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.
Colon, Colon Cancer: Click to Expand ⟱
Colon cancer can start anywhere in the colon, (5 feet long) and absorbs water from stool. Rectal cancer starts in the rectum, which is the last 12 centimeters.
Scientific Papers found: Click to Expand⟱
1548- Api,    A comprehensive view on the apigenin impact on colorectal cancer: Focusing on cellular and molecular mechanisms
- Review, Colon, NA
*BioAv↓, *Half-Life∅, selectivity↑, *toxicity↓, Wnt/(β-catenin)↓, P53↑, P21↑, PI3K↓, Akt↓, mTOR↓, TumCCA↑, TumCI↓, TumCMig↓, STAT3↓, PKM2↓, EMT↓, cl‑PARP↑, Casp3↑, Bax:Bcl2↑, VEGF↓, Hif1a↓, Dose∅, GLUT1↓, GlucoseCon↓,
173- Api,    Apigenin-induced apoptosis is enhanced by inhibition of autophagy formation in HCT116 human colon cancer cells
- in-vitro, Colon, HCT116
CycB/CCNB1↓, cDC2↓, CDC25↓, P53↑, P21↑, cl‑PARP↑, proCasp8↓, proCasp9↓, proCasp3↓,
2023- BBR,    Berberine Induces Caspase-Independent Cell Death in Colon Tumor Cells through Activation of Apoptosis-Inducing Factor
- in-vitro, Colon, NA - in-vitro, Nor, YAMC
TumCD↑, *toxicity↓, selectivity↑, ROS↑, *ROS∅, MMP↓, *MMP∅, PARP↑, BioAv↝,
5866- CA,    Carnosic acid inhibits STAT3 signaling and induces apoptosis through generation of ROS in human colon cancer HCT116 cells
- in-vitro, CRC, HCT116 - in-vitro, Colon, SW480 - in-vitro, Colon, HT29
tumCV↓, Apoptosis↑, P53↑, BAX↑, MDM2↓, Bcl-2↓, Bcl-xL↓, Casp9↑, Casp3↑, cl‑PARP↑, STAT3↓, survivin↓, cycD1/CCND1↓, CycD3↓, ROS↑, eff↓, eff↑,
2981- RES,    Resveratrol suppresses IGF-1 induced human colon cancer cell proliferation and elevates apoptosis via suppression of IGF-1R/Wnt and activation of p53 signaling pathways
- in-vitro, Colon, HT-29 - in-vitro, Colon, SW48
TumCCA↑, p27↑, cycD1/CCND1↓, TumCP↓, IGF-1R↓, Akt↓, Wnt↓, P53↑, Apoptosis↑, Sp1/3/4↓, cl‑PARP↑, β-catenin/ZEB1↓, MDM2↓,
104- RES,  QC,    Resveratrol and Quercetin in Combination Have Anticancer Activity in Colon Cancer Cells and Repress Oncogenic microRNA-27a
- in-vitro, Colon, HT-29
Casp3↑, PARP↑, survivin↓, miR-27a-3p↓, Sp1/3/4↓, ZBTB10↑, ROS⇅, TAC↑, tumCV↓,
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 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 3,   ROS⇅, 1,   TAC↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   CDC25↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

GlucoseCon↓, 1,   PKM2↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 2,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp3↑, 3,   proCasp3↓, 1,   proCasp8↓, 1,   Casp9↑, 1,   proCasp9↓, 1,   MDM2↓, 2,   necrosis↑, 1,   p27↑, 1,   survivin↓, 2,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 2,  

Transcription & Epigenetics ⓘ

miR-27a-3p↓, 1,   tumCV↓, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 4,   PARP↑, 3,   cl‑PARP↑, 4,  

Cell Cycle & Senescence ⓘ

CycB/CCNB1↓, 1,   cycD1/CCND1↓, 2,   CycD3↓, 1,   P21↑, 2,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

cDC2↓, 1,   EMT↓, 1,   IGF-1R↓, 1,   mTOR↓, 1,   PI3K↓, 1,   STAT3↓, 2,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,   VEGF↓, 1,   ZBTB10↑, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 1,   Dose∅, 1,   eff↓, 1,   eff↑, 3,   selectivity↑, 2,  
Total Targets: 59

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS∅, 1,  

Mitochondria & Bioenergetics ⓘ

MMP∅, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   Half-Life∅, 1,  

Functional Outcomes ⓘ

toxicity↓, 2,  
Total Targets: 5

Scientific Paper Hit Count for: PARP, poly ADP-ribose polymerase (PARP) cleavage
2 Apigenin (mainly Parsley)
2 Resveratrol
1 Berberine
1 Carnosic acid
1 Quercetin
1 Vitamin C (Ascorbic Acid)
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:31  Cells:%  prod#:%  Target#:239  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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