PARP Cancer Research Results

PARP, poly ADP-ribose polymerase (PARP) cleavage: Click to Expand ⟱
Source:
Type:
Poly (ADP-ribose) polymerase (PARP) cleavage is a hallmark of caspase activation. PARP (Poly (ADP-ribose) polymerase) is a family of proteins involved in a variety of cellular processes, including DNA repair, genomic stability, and programmed cell death. PARP enzymes play a crucial role in repairing single-strand breaks in DNA.
PARP has gained significant attention, particularly in the treatment of certain types of tumors, such as those with BRCA1 or BRCA2 mutations. These mutations impair the cell's ability to repair double-strand breaks in DNA through homologous recombination. Cancer cells with these mutations can become reliant on PARP for survival, making them particularly sensitive to PARP inhibitors.
PARP inhibitors, such as olaparib, rucaparib, and niraparib, have been developed as targeted therapies for cancers associated with BRCA mutations.

PARP Family:
The poly (ADP-ribose) polymerases (PARPs) are a family of enzymes involved in a number of cellular processes, including DNA repair, genomic stability, and programmed cell death.
PARP1 is the predominant family member responsible for detecting DNA strand breaks and initiating repair processes, especially through base excision repair (BER).

PARP1 Overexpression:
In several cancer types—including breast, ovarian, prostate, and lung cancers—elevated PARP1 expression and/or activity has been reported.
High PARP1 expression in certain cancers has been associated with aggressive tumor behavior and resistance to therapies (especially those that induce DNA damage).
Increased PARP1 activity may correlate with poorer overall survival in tumors that rely on DNA repair for survival.
Cerv, Cervical Cancer: Click to Expand ⟱
Cervical Cancer
Scientific Papers found: Click to Expand⟱
5472- AF,    Auranofin induces apoptosis and necrosis in HeLa cells via oxidative stress and glutathione depletion
- in-vitro, Cerv, HeLa
TrxR↓, AntiCan↑, TumCG↓, Apoptosis↑, necrosis↑, cl‑PARP↑, MMP↓, ROS↑, GSH↓, eff↓,
5592- BetA,    Betulin induces mitochondrial cytochrome c release associated apoptosis in human cancer cells
- in-vitro, Liver, HepG2 - in-vitro, Cerv, HeLa
Casp3↑, Casp9↑, cl‑PARP↑, Apoptosis↑, Cyt‑c↑, MMP↓,
7969- BUL,    Bullatacin triggered ABCB1-overexpressing cell apoptosis via the mitochondrial-dependent pathway
- NA, Cerv, KBv200
ROS↑, MMP↓, cl‑Casp3↑, cl‑Casp9↓, cl‑PARP↑, Cyt‑c↑, eff↓,
1980- CUR,  Rad,    Thioredoxin reductase-1 (TxnRd1) mediates curcumin-induced radiosensitization of squamous carcinoma cells
- in-vitro, Cerv, HeLa - in-vitro, Laryn, FaDu
selectivity↑, RadioS↑, TrxR↓, ROS↑, ERK↑, Dose∅, cl‑PARP↑,
477- CUR,    Curcumin induces G2/M arrest and triggers autophagy, ROS generation and cell senescence in cervical cancer cells
- in-vitro, Cerv, SiHa
TumCP↓, TumCCA↑, Apoptosis↑, TumAuto↑, CycB/CCNB1↓, CDC25↓, ROS↑, p62↑, LC3‑Ⅱ/LC3‑Ⅰ↑, cl‑Casp3↑, cl‑PARP↑, P53↑, P21↑,
6611- Ech,    Proliferative activity of a blend of Echinacea angustifolia and Echinacea purpurea root extracts in human vein epithelial, HeLa, and QBC-939 cell lines, but not in Beas-2b cell lines
- in-vitro, Cerv, HeLa - in-vitro, Nor, BEAS-2B - in-vitro, Nor, HUVECs
Imm↑, TumCP↑, Telomerase↓, Apoptosis↑, DNAdam↑, Casp9↑, cl‑PARP↑, β-catenin/ZEB1↓,
6834- EMD,    Emodin induces apoptosis of human cervical cancer cells through poly(ADP-ribose) polymerase cleavage and activation of caspase-9
- in-vitro, Cerv, HeLa
AntiCan↑, TumCP↓, Apoptosis↑, Casp3↑, Casp9↑, cl‑PARP↑, TumCD↑, DNAdam↑,
7103- GEN,    A Comprehensive Review of Genistein's Effects in Preclinical Models of Cervical Cancer
- Review, Cerv, NA
TumCP↓, Apoptosis↑, RadioS↑, ChemoSen↑, *antiOx↑, *Inflam↓, *Bacteria↓, *AntiViral↑, *AntiDiabetic↑, *neuroP↑, AntiCan↑, TumCG↓, TumCI↓, TumCCA↑, cl‑PARP↑, selectivity↑, CycB/CCNB1↓, CDK1↓, p‑cDC2↓, p‑ERK↓, p‑p38↑, p‑JNK↑, MMP9↓, TIMP1↑, BioAv↓, BioAv↑, Half-Life↑,
7724- IP6,    Inositol hexakisphosphate blocks tumor cell growth by activating apoptotic machinery as well as by inhibiting the Akt/NFkappaB-mediated cell survival pathway
- in-vitro, Cerv, HeLa
NF-kB↓, Akt↓, MMP↓, Cyt‑c↑, Apoptosis↑, Casp3↑, Casp9↑, PARP↑, eff↑,
4957- PEITC,    Phenethyl Isothiocyanate (PEITC) from Cruciferous Vegetables Targets Human Cancer Stem-Like Cells
- vitro+vivo, Cerv, HeLa
CSCs↓, ALDH↓, CD44↓, CD24↓, cl‑PARP↑, DR4↑, DR5↑,
4960- PEITC,    Phenethyl isothiocyanate upregulates death receptors 4 and 5 and inhibits proliferation in human cancer stem-like cells
- in-vivo, Cerv, HeLa
CD44↓, CD24↓, CSCs↓, cl‑PARP↑, DR4↑, DR5↑, TumCP↓,
5219- PG,    Propyl gallate inhibits the growth of HeLa cells via caspase-dependent apoptosis as well as a G1 phase arrest of the cell cycle
- in-vitro, Cerv, HeLa
TumCG↓, TumCCA↑, p27/CDKN1B↑, Apoptosis↑, MMP↓, Casp3↑, Casp8↑, cl‑PARP↑,
2097- TQ,    Crude extract of Nigella sativa inhibits proliferation and induces apoptosis in human cervical carcinoma HeLa cells
- in-vitro, Cerv, HeLa
Cyt‑c↑, Bax:Bcl2↑, Casp3↑, Casp9↑, Casp8↑, cl‑PARP↑, cMyc↓, hTERT/TERT↓, cycD1/CCND1↓, CDK4↓, P53↑, P21↑, TumCP↓, Apoptosis↓, selectivity↑,

Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

GSH↓, 1,   ROS↑, 4,   TrxR↓, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC25↓, 1,   MMP↓, 5,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↓, 1,   Apoptosis↑, 8,   Bax:Bcl2↑, 1,   Casp3↑, 5,   cl‑Casp3↑, 2,   Casp8↑, 2,   Casp9↑, 5,   cl‑Casp9↓, 1,   Cyt‑c↑, 4,   DR4↑, 2,   DR5↑, 2,   hTERT/TERT↓, 1,   p‑JNK↑, 1,   necrosis↑, 1,   p27/CDKN1B↑, 1,   p‑p38↑, 1,   Telomerase↓, 1,   TumCD↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   p62↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 2,   P53↑, 2,   PARP↑, 1,   cl‑PARP↑, 12,  

Cell Cycle & Senescence(tgid=11) ⓘ

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

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

ALDH↓, 1,   CD24↓, 2,   CD44↓, 2,   p‑cDC2↓, 1,   CSCs↓, 2,   ERK↑, 1,   p‑ERK↓, 1,   TumCG↓, 3,  

Migration(tgid=13) ⓘ

MMP9↓, 1,   TIMP1↑, 1,   TumCI↓, 1,   TumCP↓, 5,   TumCP↑, 1,   β-catenin/ZEB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm↑, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 1,   Dose∅, 1,   eff↓, 2,   eff↑, 1,   Half-Life↑, 1,   RadioS↑, 2,   selectivity↑, 3,  

Clinical Biomarkers(tgid=22) ⓘ

hTERT/TERT↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 3,  
Total Targets: 65

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiDiabetic↑, 1,   neuroP↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,   Bacteria↓, 1,  
Total Targets: 6

Scientific Paper Hit Count for: PARP, poly ADP-ribose polymerase (PARP) cleavage
2 Curcumin
2 Phenethyl isothiocyanate
1 Auranofin
1 Betulinic acid
1 Bullatacin
1 Radiotherapy/Radiation
1 Echinacea
1 Emodin
1 Genistein (soy isoflavone)
1 IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)
1 Propyl gallate
1 Thymoquinone
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:29  Cells:%  prod#:%  Target#:239  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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