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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. |
| Hepatocellular Carcinoma |
| 5238- | AgNPs, | β-Sitosterol-assisted silver nanoparticles activates Nrf2 and triggers mitochondrial apoptosis via oxidative stress in human hepatocellular cancer cell line |
| - | in-vitro, | HCC, | HepG2 |
| 234- | AL, | Allicin Induces Anti-human Liver Cancer Cells through the p53 Gene Modulating Apoptosis and Autophagy |
| - | in-vitro, | HCC, | Hep3B |
| 586- | Api, | 5-FU, | 5-Fluorouracil combined with apigenin enhances anticancer activity through mitochondrial membrane potential (ΔΨm)-mediated apoptosis in hepatocellular carcinoma |
| - | in-vivo, | HCC, | NA |
| 2606- | Ba, | Baicalein: A review of its anti-cancer effects and mechanisms in Hepatocellular Carcinoma |
| - | Review, | HCC, | NA |
| 2600- | Ba, | Baicalein Induces Apoptosis and Autophagy via Endoplasmic Reticulum Stress in Hepatocellular Carcinoma Cells |
| - | in-vitro, | HCC, | SMMC-7721 cell | - | in-vitro, | HCC, | Bel-7402 |
| 744- | Bor, | Borax affects cellular viability by inducing ER stress in hepatocellular carcinoma cells by targeting SLC12A5 |
| - | in-vitro, | HCC, | HepG2 | - | in-vitro, | Nor, | HL7702 |
| 5846- | CAP, | Capsaicin Alters the Expression of Genetic and Epigenetic Molecules In Hepatocellular Carcinoma Cell |
| - | in-vitro, | HCC, | HepG2 |
| 5891- | CAR, | SRF, | Carvacrol enhances anti-tumor activity and mitigates cardiotoxicity of sorafenib in thioacetamide-induced hepatocellular carcinoma model through inhibiting TRPM7 |
| - | in-vivo, | HCC, | NA |
| 1144- | CHr, | 8-bromo-7-methoxychrysin-induced apoptosis of hepatocellular carcinoma cells involves ROS and JNK |
| - | in-vitro, | HCC, | HepG2 | - | in-vitro, | HCC, | Bel-7402 | - | in-vitro, | Nor, | HL7702 |
| - | in-vitro, | HCC, | NA | - | in-vivo, | NA, | NA |
| 5225- | EMD, | Emodin inhibits growth and induces apoptosis in an orthotopic hepatocellular carcinoma model by blocking activation of STAT3 |
| - | vitro+vivo, | HCC, | HepG2 | - | in-vitro, | HCC, | Hep3B | - | in-vitro, | HCC, | HUH7 |
| 5218- | PG, | Propyl gallate inhibits hepatocellular carcinoma cell growth through the induction of ROS and the activation of autophagy |
| - | in-vitro, | HCC, | Hep3B |
| 1944- | PL, | Piperlongumine, a Novel TrxR1 Inhibitor, Induces Apoptosis in Hepatocellular Carcinoma Cells by ROS-Mediated ER Stress |
| - | in-vitro, | HCC, | HUH7 | - | in-vitro, | HCC, | HepG2 |
| 4966- | PSO, | Psoralidin induces pyroptosis in both tumor cells and macrophages as well as enhances nature killer cell cytotoxicity to suppress hepatocellular carcinoma |
| - | vitro+vivo, | HCC, | HepG2 |
| 2439- | RES, | By reducing hexokinase 2, resveratrol induces apoptosis in HCC cells addicted to aerobic glycolysis and inhibits tumor growth in mice |
| - | in-vitro, | HCC, | HCCLM3 | - | in-vitro, | Nor, | L02 | - | in-vitro, | HCC, | SMMC-7721 cell | - | in-vitro, | HCC, | Bel-7402 | - | in-vitro, | HCC, | HUH7 |
| 2110- | TQ, | Nigella sativa seed oil suppresses cell proliferation and induces ROS dependent mitochondrial apoptosis through p53 pathway in hepatocellular carcinoma cells |
| - | in-vitro, | HCC, | HepG2 | - | in-vitro, | BC, | MCF-7 | - | in-vitro, | Lung, | A549 | - | in-vitro, | Nor, | HEK293 |
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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