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.
Lung, Lung Cancer: Click to Expand ⟱
Lung CSC (Cancer Stem Cells) markers (CD133, CD44, ALDHA1, Nanog and Oct4)
Scientific Papers found: Click to Expand⟱
206- Api,    Inhibition of glutamine utilization sensitizes lung cancer cells to apigenin-induced apoptosis resulting from metabolic and oxidative stress
- in-vitro, Lung, H1299 - in-vitro, Lung, H460 - in-vitro, Lung, A549 - in-vitro, CRC, HCT116 - in-vitro, Melanoma, A375 - in-vitro, Lung, H2030 - in-vitro, CRC, SW480
Glycolysis↓, lactateProd↓, PGK1↓, ALDOA↓, GLUT1↓, ENO1↓, ATP↓, Casp9↑, Casp3↑, cl‑PARP↑, PI3K/Akt↓, HK1↓, HK2↓, ROS↑, Apoptosis↑, eff↓, NADPH↓, PPP↓,
1360- Ash,  immuno,    Withaferin A Increases the Effectiveness of Immune Checkpoint Blocker for the Treatment of Non-Small Cell Lung Cancer
- in-vitro, Lung, H1650 - in-vitro, Lung, A549 - in-vitro, CRC, HCT116 - in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
PD-L1↑, eff↓, ROS↑, ER Stress↑, Apoptosis↑, BAX↑, Bak↑, BAD↑, Bcl-2↓, XIAP↓, survivin↓, cl‑PARP↑, CHOP↑, p‑eIF2α↑, ICD↑, eff↑,
1525- Ba,  almon,    Synergistic antitumor activity of baicalein combined with almonertinib in almonertinib-resistant non-small cell lung cancer cells through the reactive oxygen species-mediated PI3K/Akt pathway
- in-vitro, Lung, H1975 - in-vivo, Lung, NA
eff↑, TumCP↓, Apoptosis↑, cl‑Casp3↑, cl‑PARP↑, cl‑Casp9↑, p‑PI3K↓, p‑Akt↓, ROS↑, eff↓,
1524- Ba,    Baicalein Induces Caspase‐dependent Apoptosis Associated with the Generation of ROS and the Activation of AMPK in Human Lung Carcinoma A549 Cells
- in-vitro, Lung, A549
DR5↑, FADD↑, FasL↑, Casp8↑, cFLIP↓, Casp3↑, Casp9↑, cl‑PARP↑, MMP↓, BID↑, Cyt‑c↑, ROS↑, eff↓, AMPK↑, Apoptosis↑, TumCCA↑, DR5↑, FasL↑, DR4∅, cFLIP↓, FADD↑, MMPs↓,
2476- Ba,    Baicalein Induces Caspase-dependent Apoptosis Associated with the Generation of ROS and the Activation of AMPK in Human Lung Carcinoma A549 Cells
- in-vitro, Lung, A549
TumCG↓, Apoptosis↑, DR5↑, FasL↑, FADD↑, Casp8↑, cFLIP↓, Casp9↑, Casp3↑, cl‑PARP↑, MMP↓, BID↑, BAX↑, Cyt‑c↑, ROS↑, eff↓, AMPK↑,
5724- BF,    A Novel Bufalin Derivative Exhibited Stronger Apoptosis-Inducing Effect than Bufalin in A549 Lung Cancer Cells and Lower Acute Toxicity in Mice
- vitro+vivo, Lung, A549
Apoptosis↑, Casp3↑, cl‑PARP↑,
434- CUR,    Curcumin induces apoptosis in lung cancer cells by 14-3-3 protein-mediated activation of Bad
- in-vitro, Lung, A549
14-3-3 proteins↓, p‑BAD↓, p‑Akt↓, Akt↓, cl‑Casp9↑, cl‑PARP↑,
1966- GamB,  Cisplatin,    Gambogic acid synergistically potentiates cisplatin-induced apoptosis in non-small-cell lung cancer through suppressing NF-κB and MAPK/HO-1 signalling
- in-vitro, Lung, A549 - in-vitro, Lung, NCIH1299
TumCCA↑, PARP↑, eff↑, ROS↑, ChemoSen↑,
2533- M-Blu,  PDT,    Methylene blue-mediated photodynamic therapy enhances apoptosis in lung cancer cells
- in-vitro, Lung, A549
MMP↓, p‑MAPK↑, ROS↑, cl‑PARP↑, Bcl-2↓, Mcl-1↓, eff↓,
1768- PG,    Propyl gallate reduces the growth of lung cancer cells through caspase‑dependent apoptosis and G1 phase arrest of the cell cycle
- in-vitro, Lung, Calu-6 - in-vitro, Lung, A549
TumCG↓, TumCCA↑, Dose∅, Bcl-2↓, cl‑PARP↑, MMP↓, Casp3↑, Casp8↑,
2010- SK,    Shikonin inhibits gefitinib-resistant non-small cell lung cancer by inhibiting TrxR and activating the EGFR proteasomal degradation pathway
- in-vitro, Lung, H1975 - in-vitro, Lung, H1650 - in-vitro, Nor, CCD19
EGFR↓, selectivity↑, Casp↑, PARP↑, Apoptosis↑, ROS↑, eff↓, selectivity↑,
2469- SK,    Shikonin induces the apoptosis and pyroptosis of EGFR-T790M-mutant drug-resistant non-small cell lung cancer cells via the degradation of cyclooxygenase-2
- in-vitro, Lung, H1975
Apoptosis↑, Pyro↑, Casp↑, cl‑PARP↑, GSDME↑, ROS↑, COX2↓, PDK1↓, Akt↓, ERK↓, eff↓, eff↓, eff↑,
1002- SSE,  Osi,  Adag,    Selenite as a dual apoptotic and ferroptotic agent synergizes with EGFR and KRAS inhibitors with epigenetic interference
- in-vitro, Lung, H1975 - in-vitro, Lung, H385
Apoptosis↑, Ferroptosis↑, DNMT1↓, TET1↑, TumCCA↑, cl‑PARP↑, cl‑Casp3↑, Cyt‑c↑, BIM↑, NOXA↑, Apoptosis↑, ROS↑, ER Stress↑, UPR↑,

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 ⓘ

Ferroptosis↑, 1,   HK1↓, 1,   ICD↑, 1,   ROS↑, 10,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 4,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALDOA↓, 1,   AMPK↑, 2,   ENO1↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,   NADPH↓, 1,   PDK1↓, 1,   PGK1↓, 1,   PI3K/Akt↓, 1,   PPP↓, 1,  

Cell Death ⓘ

14-3-3 proteins↓, 1,   Akt↓, 2,   p‑Akt↓, 2,   Apoptosis↑, 10,   BAD↑, 1,   p‑BAD↓, 1,   Bak↑, 1,   BAX↑, 2,   Bcl-2↓, 3,   BID↑, 2,   BIM↑, 1,   Casp↑, 2,   Casp3↑, 5,   cl‑Casp3↑, 2,   Casp8↑, 3,   Casp9↑, 3,   cl‑Casp9↑, 2,   cFLIP↓, 3,   Cyt‑c↑, 3,   DR4∅, 1,   DR5↑, 3,   FADD↑, 3,   FasL↑, 3,   Ferroptosis↑, 1,   GSDME↑, 1,   p‑MAPK↑, 1,   Mcl-1↓, 1,   NOXA↑, 1,   Pyro↑, 1,   survivin↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   p‑eIF2α↑, 1,   ER Stress↑, 2,   UPR↑, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,   PARP↑, 2,   cl‑PARP↑, 11,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   p‑PI3K↓, 1,   TumCG↓, 2,  

Migration ⓘ

MMPs↓, 1,   TET1↑, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   PD-L1↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose∅, 1,   eff↓, 9,   eff↑, 4,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   PD-L1↑, 1,  
Total Targets: 73

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PARP, poly ADP-ribose polymerase (PARP) cleavage
3 Baicalein
2 Shikonin
1 Apigenin (mainly Parsley)
1 Ashwagandha(Withaferin A)
1 immunotherapy
1 almonertinib
1 Bufalin/Huachansu
1 Curcumin
1 Gambogic Acid
1 Cisplatin
1 Methylene blue
1 Photodynamic Therapy
1 Propyl gallate
1 Selenite (Sodium)
1 Osimertinib
1 Adagrasib
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:15  Cells:%  prod#:%  Target#:239  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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