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| Vitexin - Apigenin-8-C-Glucoside Alternative Names: Apigenin-8-C-glucoside, apigenin-8-C-β-D-glucopyranoside Type: Flavone C-glycoside / apigenin derivative Function: Vitexin is a naturally occurring C-glycosylated flavone in which glucose is attached to apigenin at the C-8 position. It exhibits antioxidant, anti-inflammatory, metabolic, cardiovascular, neuroprotective, and antiproliferative activities and can modulate pathways involving NF-κB, Nrf2/HO-1, MAPK, PI3K/AKT, AMPK, HIF-1α, apoptosis, and oxidative stress. -see also IsoVitexinCancer: Preclinical studies indicate antiproliferative, pro-apoptotic, anti-migratory, anti-invasive, and anti-inflammatory effects across multiple cancer models. Reported mechanisms include modulation of PI3K/AKT, MAPK, NF-κB, HIF-1α, ROS, apoptosis, and cell-cycle signaling. Clinical anticancer efficacy has not been established. Alzheimer's Disease: Preclinical evidence suggests neuroprotective activity through antioxidant and anti-inflammatory effects, reduction of neuronal injury, regulation of oxidative stress and mitochondrial function, and modulation of signaling pathways relevant to cognitive impairment and amyloid-associated neurotoxicity. Clinical efficacy for Alzheimer's disease has not been established. |
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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. |
| 7896- | IVT, | VT, | Molecular targets of vitexin and isovitexin in cancer therapy: a critical review |
| - | Review, | Var, | NA |
| 7920- | VT, | Vitexin Induces Apoptosis in MCF-7 Breast Cancer Cells through the Regulation of Specific miRNAs Expression |
| - | in-vitro, | BC, | MCF7 |
| 7919- | VT, | Apoptosis triggered by vitexin in U937 human leukemia cells via a mitochondrial signaling pathway |
| - | in-vitro, | AML, | U937 |
| 7916- | VT, | Vitexin suppresses autophagy to induce apoptosis in hepatocellular carcinoma via activation of the JNK signaling pathway |
| - | in-vitro, | HCC, | NA |
| 7914- | VT, | Vitexin induces apoptosis through mitochondrial pathway and PI3K/Akt/mTOR signaling in human non-small cell lung cancer A549 cells |
| - | vitro+vivo, | Lung, | A549 |
| 7905- | VT, | Vitexin induces apoptosis and enhances daunorubicin efficacy in acute leukemia via modulation of the HIF-1α/Bcl-2/caspase-3 pathway |
| - | in-vitro, | AML, | APL NB4 |
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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