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| 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. |
| Bladder Cancer |
| 1364- | Ash, | Withaferin a Triggers Apoptosis and DNA Damage in Bladder Cancer J82 Cells through Oxidative Stress |
| - | in-vitro, | Bladder, | J82 |
| 2719- | BetA, | Betulinic Acid Restricts Human Bladder Cancer Cell Proliferation In Vitro by Inducing Caspase-Dependent Cell Death and Cell Cycle Arrest, and Decreasing Metastatic Potential |
| - | in-vitro, | CRC, | T24/HTB-9 | - | in-vitro, | Bladder, | UMUC3 | - | in-vitro, | Bladder, | 5637 |
| 2047- | Buty, | Sodium butyrate inhibits migration and induces AMPK-mTOR pathway-dependent autophagy and ROS-mediated apoptosis via the miR-139-5p/Bmi-1 axis in human bladder cancer cells |
| - | in-vitro, | CRC, | T24/HTB-9 | - | in-vitro, | Nor, | SV-HUC-1 | - | in-vitro, | Bladder, | 5637 | - | in-vivo, | NA, | NA |
| 1517- | CAP, | Capsaicin Inhibits Multiple Bladder Cancer Cell Phenotypes by Inhibiting Tumor-Associated NADH Oxidase (tNOX) and Sirtuin1 (SIRT1) |
| - | in-vitro, | Bladder, | TSGH8301 | - | in-vitro, | CRC, | T24/HTB-9 |
| 689- | EGCG, | EGCG inhibited bladder cancer SW780 cell proliferation and migration both in vitro and in vivo via down regulation of NF-κB and MMP-9 |
| - | vitro+vivo, | Bladder, | SW780 |
| 2448- | SFN, | Sulforaphane and bladder cancer: a potential novel antitumor compound |
| - | Review, | Bladder, | NA |
| 1463- | SFN, | Sulforaphane induces reactive oxygen species-mediated mitotic arrest and subsequent apoptosis in human bladder cancer 5637 cells |
| - | in-vitro, | Bladder, | 5637 |
| 1458- | SFN, | Sulforaphane Impact on Reactive Oxygen Species (ROS) in Bladder Carcinoma |
| - | Review, | Bladder, | NA |
| - | in-vitro, | Bladder, | T24/HTB-9 |
| 3416- | TQ, | Thymoquinone induces apoptosis in bladder cancer cell via endoplasmic reticulum stress-dependent mitochondrial pathway |
| - | in-vitro, | Bladder, | T24/HTB-9 | - | in-vitro, | Bladder, | 253J | - | in-vitro, | Nor, | SV-HUC-1 |
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:32 Cells:% prod#:% Target#:239 State#:% Dir#:2
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