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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. |
| Glioblastoma is a fast-growing and aggressive brain tumor. |
| 569- | ART/DHA, | Dihydroartemisinin exhibits anti-glioma stem cell activity through inhibiting p-AKT and activating caspase-3 |
| - | in-vitro, | GBM, | NA |
| 1402- | BBR, | Berberine-induced apoptosis in human glioblastoma T98G cells is mediated by endoplasmic reticulum stress accompanying reactive oxygen species and mitochondrial dysfunction |
| - | in-vitro, | GBM, | T98G |
| 2700- | BBR, | Cell-specific pattern of berberine pleiotropic effects on different human cell lines |
| - | in-vitro, | GBM, | U343 | - | in-vitro, | GBM, | MIA PaCa-2 | - | in-vitro, | Nor, | HDFa |
| 5725- | BF, | TMZ, | Bufalin Induces Apoptosis and Improves the Sensitivity of Human Glioma Stem-Like Cells to Temozolamide |
| - | in-vitro, | GBM, | NA |
| 5651- | BNL, | Cisplatin, | Natural borneol sensitizes human glioma cells to cisplatin-induced apoptosis by triggering ROS-mediated oxidative damage and regulation of MAPKs and PI3K/AKT pathway |
| - | in-vitro, | GBM, | U251 | - | in-vitro, | GBM, | U87MG |
| 5652- | BNL, | Borneol promotes apoptosis of Human Glioma Cells through regulating HIF-1a expression via mTORC1/eIF4E pathway |
| - | vitro+vivo, | GBM, | NA |
| 739- | Bor, | Borax regulates iron chaperone- and autophagy-mediated ferroptosis pathway in glioblastoma cells |
| - | in-vitro, | GBM, | U87MG | - | in-vitro, | Nor, | HMC3 |
| 738- | Bor, | Borax induces ferroptosis of glioblastoma by targeting HSPA5/NRF2/GPx4/GSH pathways |
| - | in-vitro, | GBM, | U251 | - | in-vitro, | GBM, | A172 | - | in-vitro, | Nor, | SVGp12 |
| 6544- | BSB, | Involvement of mitochondrial permeability transition pore opening in alpha-bisabolol induced apoptosis |
| - | in-vitro, | GBM, | NA |
| 5835- | CAP, | Capsaicin and dihydrocapsaicin induce apoptosis in human glioma cells via ROS and Ca2+-mediated mitochondrial pathway |
| - | in-vitro, | GBM, | U251 |
| 7185- | CHA, | Chaetocin-induced ROS-mediated apoptosis involves ATM–YAP1 axis and JNK-dependent inhibition of glucose metabolism |
| - | vitro+vivo, | GBM, | A172 | - | in-vitro, | GBM, | T98G | - | in-vitro, | GBM, | U87MG |
| 6234- | CUSP9, | In Vitro and Clinical Compassionate Use Experiences with the Drug-Repurposing Approach CUSP9v3 in Glioblastoma |
| - | Human, | GBM, | NA |
| - | in-vitro, | GBM, | U87MG |
| 6842- | EVO, | Evodiamine activates cellular apoptosis through suppressing PI3K/AKT and activating MAPK in glioma |
| - | in-vitro, | GBM, | U251 | - | in-vitro, | GBM, | LN229 |
| 1967- | GamB, | Gambogic acid induces apoptotic cell death in T98G glioma cells |
| - | in-vitro, | GBM, | T98G |
| 1153- | HNK, | Honokiol Eliminates Glioma/Glioblastoma Stem Cell-Like Cells via JAK-STAT3 Signaling and Inhibits Tumor Progression by Targeting Epidermal Growth Factor Receptor |
| - | in-vitro, | GBM, | U251 | - | in-vitro, | GBM, | U87MG | - | in-vivo, | NA, | NA |
| 2259- | MFrot, | MF, | Method and apparatus for oncomagnetic treatment |
| - | in-vitro, | GBM, | NA |
| 186- | MFrot, | MF, | Selective induction of rapid cytotoxic effect in glioblastoma cells by oscillating magnetic fields |
| - | in-vitro, | GBM, | GBM | - | in-vitro, | Lung, | NA |
| 188- | MFrot, | MF, | Spinning magnetic field patterns that cause oncolysis by oxidative stress in glioma cells |
| - | in-vitro, | GBM, | GBM115 | - | in-vitro, | GBM, | DIPG |
| 184- | MFrot, | MF, | Rotating Magnetic Fields Inhibit Mitochondrial Respiration, Promote Oxidative Stress and Produce Loss of Mitochondrial Integrity in Cancer Cells |
| - | in-vitro, | GBM, | GBM |
| 3371- | QC, | Quercetin induces MGMT+ glioblastoma cells apoptosis via dual inhibition of Wnt3a/β-Catenin and Akt/NF-κB signaling pathways |
| - | in-vitro, | GBM, | T98G |
| 1464- | SFN, | d,l-Sulforaphane Induces ROS-Dependent Apoptosis in Human Gliomablastoma Cells by Inactivating STAT3 Signaling Pathway |
| - | in-vitro, | GBM, | NA |
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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