VEGF Cancer Research Results

VEGF, Vascular endothelial growth factor: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
A signal protein produced by many cells that stimulates the formation of blood vessels. Vascular endothelial growth factor (VEGF) is a signal protein that plays a crucial role in angiogenesis, the process by which new blood vessels form from existing ones. This process is vital for normal physiological functions, such as wound healing and the menstrual cycle, but it is also a key factor in the growth and spread of tumors in cancer.
Because of its significant role in tumor growth and progression, VEGF has become a target for cancer therapies. Anti-VEGF therapies, such as monoclonal antibodies (e.g., bevacizumab) and small molecule inhibitors, aim to inhibit the action of VEGF, thereby reducing blood supply to tumors and limiting their growth. These therapies have been used in various types of cancer, including colorectal, lung, and breast 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⟱
211- Api,    Suppression of NF-κB and NF-κB-Regulated Gene Expression by Apigenin through IκBα and IKK Pathway in TRAMP Mice
- in-vivo, Pca, NA
IKKα↓, NF-kB↓, cycD1/CCND1↓, COX2↓, Bcl-2↓, Bcl-xL↓, VEGF↓, PCNA↓, BAX↑,
238- Api,    Apigenin inhibits TGF-β-induced VEGF expression in human prostate carcinoma cells via a Smad2/3- and Src-dependent mechanism
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, C4-2B
VEGF↓, TGF-β↓, Src↓, FAK↓, Akt↓, SMAD2↓, SMAD3↓,
4816- ASTX,    Potent carotenoid astaxanthin expands the anti-cancer activity of cisplatin in human prostate cancer cells
- in-vitro, Pca, NA
*antiOx↑, *Inflam↓, ChemoSen↑, E-cadherin↑, N-cadherin↓, VEGF↓, cMyc↓, PSA↓, cl‑Casp3↑, PARP1↑,
2754- BetA,    Betulinic acid inhibits prostate cancer growth through inhibition of specificity protein transcription factors
- in-vitro, Pca, LNCaP
VEGF↓, survivin↓, Sp1/3/4↓, Casp↑, PARP↑, survivin↓, angioG↓,
5940- Cela,    Celastrol Suppresses Angiogenesis-Mediated Tumor Growth through Inhibition of AKT/Mammalian Target of Rapamycin Pathway
- in-vivo, Pca, PC3
Dose↝, TumVol↓, TumW↓, angioG↓, VEGF↓, TumCMig↓, TumCP↓, TumCI↓, Akt↓, mTOR↓, P70S6K↓,
2802- CHr,    Chrysin inhibits expression of hypoxia-inducible factor-1alpha through reducing hypoxia-inducible factor-1alpha stability and inhibiting its protein synthesis
- in-vitro, Pca, DU145 - in-vivo, Pca, NA
Hif1a↓, VEGF↓, angioG↓,
155- CUR,    Osteopontin and MMP9: Associations with VEGF Expression/Secretion and Angiogenesis in PC3 Prostate Cancer Cells
- in-vitro, Pca, PC3
p‑ERK↓, VEGF↓, angioG↓, MMP2↓, MMP9↓, angioS↑,
170- CUR,    Curcumin sensitizes TRAIL-resistant xenografts: molecular mechanisms of apoptosis, metastasis and angiogenesis
- vitro+vivo, Pca, PC3
TRAILR↑, BAX↑, P21↑, p27↑, NF-kB↓, cycD1/CCND1↓, VEGF↓, uPA↓, MMP2↓, MMP9↓, Bcl-2↓, Bcl-xL↓,
169- CUR,    Curcumin inhibits the expression of vascular endothelial growth factor and androgen-independent prostate cancer cell line PC-3 in vitro
- in-vitro, Pca, PC3
VEGF↓,
26- EGCG,  QC,  docx,    Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapy
- vitro+vivo, Pca, PC3
BAD↓, cl‑PARP↑, Casp7↑, IκB↓, Ki-67↓, VEGF↓, EGFR↓, FGF↓, TGF-β↓, TNF-α↓, SCF↓, Bax:Bcl2↑, NF-kB↓, chemoP↑, ChemoSen↑, TumVol↓,
850- Gra,    Selective cytotoxic and anti-metastatic activity in DU-145 prostate cancer cells induced by Annona muricata L. bark extract and phytochemical, annonacin
- in-vitro, PC, PC3 - in-vitro, Pca, DU145
ROS∅, MMP∅, Casp3↑, Casp7↑, VEGF↓,
971- MEL,    Melatonin down-regulates HIF-1 alpha expression through inhibition of protein translation in prostate cancer cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP
Hif1a↓, VEGF↓, p‑p70S6↓,
2064- PB,  Rad,    Phenylbutyrate Attenuates the Expression of Bcl-XL, DNA-PK, Caveolin-1, and VEGF in Prostate Cancer Cells
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP
Bcl-xL↓, Cav1↓, VEGF↓, RadioS↑, chemoP↑, HDAC↓, *toxicity↓, Diff↑, Prot↓,
4939- PEITC,    Phenethyl Isothiocyanate Inhibits Angiogenesis In vitro and Ex vivo
- in-vitro, Pca, PC3 - ex-vivo, Nor, HUVECs
Risk↓, angioG↓, VEGF↓, TumCMig↓, Akt↓, EGF↓, TumCMig↓,
5185- PEITC,  SFN,    Suppression of NF-kappaB and NF-kappaB-regulated gene expression by sulforaphane and PEITC through IkappaBalpha, IKK pathway in human prostate cancer PC-3 cells
- in-vitro, Pca, PC3
NF-kB↓, p65↓, VEGF↓, cycD1/CCND1↓, Bcl-xL↓, IKKα↓,
66- QC,    Emerging impact of quercetin in the treatment of prostate cancer
- Review, Pca, NA
CycB/CCNB1↓, CDK1↓, EMT↓, PI3K↓, MAPK↓, Wnt/(β-catenin)↓, PSA↓, VEGF↓, PARP↑, Casp3↑, Casp9↑, DR5↑, ROS⇅, Shh↓, P53↑, P21↑, EGFR↓, TumCCA↑, ROS↑, miR-21↓, TumCP↓, selectivity↑, PDGF↓, EGF↓, TNF-α↓, VEGFR2↓, mTOR↓, cMyc↓, MMPs↓, GRP78/BiP↑, CHOP↑,
3369- QC,    Pharmacological basis and new insights of quercetin action in respect to its anti-cancer effects
- Review, Pca, NA
FAK↓, TumCCA↑, p‑pRB↓, CDK2↑, CycB/CCNB1↓, CDK1↓, EMT↓, PI3K↓, MAPK↓, Wnt↓, ROS↑, miR-21↑, Akt↓, NF-kB↓, FasL↑, Bak↑, BAX↑, Bcl-2↓, Casp3↓, Casp9↑, P53↑, p38↑, MAPK↑, Cyt‑c↑, PARP↓, CHOP↑, ROS↓, LDH↑, GRP78/BiP↑, ERK↑, MDA↓, SOD↑, GSH↑, NRF2↑, VEGF↓, PDGF↓, EGF↓, FGF↓, TNF-α↓, TGF-β↓, VEGFR2↓, EGFR↓, FGFR1↓, mTOR↓, cMyc↓, MMPs↓, LC3B-II↑, Beclin-1↑, IL1β↓, CRP↓, IL10↓, COX2↓, IL6↓, TLR4↓, Shh↓, HER2/EBBR2↓, NOTCH↓, DR5↑, HSP70/HSPA5↓, CSCs↓, angioG↓, MMP2↓, MMP9↓, IGFBP3↑, uPA↓, uPAR↓, RAS↓, Raf↓, TSP-1↑,
3192- SFN,    Transcriptome analysis reveals a dynamic and differential transcriptional response to sulforaphane in normal and prostate cancer cells and suggests a role for Sp1 in chemoprevention
- in-vitro, Pca, PC3
Sp1/3/4↓, selectivity↑, NRF2↑, HDAC↓, DNMTs↓, TumCCA↑, selectivity↑, HO-1↑, NQO1↑, CDK2↓, TumCP↓, BID↑, Smad1↑, Diablo↑, ICAD↑, Cyt‑c↑, IAP1↑, HSP27↑, *Cyt‑c↓, *IAP1↓, *HSP27↓, survivin↓, CDK4↓, VEGF↓, AR↓,
5112- SSE,    https://pubmed.ncbi.nlm.nih.gov/19811770/
- in-vitro, Pca, PC3
VEGF↓, IL6↓, NF-kB↓, p65↓,

Showing Research Papers: 1 to 19 of 19

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 19

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↑, 1,   HO-1↑, 1,   MDA↓, 1,   NQO1↑, 1,   NRF2↑, 2,   ROS↓, 1,   ROS↑, 2,   ROS⇅, 1,   ROS∅, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics ⓘ

EGF↓, 3,   FGFR1↓, 1,   MMP∅, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

Cav1↓, 1,   cMyc↓, 3,   LDH↑, 1,  

Cell Death ⓘ

Akt↓, 4,   BAD↓, 1,   Bak↑, 1,   BAX↑, 3,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   Bcl-xL↓, 4,   BID↑, 1,   Casp↑, 1,   Casp3↓, 1,   Casp3↑, 2,   cl‑Casp3↑, 1,   Casp7↑, 2,   Casp9↑, 2,   Cyt‑c↑, 2,   Diablo↑, 1,   DR5↑, 2,   FasL↑, 1,   IAP1↑, 1,   ICAD↑, 1,   MAPK↓, 2,   MAPK↑, 1,   p27↑, 1,   p38↑, 1,   survivin↓, 3,   TRAILR↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   p‑p70S6↓, 1,   Sp1/3/4↓, 2,  

Transcription & Epigenetics ⓘ

miR-21↓, 1,   miR-21↑, 1,   p‑pRB↓, 1,   Prot↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,   GRP78/BiP↑, 2,   HSP27↑, 1,   HSP70/HSPA5↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3B-II↑, 1,  

DNA Damage & Repair ⓘ

DNMTs↓, 1,   P53↑, 2,   PARP↓, 1,   PARP↑, 2,   cl‑PARP↑, 1,   PARP1↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 2,   CDK2↓, 1,   CDK2↑, 1,   CDK4↓, 1,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 3,   P21↑, 2,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   Diff↑, 1,   EMT↓, 2,   ERK↑, 1,   p‑ERK↓, 1,   FGF↓, 2,   HDAC↓, 2,   IGFBP3↑, 1,   mTOR↓, 3,   NOTCH↓, 1,   P70S6K↓, 1,   PI3K↓, 2,   RAS↓, 1,   SCF↓, 1,   Shh↓, 2,   Src↓, 1,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   FAK↓, 2,   Ki-67↓, 1,   MMP2↓, 3,   MMP9↓, 3,   MMPs↓, 2,   N-cadherin↓, 1,   PDGF↓, 2,   Smad1↑, 1,   SMAD2↓, 1,   SMAD3↓, 1,   TGF-β↓, 3,   TSP-1↑, 1,   TumCI↓, 1,   TumCMig↓, 3,   TumCP↓, 3,   uPA↓, 2,   uPAR↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 6,   angioS↑, 1,   EGFR↓, 3,   Hif1a↓, 2,   VEGF↓, 19,   VEGFR2↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   CRP↓, 1,   IKKα↓, 2,   IL10↓, 1,   IL1β↓, 1,   IL6↓, 2,   IκB↓, 1,   NF-kB↓, 6,   p65↓, 2,   PSA↓, 2,   TLR4↓, 1,   TNF-α↓, 3,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,   Dose↝, 1,   RadioS↑, 1,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

AR↓, 1,   CRP↓, 1,   EGFR↓, 3,   HER2/EBBR2↓, 1,   IL6↓, 2,   Ki-67↓, 1,   LDH↑, 1,   PSA↓, 2,  

Functional Outcomes ⓘ

chemoP↑, 2,   Risk↓, 1,   TumVol↓, 2,   TumW↓, 1,  
Total Targets: 142

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Cell Death ⓘ

Cyt‑c↓, 1,   IAP1↓, 1,  

Protein Folding & ER Stress ⓘ

HSP27↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

toxicity↓, 1,  
Total Targets: 6

Scientific Paper Hit Count for: VEGF, Vascular endothelial growth factor
3 Curcumin
3 Quercetin
2 Apigenin (mainly Parsley)
2 Phenethyl isothiocyanate
2 Sulforaphane (mainly Broccoli)
1 Astaxanthin
1 Betulinic acid
1 Celastrol
1 Chrysin
1 EGCG (Epigallocatechin Gallate)
1 Docetaxel
1 Graviola
1 Melatonin
1 Phenylbutyrate
1 Radiotherapy/Radiation
1 Selenite (Sodium)
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#:334  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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