflammatory and anti-apoptotic properties play a key role in cancer prevention by modulating the TLR-2 (toll-like receptor-2) and JAK-2/STAT-3 pathways and significantly inhibit STAT-3 tyrosine phosphorylation within inflammatory ce
STAT3↓,
DR5↑, several studies showed that QC upregulated the death receptor (DR)
P450↓, it hinders the activity of cytochrome P450 (CYP) enzymes in hepatocytes
MMPs↓, QC has also been shown to suppress metastatic protein expression such as MMPs (matrix metalloproteases)
IFN-γ↓, QC is its ability to inhibit inflammatory mediators including IFN-γ, IL-6, COX-2, IL-8, iNOS, TNF-α,
IL6↓,
COX2/PTGS2↓,
IL8↓,
iNOS↓,
TNF-α↓,
cl‑PARP↑, Induced caspase-8, caspase-9, and caspase-3 activation, PARP cleavage, mitochondrial membrane depolarization,
Apoptosis↑, increased apoptosis and p53 expression
P53↑,
Sp1/3/4↓, HT-29 colon cancer cells: decreased the expression of Sp1, Sp3, Sp4 mrna, and survivin,
survivin↓,
TRAILR↑, H460 Increased the expression of TRAILR, caspase-10, DFF45, TNFR 1, FAS, and decreased the expression of NF-κb, ikkα
Casp10↑,
DFF45↑,
TNFR 1↑,
Fas↑,
NF-kB↓,
IKKα↓,
cycD1/CCND1↓, SKOV3 Reduction in cyclin D1 level
Bcl-2↓, MCF-7, HCC1937, SK-Br3, 4T1, MDA-MB-231 Decreased Bcl-2 expression, increasedBax expression, inhibition of PI3K-Akt pathway
BAX↑,
PI3K↓,
Akt↓,
E-cadherin↓, MDA-MB-231 Induced the expression of E-cadherin and downregulated vimentin levels, modulation of β-catenin target genes such as cyclin D1 and c-Myc
Vim↓,
β-catenin/ZEB1↓,
cMyc↓,
EMT↓, MCF-7 Suppressed the epithelial–mesenchymal transition process, upregulated E-cadherin expression, downregulated vimentin and MMP-2 expression, decreased Notch1 expression
MMP2↓,
NOTCH1↓,
MMP7↓, PANC-1, PATU-8988 Decreased the secretion of MMP and MMP7, blocked the STAT3 signaling pathway
angioG↓, PC-3, HUVECs Reduced angiogenesis, increased TSP-1 protein and mrna expression
TSP-1↑,
CSCs↓, PC-3 and LNCaP cells Activated capase-3/7 and inhibit the expression of Bcl-2, surviving and XIAP in CSCs.
XIAP↓,
Snail↓, inhibiting the expression of vimentin, slug, snail and nuclear β-catenin, and the activity of LEF-1/TCF responsive reporter
Slug↓,
LEF1↓,
P-gp/ABCB1↓, MCF-7 and MCF-7/dox cell lines Downregulation of P-gp expression
EGFR↓, MCF-7 and MDA-MB-231 cells Suppressed EGFR signaling and inhibited PI3K/Akt/mTOR/GSK-3β
GSK‐3β↓,
mTOR↓,
RAGE↓, IA Paca-2, BxPC3, AsPC-1, HPAC and PANC1 Silencing RAGE expression
HSP27↓, Breast cancer In vivo NOD/SCID mice Inhibited the overexpression of Hsp27
VEGF↓, QC significantly reversed an elevation in profibrotic markers (VEGF, IL-6, TGF, COL-1, and COL-3)
TGF-β↓,
COL1↓,
COL3A1↓,

7834-

VA,

MBS,

Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review

Review,

AD,

*neuroP↑, Vanillic acid (4-hydroxy-3-methoxybenzoic acid) showed neuroprotective activities in various CNS disorders, such as AD, Parkinson’ disease, cerebral ischemia, and excessive iron-induced damage
*memory↑, vanillic acid improved the memory and learning deficits via multiple mechanisms
*Learn↑,
*Aβ↓, First, vanillic acid inhibited Aβ production, β-secretase (BACE-1) activity, and Aβ plaque deposits in Aβ or lipopolysaccharide (LPS)-induced AD models,
*BACE/β-secretase↓,
*NeuroI↓, vanillic acid exerted antineuroinflammatory effects by inhibition of the receptor for advanced glycation end products (RAGE)-mediated c-Jun n-terminal kinase (JNK) activation
*RAGE↓,
*antiOx↑, vanillic acid enhanced the antioxidant Nrf2/HO-1 pathway by inhibiting GSK-3β, thus reducing the oxidative stress of Aβ1−42 -injected (i.c.v.) mice.
*NRF2↑,
*HO-1↑,
*GSK‐3β↓,
*ROS↓,
*AChE↓, vanillic acid also ameliorated the cholinergic deficits as evidenced by the inhibited AChE activity in STZ-induced AD mice
*Dose↝, effective dose of vanillic acid in rodents was 30−100 mg/kg, while its content of vanillic acid in mung bean (0.97 mg/100 g) was quite low, which implied its limited contribution to the neuroprotective activity of mung bean

Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes(tgid=23) ⓘ

chemoPv↑, 1,
Total Targets: 89

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Buty↑, 1, diuretic↑, 1, GLP-1R↑, 1, Learn↑, 1, NeuroI↓, 1, SCFAs↑, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3, Catalase↑, 3, GPx↑, 1, GSH↑, 1, HO-1↑, 2, lipid-P↓, 1, MDA↓, 2, NRF2↑, 3, ROS↓, 6, SOD↑, 3, uricA↓, 1,

Mitochondria & Bioenergetics(tgid=3) ⓘ

mtDam↓, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

LDL↓, 1, SIRT1↑, 1,

Cell Death(tgid=5) ⓘ

Akt↓, 1, Akt↑, 1, BAX↓, 1, Bcl-2↑, 1, MAPK↓, 1, p38↓, 1,

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 2,

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↑, 1, GSK‐3β↓, 1, GSK‐3β↑, 1, PI3K↓, 1, STAT3↓, 1,

Migration(tgid=13) ⓘ

AntiAg↑, 1, COL1↓, 1, Fibrosis↓, 1, MMPs↓, 1, RAGE↓, 5, TGF-β1↓, 1, TJ↑, 1, α-SMA↓, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,

Barriers & Transport(tgid=15) ⓘ

IBI↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2, HMGB1↓, 1, Inflam↓, 3, JAK2↓, 1, NF-kB↓, 2,

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1, ADAM10↑, 1,

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 2, BACE/β-secretase↓, 2, NLRP3↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1, BioAv↑, 2, Dose↝, 3, eff↑, 2,

Clinical Biomarkers(tgid=22) ⓘ

BloodF↑, 1, GutMicro↑, 2, RAGE↓, 5,

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 2, cognitive↑, 1, memory↑, 2, neuroP↑, 4, RenoP↑, 1,
Total Targets: 65

Scientific Paper Hit Count for: RAGE, Receptor for advanced glycation end-product

2 Quercetin
1 Caffeic acid
1 Celastrol
1 Fucoidan
1 Ginkgolide B
1 Hibiscus sabdariffa
1 Lycopene
1 Vanillic Acid
1 Mung Bean Sprouts

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#:383  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

RAGE Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Home Page