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.


Scientific Papers found: Click to Expand⟱
5145- AgNPs,    Silver nanoparticles induce irremediable endoplasmic reticulum stress leading to unfolded protein response dependent apoptosis in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, T47D
Bacteria↓, Nowadays, silver nanoparticles (AgNP) are widely used in the medical field mainly for their antibacterial properties
Apoptosis↑, AgNP of 2 (AgNP2) and 15 nm (AgNP15) induce apoptosis in human MCF-7 and T-47D breast cancer cells.
ER Stress↑, Treatment with AgNP2 and AgNP15 led to accumulation and aggregation of misfolded proteins causing an endoplasmic reticulum (ER) stress and activating the unfolded protein response (UPR).
UPR↑,
PERK↑, The three main ER sensors, PERK, IRE-1α and ATF-6, were rapidly activated in response to AgNP2 and AgNP15
IRE1↑,
ATF6↑,
ATF4↑, AgNP2 and AgNP15 induced upregulation of the transcription factors ATF-4 and GADD153/CHOP
CHOP↑,
Casp9↑, Moreover, the initiating caspase-9 and the effector caspase-7 were activated in response to these NPs.
Casp7↑,
Mcl-1↓, In contrast, a downregulation of Mcl-1 and xIAP protein expression as well as a processing of PARP were observed.
XIAP↓,
PARP↝,
selectivity↑, Of note, the non-cancerous MCF-10A cells were more resistant to both AgNP2 and AgNP15 when compared to MCF-7 and T-47D cell lines.

5728- BF,    Effects of bufalin on the proliferation of human lung cancer cells and its molecular mechanisms of action
- in-vitro, Lung, A549
TumCP↓, we have demonstrated that bufalin suppressed the proliferation of human NSCLC A549 cell line in time- and dose-dependent manners.
Apoptosis↑, Bufalin induced the apoptosis and cell cycle arrest by affecting the protein expressions of Bcl-2/Bax, cytochrome c, caspase-3, PARP, p53, p21WAF1, cyclinD1, and COX-2 in A549 cells.
TumCCA↑,
Bcl-2↝,
BAX↝,
Cyt‑c↝,
Casp3↝,
PARP↝,
P21↝,
cycD1/CCND1↝,
COX2↝,
p‑VEGFR2↓, bufalin reduced the protein levels of receptor expressions and/or phosphorylation of VEGFR1, VEGFR2, EGFR and/or c-Met in A549 cells.
EGFR↓,
Akt↓, bufalin inhibited the protein expressions and phosphorylation of Akt, NF-κB, p44/42 MAPK (ERK1/2) and p38 MAPK in A549 cells.
NF-kB↓,
p44↓,

810- GAR,  GEM,    Garcinol sensitizes human pancreatic adenocarcinoma cells to gemcitabine in association with microRNA signatures
- in-vitro, PC, NA
TumCP↓, Garcinol synergizes with gemcitabine to inhibit cell proliferation and induce apoptosis
Apoptosis↑,
PARP↝,
VEGF↝,
MMPs↝,
Casp↝,
NF-kB↝,
miR-21↝,

4906- Sal,    A Concise Review of Prodigious Salinomycin and Its Derivatives Effective in Treatment of Breast Cancer: (2012–2022)
- Review, BC, NA
CSCs↓, Salinomycin (SAL), a polyether ionophore antibiotic being used in the poultry industry, was identified as a powerful anti-cancer compound that possesses broad-spectrum activities, especially against CSCs.
Casp3↑, SAL has been shown to affect the mitochondria, leading to caspase-3 cleaving poly-ADP ribose polymerase (PARP), resulting in apoptosis.
cl‑PARP↝,
Apoptosis↑,
ROS↑, SAL has shown the ability to affect prostate cancer (PC-3) cell lines through the production of reactive oxygen species (ROS), leading to programmed cell death.
ABC↓, potential use of SAL as an ABC transporter inhibitor
OXPHOS↓, Inhibition of Oxidative Phosphorylation and Glycolysis
Glycolysis↓,
eff↑, SAL in combination with glucose analogs (2-DG, 2-FDG) increased the toxicity of SAL towards cancer cells and showed that cancer cells are dependent on glycolysis for ATP production
TumAuto↑, Induction of Autophagy, ROS, and DNA Damage
DNAdam↑,
Wnt↓, Inhibition of the Wnt Signaling Cascade
Ferritin↓, SAL was tested, and at 0.5 μM iron accumulation in the lysosome, a reduction in iron keeper ferritin expression and elevated iron regulatory protein-2 (IRP2) were observed
Iron↑, a novel mechanism of action of SAL affecting breast CSCs is iron accumulation in the lysosome. and an increased amount of iron in the lysosome produces ROS, which leads to apoptosis

4504- SeNPs,  Chit,  FA,  doxoR,    pH-responsive selenium nanoparticles stabilized by folate-chitosan delivering doxorubicin for overcoming drug-resistant cancer cells
- in-vitro, Var, NA
ChemoSen↑, enhance the activity of DOX by approximately 10-fold for a reduced IC50 value compared to free DOX
Apoptosis↑, Mechanistic studies suggested that DOX-SeNPs@TMC-FA induced cell death through the apoptosis pathway by involvement of caspase-3 and PARP proteins.
Casp3↑,
PARP↝,


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

Iron↑, 1,   OXPHOS↓, 1,   ROS↑, 1,  

Metal & Cofactor Biology

Ferritin↓, 1,  

Mitochondria & Bioenergetics

XIAP↓, 1,  

Core Metabolism/Glycolysis

Glycolysis↓, 1,  

Cell Death

Akt↓, 1,   Apoptosis↑, 5,   BAX↝, 1,   Bcl-2↝, 1,   Casp↝, 1,   Casp3↑, 2,   Casp3↝, 1,   Casp7↑, 1,   Casp9↑, 1,   Cyt‑c↝, 1,   Mcl-1↓, 1,  

Transcription & Epigenetics

miR-21↝, 1,  

Protein Folding & ER Stress

ATF6↑, 1,   CHOP↑, 1,   ER Stress↑, 1,   IRE1↑, 1,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes

TumAuto↑, 1,  

DNA Damage & Repair

DNAdam↑, 1,   PARP↝, 4,   cl‑PARP↝, 1,  

Cell Cycle & Senescence

cycD1/CCND1↝, 1,   P21↝, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State

CSCs↓, 1,   Wnt↓, 1,  

Migration

MMPs↝, 1,   p44↓, 1,   TumCP↓, 2,  

Angiogenesis & Vasculature

ATF4↑, 1,   EGFR↓, 1,   VEGF↝, 1,   p‑VEGFR2↓, 1,  

Immune & Inflammatory Signaling

COX2↝, 1,   NF-kB↓, 1,   NF-kB↝, 1,  

Drug Metabolism & Resistance

ABC↓, 1,   ChemoSen↑, 1,   eff↑, 1,   selectivity↑, 1,  

Clinical Biomarkers

EGFR↓, 1,   Ferritin↓, 1,  

Infection & Microbiome

Bacteria↓, 1,  
Total Targets: 50

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PARP, poly ADP-ribose polymerase (PARP) cleavage
1 Silver-NanoParticles
1 Bufalin/Huachansu
1 Garcinol
1 Gemcitabine (Gemzar)
1 salinomycin
1 Selenium NanoParticles
1 chitosan
1 Folic Acid, Vit B9
1 doxorubicin
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#:239  State#:%  Dir#:4
wNotes=on sortOrder:rid,rpid

 

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