| Features: | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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)
|
| Source: |
| Type: |
| Caspases are a cysteine protease that speed up a chemical reaction via pointing their target substrates following an aspartic acid residue.1 They are grouped into apoptotic (caspase-2, 3, 6, 7, 8, 9 and 10) and inflammatory (caspase-1, 4, 5, 11 and 12) mediated caspases. Caspase-1 may have both tumorigenic or antitumorigenic effects on cancer development and progression, but it depends on the type of inflammasome, methodology, and cancer. Catalase is an enzyme found in nearly all living cells exposed to oxygen. Its primary role is to protect cells from oxidative damage by catalyzing the conversion of hydrogen peroxide (H₂O₂), a potentially damaging byproduct of metabolism, into water (H₂O) and oxygen (O₂). This detoxification process is crucial because excess H₂O₂ can lead to the formation of reactive oxygen species (ROS) that damage proteins, lipids, and DNA. Catalase and Cancer Oxidative Stress and Cancer: Cancer cells often experience increased levels of oxidative stress due to rapid proliferation and metabolic changes. This stress can lead to DNA damage, promoting tumorigenesis. Catalase helps mitigate oxidative stress, and its expression can influence the survival and proliferation of cancer cells. Expression Levels in Different Cancers: Overexpression: In some cancers, such as breast cancer and certain types of leukemia, catalase may be overexpressed. This overexpression can help cancer cells survive in oxidative environments, potentially leading to more aggressive tumor behavior. Downregulation: Conversely, in other cancers, such as colorectal cancer, reduced catalase expression has been observed. This downregulation can lead to increased oxidative stress, contributing to tumor progression and metastasis. Prognostic Implications: Survival Rates: Studies have shown that high levels of catalase expression can be associated with poor prognosis in certain cancers, as it may enable cancer cells to resist apoptosis (programmed cell death) induced by oxidative stress. Some types of cancer cells have been reported to exhibit lower catalase activity, possibly increasing their vulnerability to oxidative damage under certain conditions. This vulnerability has even been exploited in some therapeutic strategies (for example, approaches that generate excess H₂O₂ or other ROS specifically targeting cancer cells have been researched). |
| 1767- | PG, | Propyl gallate induces cell death in human pulmonary fibroblast through increasing reactive oxygen species levels and depleting glutathione |
| - | in-vitro, | Nor, | NA |
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#:46 State#:% Dir#:%
wNotes=0 sortOrder:rid,rpid