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| Polyphenols are a large and structurally diverse family of plant-derived phenolic compounds characterized by multiple phenolic hydroxyl groups and encompassing major subclasses including flavonoids, phenolic acids, stilbenes, lignans, and tannins. They occur widely in fruits, vegetables, herbs, tea, coffee, cocoa, and medicinal plant extracts. Polyphenols exhibit broad biological activity involving redox regulation, inflammatory signaling, kinase pathways, apoptosis, cell-cycle control, angiogenesis, metabolism, and epigenetic regulation. In cancer models, many polyphenols inhibit proliferation, promote apoptosis or senescence, suppress invasion and angiogenesis, and can alter sensitivity to chemotherapy or radiotherapy. Effects are highly compound-, dose-, and context-dependent; antioxidant activity in normal tissues may coexist with pro-oxidant ROS induction in cancer cells. Oral bioavailability is frequently limited by poor absorption and extensive intestinal, hepatic, and microbial metabolism, making high-concentration in-vitro findings difficult to extrapolate directly to human systemic exposure. Polyphenols — broad umbrella class of plant-derived phenolic compounds.
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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. |
| 7416- | CS, | Poly, | Phenolic-Rich Extracts from Artichoke By-Products Promote Apoptosis in Human Colorectal Cancer Cell Lines |
| - | in-vitro, | Colon, | Caco-2 | - | in-vitro, | Colon, | HT29 |
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
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