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| Recombinant TRAIL - Recombinant Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Recommended Abbreviation: rTRAIL Alternative Names: Recombinant TRAIL, recombinant TNFSF10, Apo2L/TRAIL Type: Recombinant protein / biologic anticancer agent / death-receptor agonist Function: Recombinant TRAIL binds primarily to the death receptors DR4 (TNFRSF10A) and DR5 (TNFRSF10B), causing death-inducing signaling complex formation, caspase-8 activation, downstream caspase activation, and apoptosis. Many cancer cells are more sensitive to TRAIL-induced apoptosis than normal cells, although resistance is common. Cancer: ↑ TRAIL-induced death-receptor signaling is generally favorable because it promotes extrinsic apoptosis in susceptible cancer cells. Recombinant TRAIL and TRAIL-receptor agonists have shown substantial preclinical anticancer activity, although clinical efficacy has been limited by short circulating half-life, receptor biology, and intrinsic or acquired TRAIL resistance. |
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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. |
| 8152- | lamb, | TRAIL/rTRAIL, | Lambertianic Acid Sensitizes Non-Small Cell Lung Cancers to TRAIL-Induced Apoptosis via Inhibition of XIAP/NF-κB and Activation of Caspases and Death Receptor 4 |
| - | in-vitro, | NSCLC, | A549 | - | in-vitro, | Lung, | H1299 |
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