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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. |
| Cervical Cancer |
| 4388- | AgNPs, | Differential Cytotoxic Potential of Silver Nanoparticles in Human Ovarian Cancer Cells and Ovarian Cancer Stem Cells |
| - | in-vitro, | Cerv, | NA |
| 324- | AgNPs, | CPT, | Silver Nanoparticles Potentiates Cytotoxicity and Apoptotic Potential of Camptothecin in Human Cervical Cancer Cells |
| - | in-vitro, | Cerv, | HeLa |
| 5592- | BetA, | Betulin induces mitochondrial cytochrome c release associated apoptosis in human cancer cells |
| - | in-vitro, | Liver, | HepG2 | - | in-vitro, | Cerv, | HeLa |
| 1145- | CHr, | Chrysin inhibits propagation of HeLa cells by attenuating cell survival and inducing apoptotic pathways |
| - | in-vitro, | Cerv, | HeLa |
| 477- | CUR, | Curcumin induces G2/M arrest and triggers autophagy, ROS generation and cell senescence in cervical cancer cells |
| - | in-vitro, | Cerv, | SiHa |
| 1245- | EMD, | Emodin Exhibits Strong Cytotoxic Effect in Cervical Cancer Cells by Activating Intrinsic Pathway of Apoptosis |
| - | in-vitro, | Cerv, | HeLa |
| 1323- | EMD, | Anticancer action of naturally occurring emodin for the controlling of cervical cancer |
| - | Review, | Cerv, | NA |
| 3460- | EP, | Picosecond pulsed electric fields induce apoptosis in HeLa cells via the endoplasmic reticulum stress and caspase-dependent signaling pathways |
| - | in-vitro, | Cerv, | HeLa |
| 1015- | NarG, | Naringin induces endoplasmic reticulum stress-mediated apoptosis, inhibits β-catenin pathway and arrests cell cycle in cervical cancer cells |
| - | in-vitro, | Cerv, | SiHa | - | in-vitro, | Cerv, | HeLa | - | in-vitro, | Cerv, | C33A |
| 5183- | PEITC, | Cisplatin, | Phenethyl Isothiocyanate Induces Apoptosis Through ROS Generation and Caspase-3 Activation in Cervical Cancer Cells |
| - | in-vitro, | Cerv, | HeLa | - | in-vitro, | Nor, | HaCaT |
| 5219- | PG, | Propyl gallate inhibits the growth of HeLa cells via caspase-dependent apoptosis as well as a G1 phase arrest of the cell cycle |
| - | in-vitro, | Cerv, | HeLa |
| 5213- | PI, | Induction of apoptosis by piperine in human cervical adenocarcinoma via ROS mediated mitochondrial pathway and caspase-3 activation |
| - | in-vitro, | Cerv, | HeLa |
| 5158- | PLB, | Plumbagin induces reactive oxygen species, which mediate apoptosis in human cervical cancer cells |
| - | in-vitro, | Cerv, | ME-180 |
| 4968- | PSO, | Psoralidin: emerging biological activities of therapeutic benefits and its potential utility in cervical cancer |
| - | in-vitro, | Cerv, | NA |
| 1993- | PTL, | Parthenolide induces apoptosis and autophagy through the suppression of PI3K/Akt signaling pathway in cervical cancer |
| - | in-vitro, | Cerv, | HeLa |
| 36- | QC, | Quercetin induces G2 phase arrest and apoptosis with the activation of p53 in an E6 expression-independent manner in HPV-positive human cervical cancer-derived cells |
| - | in-vitro, | Cerv, | HeLa | - | in-vitro, | Cerv, | SiHa |
| 3362- | QC, | The effect of quercetin on cervical cancer cells as determined by inducing tumor endoplasmic reticulum stress and apoptosis and its mechanism of action |
| - | in-vitro, | Cerv, | HeLa |
| 884- | RES, | PTS, | Resveratrol and Pterostilbene Exhibit Anticancer Properties Involving the Downregulation of HPV Oncoprotein E6 in Cervical Cancer Cells |
| - | in-vitro, | Cerv, | HeLa |
| 1403- | SDT, | BBR, | From 2D to 3D In Vitro World: Sonodynamically-Induced Prooxidant Proapoptotic Effects of C60-Berberine Nanocomplex on Cancer Cells |
| - | in-vitro, | Cerv, | HeLa | - | in-vitro, | Lung, | LLC1 |
| 2097- | TQ, | Crude extract of Nigella sativa inhibits proliferation and induces apoptosis in human cervical carcinoma HeLa cells |
| - | in-vitro, | Cerv, | HeLa |
| 1838- | VitK3, | PDT, | Photodynamic Effects of Vitamin K3 on Cervical Carcinoma Cells Activating Mitochondrial Apoptosis Pathways |
| - | in-vitro, | Cerv, | 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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