| Features: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Hydroxycinnamic acid compounds (p-coumaric, caffeic acid (CA), ferulic acid) occur most frequently as simple esters with hydroxy carboxylic acids or glucose, while the hydroxybenzoic acid compounds (p-hydroxybenzoic, gallic acid, ellagic acid) are present mainly in the form of glucosides. https://www.sciencedirect.com/topics/chemistry/hydroxycinnamic-acid Hydroxycinnamic acids (HCAs) are plant-derived phenolic acids (including caffeic, ferulic, p-coumaric, and sinapic acids) with documented antioxidant, anti-inflammatory (NF-κB↓), and context-dependent anticancer effects in cellular and preclinical models. Mechanistic themes include activation of the Nrf2/ARE antioxidant response, suppression of pro-inflammatory and survival pathways (such as NF-κB and PI3K/AKT), modulation of MAPK signaling, and downstream effects on cell-cycle, apoptosis, invasion, and angiogenesis. Oral exposure is influenced by rapid metabolism (phase II conjugates) and food matrix effects, which affects systemic bioavailability and translational relevance. Biological effects vary by specific hydroxycinnamic derivative and its conjugated/esterified form. (Caffeic acid ≠ ferulic acid ≠ sinapic acid) -Ferulic acid and p‐coumaric acid are naturally occurring hydroxycinnamic acids found in many plant-based foods (such as whole grains, fruits, and vegetables) CA showed pro-oxidant potential due to its ability to interact with metals like copper, inducing lipid peroxidation and causing DNA damage within tumor cells through either oxidation or covalent adduct formation. Summary: -HCAs are classically antioxidant -Such as caffeic acid, ferulic acid, and sinapic acid (SA) -May increase sensitivity to chemotherapy -Bioavailability is problem. Formulation strategies (e.g., liposomal or encapsulated forms) are investigated to improve systemic exposure. -Propolis has caffeic acid (Caffeic acid (0.639–4.172 mg/g propolis) -SA at higher concentrations may acts as a potent pro-oxidant agent -SA may act in collaboration with other chemotherapeutic agents to improve treatment sensitivity. -Co-administration of caffeic acid or CAPE with other anti-tumor compounds (e.g., gallic acid) has shown additive or synergistic effects in selected models -Combination of caffeic acid and endogenous copper ions can result in oxidative damage -Ferulic Acid (abundant in whole grains,popcorn): upregulate apoptotic protein and downregulate anti-apoptotic protein.upregulating (BAX), (p53), (CYCS) and downregulating (Bcl-2),
Time-Scale Flag (TSF): P / R / G
|
| Source: |
| Type: |
| 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. |
| 1641- | HCAs, | Lung cancer induced by Benzo(A)Pyrene: ChemoProtective effect of sinapic acid in swiss albino mice |
| - | in-vitro, | Lung, | A549 | - | in-vivo, | Lung, | NA |
| 1644- | HCAs, | PBG, | Artepillin C (3,5-diprenyl-4-hydroxycinnamic acid) sensitizes LNCaP prostate cancer cells to TRAIL-induced apoptosis |
| - | in-vitro, | Pca, | LNCaP |
| 1657- | HCAs, | Anticancer Activity of Sinapic Acid by Inducing Apoptosis in HT-29 Human Colon Cancer Cell Line 2023 |
| - | in-vitro, | CRC, | HT-29 |
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#:95 Target#:42 State#:% Dir#:%
wNotes=0 sortOrder:rid,rpid