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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. |
| Bladder Cancer |
| 381- | AgNPs, | Silver Nanoparticles Exert Apoptotic Activity in Bladder Cancer 5637 Cells Through Alteration of Bax/Bcl-2 Genes Expression |
| - | in-vitro, | Bladder, | 5637 |
| 5130- | ART/DHA, | Dihydroartemisinin Induces Apoptosis in Human Bladder Cancer Cell Lines Through Reactive Oxygen Species, Mitochondrial Membrane Potential, and Cytochrome C Pathway |
| - | in-vitro, | Bladder, | T24/HTB-9 |
| 1364- | Ash, | Withaferin a Triggers Apoptosis and DNA Damage in Bladder Cancer J82 Cells through Oxidative Stress |
| - | in-vitro, | Bladder, | J82 |
| 1521- | Ba, | Baicalein induces apoptosis via ROS-dependent activation of caspases in human bladder cancer 5637 cells |
| - | in-vitro, | Bladder, | 5637 |
| 1393- | BBR, | EPI, | Berberine promotes antiproliferative effects of epirubicin in T24 bladder cancer cells by enhancing apoptosis and cell cycle arrest |
| - | in-vitro, | Bladder, | T24/HTB-9 |
| 2719- | BetA, | Betulinic Acid Restricts Human Bladder Cancer Cell Proliferation In Vitro by Inducing Caspase-Dependent Cell Death and Cell Cycle Arrest, and Decreasing Metastatic Potential |
| - | in-vitro, | CRC, | T24/HTB-9 | - | in-vitro, | Bladder, | UMUC3 | - | in-vitro, | Bladder, | 5637 |
| 2047- | Buty, | Sodium butyrate inhibits migration and induces AMPK-mTOR pathway-dependent autophagy and ROS-mediated apoptosis via the miR-139-5p/Bmi-1 axis in human bladder cancer cells |
| - | in-vitro, | CRC, | T24/HTB-9 | - | in-vitro, | Nor, | SV-HUC-1 | - | in-vitro, | Bladder, | 5637 | - | in-vivo, | NA, | NA |
| 1517- | CAP, | Capsaicin Inhibits Multiple Bladder Cancer Cell Phenotypes by Inhibiting Tumor-Associated NADH Oxidase (tNOX) and Sirtuin1 (SIRT1) |
| - | in-vitro, | Bladder, | TSGH8301 | - | in-vitro, | CRC, | T24/HTB-9 |
| 689- | EGCG, | EGCG inhibited bladder cancer SW780 cell proliferation and migration both in vitro and in vivo via down regulation of NF-κB and MMP-9 |
| - | vitro+vivo, | Bladder, | SW780 |
| 2448- | SFN, | Sulforaphane and bladder cancer: a potential novel antitumor compound |
| - | Review, | Bladder, | NA |
| 1463- | SFN, | Sulforaphane induces reactive oxygen species-mediated mitotic arrest and subsequent apoptosis in human bladder cancer 5637 cells |
| - | in-vitro, | Bladder, | 5637 |
| 1458- | SFN, | Sulforaphane Impact on Reactive Oxygen Species (ROS) in Bladder Carcinoma |
| - | Review, | Bladder, | NA |
| - | in-vitro, | Bladder, | T24/HTB-9 |
| 3416- | TQ, | Thymoquinone induces apoptosis in bladder cancer cell via endoplasmic reticulum stress-dependent mitochondrial pathway |
| - | in-vitro, | Bladder, | T24/HTB-9 | - | in-vitro, | Bladder, | 253J | - | in-vitro, | Nor, | SV-HUC-1 |
| 2279- | VitK2, | Vitamin K2 Induces Mitochondria-Related Apoptosis in Human Bladder Cancer Cells via ROS and JNK/p38 MAPK Signal Pathways |
| - | in-vitro, | Bladder, | T24/HTB-9 | - | in-vitro, | Bladder, | J82 | - | in-vitro, | Nor, | HEK293 | - | in-vitro, | Nor, | L02 | - | in-vivo, | NA, | 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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