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.
GBM, Glioblastoma: Click to Expand ⟱
Glioblastoma is a fast-growing and aggressive brain tumor.
Scientific Papers found: Click to Expand⟱
1402- BBR,    Berberine-induced apoptosis in human glioblastoma T98G cells is mediated by endoplasmic reticulum stress accompanying reactive oxygen species and mitochondrial dysfunction
- in-vitro, GBM, T98G
tumCV↓, ROS↑, Ca+2↑, ER Stress↑, eff↓, Bax:Bcl2↑, MMP↓, Casp9↑, Casp3↑, cl‑PARP↑,
5725- BF,  TMZ,    Bufalin Induces Apoptosis and Improves the Sensitivity of Human Glioma Stem-Like Cells to Temozolamide
- in-vitro, GBM, NA
TumCG↓, TumCP↓, CSCs↓, cl‑Casp3↑, PARP↑, Telomerase↓, eff↑,
1912- HCQ,  TMZ,    Chloroquine enhances temozolomide cytotoxicity in malignant gliomas by blocking autophagy
- in-vivo, GBM, U87MG
LC3B-II↑, CHOP↑, cl‑PARP↑,
3371- QC,    Quercetin induces MGMT+ glioblastoma cells apoptosis via dual inhibition of Wnt3a/β-Catenin and Akt/NF-κB signaling pathways
- in-vitro, GBM, T98G
TIMP2↑, TumCG↓, TumCMig↓, Apoptosis↑, TumCCA↑, MMP↓, ROS↑, Bax:Bcl2↑, cl‑Casp9↑, cl‑Casp3↑, DNAdam↑, γH2AX↑, MGMT↓, cl‑PARP↑,
1344- SK,    Novel multiple apoptotic mechanism of shikonin in human glioma cells
- in-vitro, GBM, U87MG - in-vitro, GBM, Hs683 - in-vitro, GBM, M059K
ROS↑, GSH↓, MMP↓, P53↑, cl‑PARP↑, Catalase↓, SOD1↑, Bcl-2↓, BAX↑, eff↓,
2127- TQ,    Therapeutic Potential of Thymoquinone in Glioblastoma Treatment: Targeting Major Gliomagenesis Signaling Pathways
- Review, GBM, NA
chemoP↑, ChemoSen↑, BioAv↑, PTEN↑, PI3K↓, Akt↓, TumCCA↓, NF-kB↓, p‑Akt↓, p65↓, XIAP↓, Bcl-2↓, COX2↓, VEGF↓, mTOR↓, RAS↓, Raf↓, MEK↓, ERK↓, MMP2↓, MMP9↓, TumCMig↓, TumCI↓, Casp↑, cl‑PARP↑, ROS⇅, ROS↑, MMP↓, eff↑, Telomerase↓, DNAdam↑, Apoptosis↑, STAT3↓, RadioS↑,
4468- VitC,  SSE,    Selenium modulates cancer cell response to pharmacologic ascorbate
- in-vivo, GBM, U87MG - in-vitro, CRC, HCT116
eff↓, TumCD↑, ChemoSen↑, ROS⇅, DNAdam↑, PARP↑, NAD↓, Glycolysis↓, Fenton↑, lipid-P↑, eff↓, H2O2↑, other↝,
3138- VitC,    The Hypoxia-inducible Factor Renders Cancer Cells More Sensitive to Vitamin C-induced Toxicity
- in-vitro, RCC, RCC4 - in-vitro, CRC, HCT116 - in-vitro, BC, MDA-MB-435 - in-vitro, Ovarian, SKOV3 - in-vitro, Colon, SW48 - in-vitro, GBM, U251
eff↑, Warburg↓, BioAv↑, ROS↑, DNAdam↑, ATP↓, eff↑, necrosis↑, PARP↑,

Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   Fenton↑, 1,   GSH↓, 1,   H2O2↑, 1,   lipid-P↑, 1,   ROS↑, 5,   ROS⇅, 2,   SOD1↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MEK↓, 1,   MMP↓, 4,   Raf↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,   NAD↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 1,   Bax:Bcl2↑, 2,   Bcl-2↓, 2,   Casp↑, 1,   Casp3↑, 1,   cl‑Casp3↑, 2,   Casp9↑, 1,   cl‑Casp9↑, 1,   necrosis↑, 1,   Telomerase↓, 2,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

LC3B-II↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 4,   MGMT↓, 1,   P53↑, 1,   PARP↑, 3,   cl‑PARP↑, 5,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   ERK↓, 1,   mTOR↓, 1,   PI3K↓, 1,   PTEN↑, 1,   RAS↓, 1,   STAT3↓, 1,   TumCG↓, 2,  

Migration ⓘ

Ca+2↑, 1,   MMP2↓, 1,   MMP9↓, 1,   TIMP2↑, 1,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,   p65↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   ChemoSen↑, 2,   eff↓, 4,   eff↑, 4,   RadioS↑, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,  
Total Targets: 68

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PARP, poly ADP-ribose polymerase (PARP) cleavage
2 temozolomide
2 Vitamin C (Ascorbic Acid)
1 Berberine
1 Bufalin/Huachansu
1 hydroxychloroquine
1 Quercetin
1 Shikonin
1 Thymoquinone
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:27  Cells:%  prod#:%  Target#:239  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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