| 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. |
| Liver Cancer |
| 233- | AL, | 5-FU, | Allicin sensitizes hepatocellular cancer cells to anti-tumor activity of 5-fluorouracil through ROS-mediated mitochondrial pathway |
| - | in-vivo, | Liver, | NA |
| 5592- | BetA, | Betulin induces mitochondrial cytochrome c release associated apoptosis in human cancer cells |
| - | in-vitro, | Liver, | HepG2 | - | in-vitro, | Cerv, | HeLa |
| 5907- | CAR, | Anti-proliferative and pro-apoptotic effect of carvacrol on human hepatocellular carcinoma cell line HepG-2 |
| - | in-vitro, | Liver, | HepG2 |
| 7168- | CHA, | The anticancer effect of chaetocin is enhanced by inhibition of autophagy |
| - | vitro+vivo, | Liver, | HepG2 | - | in-vitro, | Liver, | HepG3 | - | in-vitro, | Liver, | HUH7 |
| 821- | GAR, | Garcinol inhibits cell growth in hepatocellular carcinoma Hep3B cells through induction of ROS-dependent apoptosis |
| - | in-vitro, | Liver, | Hep3B |
| 7138- | GI, | 6-Shogaol exerts anti-proliferative and pro-apoptotic effects through the modulation of STAT3 and MAPKs signaling pathways |
| - | vitro+vivo, | BC, | MDA-MB-231 | - | in-vitro, | Pca, | DU145 | - | in-vitro, | Liver, | HepG2 | - | in-vitro, | Lung, | A549 |
| 1918- | JG, | ROS -mediated p53 activation by juglone enhances apoptosis and autophagy in vivo and in vitro |
| - | in-vitro, | Liver, | HepG2 | - | in-vivo, | NA, | NA |
| 1459- | SFN, | AF, | Auranofin Enhances Sulforaphane-Mediated Apoptosis in Hepatocellular Carcinoma Hep3B Cells through Inactivation of the PI3K/Akt Signaling Pathway |
| - | in-vitro, | Liver, | Hep3B | - | in-vitro, | Liver, | HepG2 |
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:14 Cells:% prod#:% Target#:239 State#:% Dir#:2
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