pRB Cancer Research Results

pRB, retinoblastoma protein: Click to Expand ⟱
Source: Tumor suspressor
Type:
pRB, or retinoblastoma protein, is a crucial tumor suppressor that plays a significant role in regulating the cell cycle. It is encoded by the RB1 gene, and its primary function is to control the progression of cells from the G1 phase to the S phase of the cell cycle. When functioning properly, pRB binds to and inhibits E2F transcription factors, which are necessary for the expression of genes required for DNA synthesis and cell division.
pRB is often found to be downregulated or functionally inactivated due to mutations in the RB1 gene or through other mechanisms.


Scientific Papers found: Click to Expand⟱
3162- Ash,    Molecular insights into cancer therapeutic effects of the dietary medicinal phytochemical withaferin A
- Review, Var, NA
lipid-P↓, Oral cancer 20 mg/Kg ↓Lipid peroxidation : ↑SOD, glutathione peroxidase, p53, Bcl-2
SOD↑,
GPx↑,
P53↑,
Bcl-2↑,
E6↓, Cervival cancer 8mg/Kg ↓E6, E7: ↑p53, pRb, Cyclin B1, P34 Cdc2, p21, PCNA
E7↓,
pRB↑,
CycB/CCNB1↑,
CDC2↑,
P21↑,
PCNA↓,
ALDH1A1↓, Mammary cancer 0-1 mg/mouse (5-10) ↓Mammosphere number, ALDH1 activity. Vimentin, glycolysis
Vim↓,
Glycolysis↓,
cMyc↓, Mesotheliome cancer 5 mg/Kg ↓Proteasomal chymotrypsin, C-Myc : ↑ Bax, CARP-1
BAX↑,
NF-kB↓,
Casp3↑, caspase-3 activation
CHOP/DDIT3↑, WA is found to increase activation of Elk1 and CHOP (CCAAT-enhancer-binding protein homologous protein) by RSK, as well as up-regulation of DR5 by selectively suppressing pathway ERK
DR5↑,
ERK↓,
Wnt↓, WA inhibits Wnt/β-catenin pathway via suppression of AKT signalling, which inhibits cancer cell motility and sensitises for cell death
β-catenin/ZEB1↓,
Akt↓,
HSP90↓, WA-dependent inhibition of heat shock protein (HSP) chaperone functions. WA inhibits the activity of HSP90-mediated function

3238- EGCG,    Green tea catechin, epigallocatechin-3-gallate (EGCG): mechanisms, perspectives and clinical applications
- Review, Var, NA
Telomerase↓, EGCG stimulates telomere fragmentation through inhibiting telomerase activity.
DNMTs↓, EGCG reduced DNMTs,
cycD1/CCND1↓, EGCG also reduced the protein expression of cyclin D1, cyclin E, CDK2, CDK4, and CDK6. EGCG also inhibited the activity of CDK2 and CDK4, and caused Rb hypophosphorylation
cycE/CCNE↓,
CDK2↓,
CDK4↓,
CDK6↓,
HATs↓, EGCG can inhibit certain biomedically important molecular targets such as DNMTs, HATs, and HDACs
HDAC↓,
selectivity↑, EGCG has shown higher cytotoxicity in cancer cells than in their normal counterparts.
uPA↓, EGCG blocks urokinase, an enzyme which is essential for cancer growth and metastasis
NF-kB↓, EGCG inhibits NFκB and expression of TNF-α, reduces cancer promotion
TNF-α↓,
*ROS↓, It acts as strong ROS scavenger and antioxidant,
*antiOx↑,
Hif1a↓, ↓ HIF-1α; ↓ VEGF; ↓ VEGFR1;
VEGF↓,
MMP2↓, ↓ MMP-2; ↓ MMP-9; ↓ FAK;
MMP9↓,
FAK↓,
TIMP2↑, TIMP-2; ↑
Mcl-1↓, ↓ Mcl-1; ↓ survivin; ↓ XIAP
survivin↓,
XIAP↓,
PCNA↓, ↓ PCNA; ↑ 16; ↑ p18; ↑ p21; ↑ p27; ↑ pRb; ↑ p53; ↑ mdm2
p16↑,
P21↑,
p27/CDKN1B↑,
pRB↑,
P53↑,
MDM2↑,
ROS↑, ↑ ROS; ↑ caspase-3; ↑ caspase-8; ↑ caspase-9; ↑ cytochrome c; ↑ Smac/DIABLO; ↓↑ Bax; Z Bak; ↓ cleaved PPAR;
Casp3↑,
Casp8↑,
Casp9↑,
Cyt‑c↑,
Diablo↑,
BAX⇅,
cl‑PPARα↓,
PDGF↓, ↓ PDGF; ↓ PDGFRb; ↓ EGFR;
EGFR↓,
FOXO↑, activated FOXO transcription factors
AP-1↓, The inhibition of AP-1 activity by EGCG was associated with inhibition of JNK activation but not ERK activation.
JNK↓,
COX2/PTGS2↓, EGCG reduces the activity of COX-2 following interleukin-1A stimulation of human chondrocytes
angioG↓, EGCG inhibits angiogenesis by enhancing FOXO transcriptional activity

7718- IP6,    Inositol hexaphosphate inhibits growth, and induces G1 arrest and apoptotic death of prostate carcinoma DU145 cells: modulation of CDKI-CDK-cyclin and pRb-related protein-E2F complexes
- in-vitro, Pca, DU145
chemoPv↑, Cancer chemopreventive effects of inositol hexaphosphate (IP6), a dietary constituent, have been demonstrated against a variety of experimental tumors
TumCG↓, A significant dose- as well as time-dependent growth inhibition was observed in IP6-treated cells, which was associated with an increase in G1 arrest.
TumCCA↑,
P21↓, IP6 strongly increased the expression of CDKIs (cyclin-dependent kinase inhibitors), Cip1/p21 and Kip1/p27
p27/CDKN1B↑,
CDK2↓, IP6 inhibited kinase activities associated with CDK2, 4 and 6, and cyclin E and D1.
CDK4↓,
CDK6↓,
cycE/CCNE↓,
cycD1/CCND1↓,
pRB↑, IP6 increased hypophosphorylated levels of Rb-related proteins, pRb/p107 and pRb2/p130,
Apoptosis↑, IP6 caused a marked increase in apoptosis, which was accompanied by increased levels of cleaved PARP and active caspase 3.
cl‑PARP↑,
Casp3↑,


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

GPx↑, 1,   lipid-P↓, 1,   ROS↑, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC2↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,   Glycolysis↓, 1,   cl‑PPARα↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   BAX⇅, 1,   Bcl-2↑, 1,   Casp3↑, 3,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   Diablo↑, 1,   DR5↑, 1,   JNK↓, 1,   Mcl-1↓, 1,   MDM2↑, 1,   p27/CDKN1B↑, 2,   survivin↓, 1,   Telomerase↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

HATs↓, 1,   pRB↑, 3,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   HSP90↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNMTs↓, 1,   p16↑, 1,   P53↑, 2,   cl‑PARP↑, 1,   PCNA↓, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 2,   CDK4↓, 2,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 2,   P21↓, 1,   P21↑, 2,   TumCCA↑, 1,  

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

ALDH1A1↓, 1,   ERK↓, 1,   FOXO↑, 1,   HDAC↓, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   FAK↓, 1,   MMP2↓, 1,   MMP9↓, 1,   PDGF↓, 1,   TIMP2↑, 1,   uPA↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   NF-kB↓, 2,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

E6↓, 1,   E7↓, 1,   EGFR↓, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoPv↑, 1,  
Total Targets: 71

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   ROS↓, 1,  
Total Targets: 2

Scientific Paper Hit Count for: pRB, retinoblastoma protein
1 Ashwagandha(Withaferin A)
1 EGCG (Epigallocatechin Gallate)
1 IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)
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#:478  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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