CD31 Cancer Research Results

CD31, platelet endothelial cell adhesion molecule-1 (PECAM-1): Click to Expand ⟱
Source:
Type: marker
CD31, also known as platelet endothelial cell adhesion molecule-1 (PECAM-1), is a transmembrane receptor that plays a crucial role in various cellular processes, including cell adhesion, migration, and signaling.
High CD31 expression has been linked to poor prognosis and increased metastasis. (except Leukemia and brain cancers).
CD31 is a marker that is commonly used to identify microvessels in tissue sections.


Scientific Papers found: Click to Expand⟱
557- ART/DHA,    Artemisinin and Its Derivatives in Cancer Care
- Review, Var, NA
*BioAv↓, with High fat and high calorie meals
*BioAv↑, DHA dihydroartemisinin have improved bioavailability
Apoptosis↑,
EGFR↓,
CD31↓,
Ki-67↓,
P53↓,
TfR1/CD71↑,
P-gp↓, many artemisinin derivatives act as P-gp inhibitors
PD-1↝, Caution when used with mmunotherapy (PD1/PDL1 inhibitors)

2773- Bos,    Targeted inhibition of tumor proliferation, survival, and metastasis by pentacyclic triterpenoids: Potential role in prevention and therapy of cancer
- Review, Var, NA
Inflam↓, BA has been shown to be effective against chronic inflammation-driven diseases such as adjuvant or bovine serum albumin-induced arthritis, osteoarthritis, Crohn’s disease, ulcerative colitis, and ileitis, and galactosamine/endotoxin-induced hepa
TumCCA↑, BA induced apoptosis was mediated by cell cycle arrest in the G1 phase and by activating caspases 3, 8 and 9 in HT-29 cells
Casp3↑,
Casp8↑,
Casp9↑,
STAT3↑, BA inhibited the growth of multiple myeloma cells by suppression of STAT3 pathway and by activation of protein tyrosine phosphatase SHP1
SHP1↓,
NF-kB↓, BA down regulated the expression of NF-kB, cyclin D1, COX2, Ki-67, CD-31 and IAPs in the tumor tissue.
cycD1/CCND1↓,
COX2↓,
Ki-67↓,
CD31↓,
IAP1↓,
MMPs↓, AKBA induced cell cycle arrest was mediated by down-regulating the expression of cyclinD1, suppresses MMP activity, and also induced apoptosis by suppressing Bcl-2, and Bcl-xL expression
Bcl-2↓,
Bcl-xL↓,

1169- Bos,    Boswellic Acid Inhibits Growth and Metastasis of Human Colorectal Cancer in Orthotopic Mouse Model By Downregulating Inflammatory, Proliferative, Invasive, and Angiogenic Biomarkers
- in-vivo, CRC, NA
TumCG↓,
TumVol↓,
Weight∅, without significant decreases in body weight
ascitic↓,
TumMeta↓,
Ki-67↓,
CD31↓,
NF-kB↓,
COX2↓,
Bcl-2↓,
Bcl-xL↓,
IAP1↓,
survivin↓,
cycD1/CCND1↓,
ICAM-1↓,
MMP9↓,
CXCR4↓,
VEGF↓,

465- CUR,    Curcumin inhibits the growth of liver cancer by impairing myeloid-derived suppressor cells in murine tumor tissues
- vitro+vivo, Liver, HepG2 - vitro+vivo, Liver, HUH7 - vitro+vivo, Liver, MHCC-97H
TumCG↓,
MDSCs↓,
TLR4↓,
NF-kB↓,
IL6↓,
IL1↓, IL-1β
PGE2↓,
COX2↓,
GM-CSF↓,
angioG↓,
VEGF↓,
CD31↓,
GM-CSF↓,
α-SMA↓,
p‑IKKα↓, p-IKKα, p-IKKβ
MyD88↓,

801- GAR,  Cisplatin,    Garcinol sensitizes human head and neck carcinoma to cisplatin in a xenograft mouse model despite downregulation of proliferative biomarkers
- in-vivo, HNSCC, NA
Apoptosis↑, enhanced the apoptotic effect of cisplatin
cycD1/CCND1↓,
Bcl-2↓,
survivin↓,
VEGF↓,
TumCG↓,
Ki-67↓, index (Ki-67) and microvessel density (CD31) were downregulated in tumor tissues by the combination of cisplatin and garcinol.
CD31↓,

972- MAG,    Magnolol suppresses hypoxia-induced angiogenesis via inhibition of HIF-1α/VEGF signaling pathway in human bladder cancer cells
- vitro+vivo, Bladder, T24/HTB-9
angioG↓,
VEGF↓,
H2O2↓,
Hif1a↓,
VEGFR2↓,
Akt↓,
mTOR↓,
P70S6K↓,
4E-BP1↓,
TumCG↓,
CD31↓,
CA↓, carbonic anhydrase IX

4968- PSO,    Psoralidin: emerging biological activities of therapeutic benefits and its potential utility in cervical cancer
- in-vitro, Cerv, NA
*Inflam↓, showing anti-inflammatory, anti-oxidant, estrogenic, neuroprotective, anti-diabetic, anti-depressant, antimicrobial, and anti-tumor activities substantiate its promising biological effects.
*antiOx↑,
*neuroP↑,
*AntiDiabetic↑,
*Bacteria↓,
AntiTum↑,
CSCs↓, Its capacity to effectively target cancer stem cells (CSCs) in general adds to its therapeutic potential.
ROS↑, Psoralidin carries out its anti-cancer activity by inducing oxidative stress, autophagy, and apoptosis.
TumAuto↑,
Apoptosis↑,
ChemoSen↑, This unique characteristic suggests its potential to be used as an adjunct molecule in combination with existing treatment to enhance the efficacy of chemo/radiotherapy for treating CaCx.
RadioS↑,
BioAv↓, low bioavailability and intestinal efflux limit the use of psoralidin in clinical applications
*cardioP↑, Psoralidin demonstrated cardioprotective effects.
*ROS↓, Furthermore, psoralidin administration resulted in a decrease in ROS levels and lactate dehydrogenase (LDH) release, indicating reduced oxidative stress and cellular damage in the heart.
*LDH↓,
TumCP↓, LNCaP Induction of apoptosis ↓Cell proliferation ↑TRAIL
TRAIL⇅,
TumCMig↓, PC-3, PzHPV-7, C4-2B 5–20 µM ↓Cell proliferation, ↓Migration, Invasion ROS generation
EMT↓, RWPE-1, xenograft mice 4 µM ↓Cell proliferation, Induction of apoptosis, Autophagy induction, EMT Inhibition ↓NF-кB signaling
NF-kB↓,
P53↑, HepG2 64 µM Induction of apoptosis ↑p53
Casp3↑, figure 4
NOTCH↓,
CSCs↓, Anti-CSC activity
angioG↓, Anti-angiogenesis
VEGF↓, it inhibited angiogenesis by downregulating the expression of pro-angiogenic molecules VEGF, Ki67, and CD31
Ki-67↓,
CD31↓,
TRAILR↑, psoralidin treatment induced the activation of death receptors 1 (DR 1) and DR 2 after 48 h of treatment
MMP↓, Psoralidin significantly increased the loss of ΔΨm, affecting a large percentage of cancer cells (58.38% ± 1.41%) and causing a major disruption of the mitochondrial membrane potential.
BioAv↓, hydrophobic nature, inadequate pharmacokinetic profile of psoralidin, and intestinal efflux, which hampers its clinical application
BioAv↑, bioavailability of psoralidin significantly improved with a value of 339% w.r.t to reference through its nanoencapsulation (NCs) using chitosan and Eudragit S100

3288- SIL,    Silymarin in cancer therapy: Mechanisms of action, protective roles in chemotherapy-induced toxicity, and nanoformulations
- Review, Var, NA
Inflam↓, Silymarin, a milk thistle extract, has anti-inflammatory, immunomodulatory, anti-lipid peroxidative, anti-fibrotic, anti-oxidative, and anti-proliferative properties.
lipid-P↓,
TumMeta↓, Silymarin exhibits not only anti-cancer functions through modulating various hallmarks of cancer, including cell cycle, metastasis, angiogenesis, apoptosis, and autophagy, by targeting a plethora of molecules
angioG↓,
chemoP↑, but also plays protective roles against chemotherapy-induced toxicity, such as nephrotoxicity,
EMT↓, Figure 2, Metastasis
HDAC↓,
HATs↑,
MMPs↓,
uPA↓,
PI3K↓,
Akt↓,
VEGF↓, Angiogenesis
CD31↓,
Hif1a↓,
VEGFR2↓,
Raf↓,
MEK↓,
ERK↓,
BIM↓, apoptosis
BAX↑,
Bcl-2↓,
Bcl-xL↓,
Casp↑,
MAPK↓,
P53↑,
LC3II↑, Autophagy
mTOR↓,
YAP/TEAD↓,
*BioAv↓, Additionally, the oral bioavailability of silymarin in rats is only 0.73 %
MMP↓, silymarin treatment reduced mitochondrial transmembrane potential, leading to an increase in cytosolic cytochrome c (Cyt c), downregulating proliferation-associated proteins (PCNA, c-Myc, cyclin D1, and β-catenin)
Cyt‑c↑,
PCNA↓,
cMyc↓,
cycD1/CCND1↓,
β-catenin/ZEB1↓,
survivin↓, and anti-apoptotic proteins (survivin and Bcl-2), and upregulating pro-apoptotic proteins (caspase-3, Bax, APAF-1, and p53)
APAF1↑,
Casp3↑,
MDSCs↓, ↓MDSCs, ↓IL-10, ↑IL-2 and IFN-γ
IL10↓,
IL2↑,
IFN-γ↑,
hepatoP↑, Moreover, in a randomized clinical trial, silymarin attenuated hepatoxicity in non-metastatic breast cancer patients undergoing a doxorubicin/cyclophosphamide-paclitaxel regimen
cardioP↑, For example, Rašković et al. studied the hepatoprotective and cardioprotective effects of silymarin (60 mg/kg orally) in rats following DOX
GSH↑, silymarin could protect the kidney and heart from ADR toxicity by protecting against glutathione (GSH) depletion and inhibiting lipid peroxidation
neuroP↑, silymarin attenuated the neurotoxicity of docetaxel by reducing apoptosis, inflammation, and oxidative stress

2411- UA,    Ursolic acid in health and disease
- Review, Var, NA
Inflam↓, UA because of its beneficial effects, which include anti-inflammatory, anti-oxidant, anti-apoptotic, and anti-carcinogenic effects
antiOx↑,
NF-kB↓, Colon cancer HCT116, HT29 20 μM for 8 hour ↓ NF-kB, Bcl-xL, Bcl-2, and cyclin D1
Bcl-xL↓,
Bcl-2↓,
cycD1/CCND1↓,
Ki-67↓, ↓ Ki67, CD31, STAT3, and EGFR, ↑ p53 and p21 mRNA expression
CD31↓,
STAT3↓,
EGFR↓,
P53↑,
P21↓,
HK2↓, MCF-7, MDA-MB-231 20 μM for 24 hours ↓ HK2, PKM2, ATP, and lactate ↓ pERK1/2, and depolarization of mitochondrial membrane potential, ↑ Nitric oxide and ATM
PKM2↓,
ATP↓,
lactateProd↓,
p‑ERK↓,
MMP↓,
NO↑,
ATM↑,
Casp3↑, T24 cancer cells ↑ Caspase 3 activity ↑ AMPK activation ↑ JNK activation
AMPK↑,
JNK↑,
FAO↑, 80 μM UA reduces triglyceride (TG) and cholesterol levels by increasing fatty acid oxidation and decreasing fatty acid synthesis in hepatocytes
FASN↓,
*GSH↑, ↑ Vitamin C, E, GSH, SOD, CAT, GPx, GST, and GR in heart
*SOD↑,
*Catalase↑,
*GPx↑,
*GSTs↑,
neuroP↑, This demonstrates that UA has a protective effect against various inflammatory conditions of the brain.


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:


Redox & Oxidative Stress

antiOx↑, 1,   GSH↑, 1,   H2O2↓, 1,   lipid-P↓, 1,   ROS↑, 1,  

Metal & Cofactor Biology

TfR1/CD71↑, 1,  

Mitochondria & Bioenergetics

ATP↓, 1,   MEK↓, 1,   MMP↓, 3,   Raf↓, 1,  

Core Metabolism/Glycolysis

AMPK↑, 1,   cMyc↓, 1,   FAO↑, 1,   FASN↓, 1,   HK2↓, 1,   lactateProd↓, 1,   PKM2↓, 1,  

Cell Death

Akt↓, 2,   APAF1↑, 1,   Apoptosis↑, 3,   BAX↑, 1,   Bcl-2↓, 5,   Bcl-xL↓, 4,   BIM↓, 1,   Casp↑, 1,   Casp3↑, 4,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   IAP1↓, 2,   JNK↑, 1,   MAPK↓, 1,   survivin↓, 3,   TRAIL⇅, 1,   TRAILR↑, 1,   YAP/TEAD↓, 1,  

Transcription & Epigenetics

HATs↑, 1,  

Autophagy & Lysosomes

LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair

ATM↑, 1,   P53↓, 1,   P53↑, 3,   PCNA↓, 1,  

Cell Cycle & Senescence

cycD1/CCND1↓, 5,   P21↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State

4E-BP1↓, 1,   CSCs↓, 2,   EMT↓, 2,   ERK↓, 1,   p‑ERK↓, 1,   HDAC↓, 1,   mTOR↓, 2,   NOTCH↓, 1,   P70S6K↓, 1,   PI3K↓, 1,   SHP1↓, 1,   STAT3↓, 1,   STAT3↑, 1,   TumCG↓, 4,  

Migration

CA↓, 1,   CD31↓, 9,   Ki-67↓, 6,   MMP9↓, 1,   MMPs↓, 2,   TumCMig↓, 1,   TumCP↓, 1,   TumMeta↓, 2,   uPA↓, 1,   α-SMA↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature

angioG↓, 4,   EGFR↓, 2,   Hif1a↓, 2,   NO↑, 1,   VEGF↓, 6,   VEGFR2↓, 2,  

Barriers & Transport

P-gp↓, 1,  

Immune & Inflammatory Signaling

COX2↓, 3,   CXCR4↓, 1,   GM-CSF↓, 2,   ICAM-1↓, 1,   IFN-γ↑, 1,   p‑IKKα↓, 1,   IL1↓, 1,   IL10↓, 1,   IL2↑, 1,   IL6↓, 1,   Inflam↓, 3,   MDSCs↓, 2,   MyD88↓, 1,   NF-kB↓, 5,   PD-1↝, 1,   PGE2↓, 1,   TLR4↓, 1,  

Drug Metabolism & Resistance

BioAv↓, 2,   BioAv↑, 1,   ChemoSen↑, 1,   RadioS↑, 1,  

Clinical Biomarkers

ascitic↓, 1,   EGFR↓, 2,   IL6↓, 1,   Ki-67↓, 6,  

Functional Outcomes

AntiTum↑, 1,   cardioP↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   neuroP↑, 2,   TumVol↓, 1,   Weight∅, 1,  
Total Targets: 110

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   GSTs↑, 1,   ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis

LDH↓, 1,  

Immune & Inflammatory Signaling

Inflam↓, 1,  

Drug Metabolism & Resistance

BioAv↓, 2,   BioAv↑, 1,  

Clinical Biomarkers

LDH↓, 1,  

Functional Outcomes

AntiDiabetic↑, 1,   cardioP↑, 1,   neuroP↑, 1,  

Infection & Microbiome

Bacteria↓, 1,  
Total Targets: 16

Scientific Paper Hit Count for: CD31, platelet endothelial cell adhesion molecule-1 (PECAM-1)
2 Boswellia (frankincense)
1 Artemisinin
1 Curcumin
1 Garcinol
1 Cisplatin
1 Magnolol
1 Psoralidin
1 Silymarin (Milk Thistle) silibinin
1 Ursolic acid
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#:295  State#:%  Dir#:1
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