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.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
4584- AgNPs,    Silver Nanoparticles Synthesized Using Carica papaya Leaf Extract (AgNPs-PLE) Causes Cell Cycle Arrest and Apoptosis in Human Prostate (DU145) Cancer Cells
- in-vitro, Pca, DU145
selectivity↑, ROS↑, BAX↑, cl‑Casp3↑, p‑PARP↑, TumCCA↑, cycD1/CCND1↓, p27↑, P21↑, AntiCan↑,
1563- Api,  MET,    Metformin-induced ROS upregulation as amplified by apigenin causes profound anticancer activity while sparing normal cells
- in-vitro, Nor, HDFa - in-vitro, PC, AsPC-1 - in-vitro, PC, MIA PaCa-2 - in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP - in-vivo, NA, NA
selectivity↑, selectivity↑, selectivity↓, ROS↑, eff↑, tumCV↓, MMP↓, Dose∅, eff↓, DNAdam↑, Apoptosis↑, TumAuto↑, Necroptosis↑, p‑P53↑, BIM↑, BAX↑, p‑PARP↑, Casp3↑, Casp8↑, Casp9↑, Cyt‑c↑, Bcl-2↓, AIF↑, p62↑, LC3B↑, MLKL↑, p‑MLKL↓, RIP3↑, p‑RIP3↑, TumCG↑, TumW↓,
2603- Ba,    Baicalein inhibits prostate cancer cell growth and metastasis via the caveolin-1/AKT/mTOR pathway
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
TumCG↓, Apoptosis↑, Cav1↓, p‑Akt↓, p‑mTOR↓, Bax:Bcl2↑, survivin↓, cl‑PARP↑, BioAv↓,
1404- BBR,    Berberine-induced apoptosis in human prostate cancer cells is initiated by reactive oxygen species generation
- in-vitro, Pca, PC3
Apoptosis↑, *Apoptosis∅, MMP↓, cl‑Casp3↑, cl‑Casp9↑, cl‑PARP↑, ROS↑, eff↓, Cyt‑c↑,
5178- BBR,    Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
TumCP↑, TumCCA↑, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, CDK6↓, P21↑, p27↑, Apoptosis↑, Bax:Bcl2↑, MMP↓, Casp9↑, Casp3↑, PARP↑, DNAdam↑, selectivity↑, Cyt‑c↑,
2754- BetA,    Betulinic acid inhibits prostate cancer growth through inhibition of specificity protein transcription factors
- in-vitro, Pca, LNCaP
VEGF↓, survivin↓, Sp1/3/4↓, Casp↑, PARP↑, survivin↓, angioG↓,
1580- Citrate,    Citrate activates autophagic death of prostate cancer cells via downregulation CaMKII/AKT/mTOR pathway
- in-vitro, Pca, PC3 - in-vivo, PC, NA - in-vitro, Pca, LNCaP - in-vitro, Pca, WPMY-1
Apoptosis↑, Ca+2↓, Akt↓, mTOR↓, selectivity↑, TumCP↓, cl‑Casp3↑, cl‑PARP↑, LC3‑Ⅱ/LC3‑Ⅰ↑, p62↓, ATG5↑, ATG7↑, Beclin-1↑, TumAuto↑, CaMKII ↓,
136- CUR,  docx,    Combinatorial effect of curcumin with docetaxel modulates apoptotic and cell survival molecules in prostate cancer
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
Bcl-2↓, Bcl-xL↓, Mcl-1↓, BAX↑, BID↑, PARP↑, NF-kB↓, CDK1↓, COX2↓, RTK-RAS↓, PI3K/Akt↓, EGFR↓, HER2/EBBR2↓, P53↑, ChemoSen↑,
152- CUR,    Anti-cancer activity of curcumin loaded nanoparticles in prostate cancer
- in-vivo, Pca, NA
β-catenin/ZEB1↓, AR↓, STAT3↓, p‑Akt↓, Mcl-1↓, Bcl-xL↓, cl‑PARP↑, miR-21↓, miR-205↑, TumCG↓, TumCP↓, TumCI↓, angioG↓, TumMeta↓,
118- CUR,    Curcumin analog WZ35 induced cell death via ROS-dependent ER stress and G2/M cell cycle arrest in human prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145
ROS↑, Bcl-2↓, PARP↑, cDC2↓, CycB/CCNB1↓, MDM2↓, eff↓, eIF2α↑, ATF4↑, CHOP↑, ER Stress↑, TumCCA↑,
132- CUR,    Targeting multiple pro-apoptotic signaling pathways with curcumin in prostate cancer cells
- in-vitro, Pca, PC3
TumCCA↑, ROS↑, TumAuto↑, UPR↑, ER Stress↑, Casp3↑, Casp9↑, Casp12↑, PARP↑, other↝, GRP78/BiP↑, PDI↑, eIF2α↑, other↝,
462- CUR,    Curcumin promotes cancer-associated fibroblasts apoptosis via ROS-mediated endoplasmic reticulum stress
- in-vitro, Pca, PC3
Bcl-2↓, MMP↓, cl‑Casp3↑, BAX↑, BIM↑, p‑PARP↑, PUMA↑, p‑P53↑, ROS↑, p‑ERK↑, p‑eIF2α↑, CHOP↑, ATF4↑,
26- EGCG,  QC,  docx,    Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapy
- vitro+vivo, Pca, PC3
BAD↓, cl‑PARP↑, Casp7↑, IκB↓, Ki-67↓, VEGF↓, EGFR↓, FGF↓, TGF-β↓, TNF-α↓, SCF↓, Bax:Bcl2↑, NF-kB↓, chemoP↑, ChemoSen↑, TumVol↓,
4639- HT,    Hydroxytyrosol Induces Apoptosis, Cell Cycle Arrest and Suppresses Multiple Oncogenic Signaling Pathways in Prostate Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, C4-2B
TumCP↓, selectivity↑, TumCCA↑, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, P21↑, p27↑, Apoptosis↑, Casp↑, cl‑PARP↑, Bax:Bcl2↑, p‑Akt↓, p‑STAT3↓, NF-kB↓, AR↓, ROS↑, *BioAv↓, *toxicity∅,
150- NRF,  CUR,  docx,    Subverting ER-Stress towards Apoptosis by Nelfinavir and Curcumin Coexposure Augments Docetaxel Efficacy in Castration Resistant Prostate Cancer Cells
- in-vitro, Pca, C4-2B
p‑Akt↓, p‑eIF2α↑, ER Stress↑, ATF4↑, CHOP↑, TRIB3↑, ChemoSen↑, Casp3↑, cl‑PARP↑, BID↑, XBP-1↑,
66- QC,    Emerging impact of quercetin in the treatment of prostate cancer
- Review, Pca, NA
CycB/CCNB1↓, CDK1↓, EMT↓, PI3K↓, MAPK↓, Wnt/(β-catenin)↓, PSA↓, VEGF↓, PARP↑, Casp3↑, Casp9↑, DR5↑, ROS⇅, Shh↓, P53↑, P21↑, EGFR↓, TumCCA↑, ROS↑, miR-21↓, TumCP↓, selectivity↑, PDGF↓, EGF↓, TNF-α↓, VEGFR2↓, mTOR↓, cMyc↓, MMPs↓, GRP78/BiP↑, CHOP↑,
71- QC,    Role of Bax in quercetin-induced apoptosis in human prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PrEC - in-vitro, Pca, YPEN-1 - in-vitro, Pca, HCT116
Casp8↑, Casp9↑, PARP↑, BAD↓, BAX↑, PI3K/Akt↓, Cyt‑c↑, selectivity↑,
90- QC,  HP,    Combination of quercetin and hyperoside inhibits prostate cancer cell growth and metastasis via regulation of microRNA‑21
- in-vitro, Pca, PC3
ROS↑, cl‑Casp3↑, cl‑PARP↑, miR-21↓, PDCD4↑, TAC↑, tumCV↓, TumCI↓,
86- QC,  PacT,    Quercetin regulates insulin like growth factor signaling and induces intrinsic and extrinsic pathway mediated apoptosis in androgen independent prostate cancer cells (PC-3)
- vitro+vivo, Pca, PC3
BAD↑, IGFBP3↑, Cyt‑c↑, cl‑Casp9↑, Casp10↑, cl‑PARP↑, Casp3↑, IGF-1R↓, PI3K↓, p‑Akt↓, cycD1/CCND1↓, IGF-1↓, IGF-2↓, IGF-1R↓, MMP↓, Apoptosis↑, NA?,

Showing Research Papers: 1 to 19 of 19

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 19

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned ⓘ

NA?, 1,  

Redox & Oxidative Stress ⓘ

ROS↑, 9,   ROS⇅, 1,   TAC↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   EGF↓, 1,   MMP↓, 5,  

Core Metabolism/Glycolysis ⓘ

ATG7↑, 1,   Cav1↓, 1,   cMyc↓, 1,   PI3K/Akt↓, 2,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 5,   Apoptosis↑, 7,   BAD↓, 2,   BAD↑, 1,   BAX↑, 5,   Bax:Bcl2↑, 4,   Bcl-2↓, 4,   Bcl-xL↓, 2,   BID↑, 2,   BIM↑, 2,   Casp↑, 2,   Casp10↑, 1,   Casp12↑, 1,   Casp3↑, 6,   cl‑Casp3↑, 5,   Casp7↑, 1,   Casp8↑, 2,   Casp9↑, 5,   cl‑Casp9↑, 2,   Cyt‑c↑, 5,   DR5↑, 1,   MAPK↓, 1,   Mcl-1↓, 2,   MDM2↓, 1,   MLKL↑, 1,   p‑MLKL↓, 1,   Necroptosis↑, 1,   p27↑, 3,   PDCD4↑, 1,   PUMA↑, 1,   survivin↓, 3,  

Kinase & Signal Transduction ⓘ

CaMKII ↓, 1,   HER2/EBBR2↓, 1,   RTK-RAS↓, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

miR-205↑, 1,   miR-21↓, 3,   other↝, 2,   tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

CHOP↑, 4,   eIF2α↑, 2,   p‑eIF2α↑, 2,   ER Stress↑, 3,   GRP78/BiP↑, 2,   UPR↑, 1,   XBP-1↑, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   LC3B↑, 1,   p62↓, 1,   p62↑, 1,   TumAuto↑, 3,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 2,   p‑P53↑, 2,   PARP↑, 7,   p‑PARP↑, 3,   cl‑PARP↑, 9,  

Cell Cycle & Senescence ⓘ

CDK1↓, 2,   CDK2↓, 2,   CDK4↓, 2,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 4,   cycE/CCNE↓, 2,   P21↑, 4,   TumCCA↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

cDC2↓, 1,   EMT↓, 1,   p‑ERK↑, 1,   FGF↓, 1,   IGF-1↓, 1,   IGF-1R↓, 2,   IGF-2↓, 1,   IGFBP3↑, 1,   mTOR↓, 2,   p‑mTOR↓, 1,   PI3K↓, 2,   SCF↓, 1,   Shh↓, 1,   STAT3↓, 1,   p‑STAT3↓, 1,   TumCG↓, 2,   TumCG↑, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

Ca+2↓, 1,   Ki-67↓, 1,   MMPs↓, 1,   PDGF↓, 1,   RIP3↑, 1,   p‑RIP3↑, 1,   TGF-β↓, 1,   TRIB3↑, 1,   TumCI↓, 2,   TumCP↓, 4,   TumCP↑, 1,   TumMeta↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   ATF4↑, 3,   EGFR↓, 3,   PDI↑, 1,   VEGF↓, 3,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IκB↓, 1,   NF-kB↓, 3,   PSA↓, 1,   TNF-α↓, 2,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 2,   CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 3,   Dose∅, 1,   eff↓, 3,   eff↑, 1,   selectivity↓, 1,   selectivity↑, 8,  

Clinical Biomarkers ⓘ

AR↓, 2,   EGFR↓, 3,   HER2/EBBR2↓, 1,   Ki-67↓, 1,   PSA↓, 1,   TRIB3↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoP↑, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 140

Pathway results for Effect on Normal Cells:


Cell Death ⓘ

Apoptosis∅, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  

Functional Outcomes ⓘ

toxicity∅, 1,  
Total Targets: 3

Scientific Paper Hit Count for: PARP, poly ADP-ribose polymerase (PARP) cleavage
6 Curcumin
5 Quercetin
3 Docetaxel
2 Berberine
1 Silver-NanoParticles
1 Apigenin (mainly Parsley)
1 Metformin
1 Baicalein
1 Betulinic acid
1 Citric Acid
1 EGCG (Epigallocatechin Gallate)
1 HydroxyTyrosol
1 nelfinavir/Viracept
1 Hyperoside
1 Paclitaxel
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:22  Cells:%  prod#:%  Target#:239  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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