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| Ginkgolic acids (GAs) are a group of naturally occurring 2-hydroxy-6-alkylsalicylic acids found in Ginkgo biloba leaves, seeds and especially the seed coat. Major congeners include ginkgolic acid C13:0, C15:1 and C17:1. Ginkgolic acids have demonstrated antimicrobial, antiviral, autophagy-modulating and anticancer activities in preclinical studies. In cancer models, GAs can suppress proliferation, migration and invasion and promote apoptosis through mechanisms including inhibition of SUMOylation, STAT3 signalling, Hsp90 activity and other oncogenic pathways. Individual congeners can differ substantially in potency and biological activity, so specific forms such as C15:1 or C17:1 should be recorded separately when identified. Ginkgolic acids are kept separate from standardized Ginkgo biloba extracts because they are considered potentially toxic constituents and are deliberately reduced to very low concentrations in purified medicinal ginkgo preparations. Current anticancer evidence is predominantly preclinical. |
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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. |
| 7214- | GAs, | Ginkgolic Acid Suppresses Nasopharyngeal Carcinoma Growth by Inducing Apoptosis and Inhibiting AKT/NF-κB Signaling |
| - | vitro+vivo, | NPC, | CNE2 |
| 7233- | GAs, | Antitumor effects of ginkgolic acid in human cancer cell occur via cell cycle arrest and decrease the Bcl-2/Bax ratio to induce apoptosis |
| - | in-vitro, | Laryn, | HEp2 |
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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