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| An ester formed by the condensation of gallic acid and propanol. Propyl gallate (PG), chemically known as propyl-3,4,5-trihydroxybenzoate, is widely present in processed food and cosmetics, hair products, and lubricants. PG alone demonstrated antioxidative and cytoprotective properties against cellular damage and gained a pro-oxidative property in combination with copper (II). It was reported that PG was one of the most active compounds capable of generating H2O2 in DMEM media Main cancer-relevant pathways modulated by propyl gallate A. Redox imbalance & oxidative stress (dominant) -↑ Intracellular ROS (context- and dose-dependent) -Pro-oxidant in cancer cells with high basal ROS -Mitochondrial superoxide accumulation -Thiol depletion (↓ GSH, ↓ Trx buffering capacity) Importance: ★★★★★ (Primary mechanism) B. Mitochondrial dysfunction & intrinsic apoptosis -↑ MOMP → caspase cascade -Loss of mitochondrial membrane potential (ΔΨm) -Cytochrome-c release -Caspase-9 → caspase-3 activation -↑ Bax / ↓ Bcl-2 ratio Importance: ★★★★☆ C. ER stress & unfolded protein response (UPR) -↑ PERK–eIF2α–ATF4–CHOP -ROS-linked protein misfolding -Pro-apoptotic UPR signaling dominates over adaptive UPR Importance: ★★★☆☆ D. Cell cycle disruption -G1 or G2/M arrest (cell-type dependent) -↓ Cyclin D1, Cyclin B1 -↑ p21, p27 Importance: ★★☆☆☆ E. MAPK stress signaling -↑ JNK / p38 -Stress-activated apoptosis signaling -Often precedes mitochondrial failure Importance: ★★☆☆☆ F. Inflammation & survival pathways (secondary) -↓ NF-κB, ↓ STAT3 (indirect) -Suppression is largely ROS-mediated, not direct inhibition -Reduced anti-apoptotic gene transcription Importance: ★★☆☆☆ G. NRF2–ARE signaling (dual role) -Low dose: NRF2 activation → cytoprotection -High dose / cancer cells: NRF2 overwhelmed → apoptosis Importance: ★★☆☆☆ (Highly context dependent; double-edged)
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| Also known as CP32. Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death. As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression. Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy. Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent. On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer. Procaspase-3 is a apoptotic marker protein. Prognostic significance: • High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers. • Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers. |
| 1768- | PG, | Propyl gallate reduces the growth of lung cancer cells through caspase‑dependent apoptosis and G1 phase arrest of the cell cycle |
| - | in-vitro, | Lung, | Calu-6 | - | in-vitro, | Lung, | A549 |
| 5217- | PG, | Role of redox signaling regulation in propyl gallate-induced apoptosis of human leukemia cells |
| - | in-vitro, | AML, | THP1 | - | in-vitro, | AML, | Jurkat | - | in-vitro, | AML, | HL-60 |
| 5218- | PG, | Propyl gallate inhibits hepatocellular carcinoma cell growth through the induction of ROS and the activation of autophagy |
| - | in-vitro, | HCC, | Hep3B |
| 5219- | PG, | Propyl gallate inhibits the growth of HeLa cells via caspase-dependent apoptosis as well as a G1 phase arrest of the cell cycle |
| - | in-vitro, | Cerv, | HeLa |
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:% Cells:% prod#:138 Target#:42 State#:% Dir#:2
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