| Source: |
| Type: |
| 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. |
| Acute Myeloid Leukemia |
| 5341- | Ajoene, | Ajoene (natural garlic compound): a new anti-leukaemia agent for AML therapy |
| - | Review, | AML, | NA |
| 591- | Api, | doxoR, | Polyphenols act synergistically with doxorubicin and etoposide in leukaemia cell lines |
| - | in-vitro, | AML, | Jurkat | - | in-vitro, | AML, | THP1 |
| 270- | Api, | Apigenin induces apoptosis in human leukemia cells and exhibits anti-leukemic activity in vivo via inactivation of Akt and activation of JNK |
| - | in-vivo, | AML, | U937 |
| 268- | Api, | Induction of apoptosis by apigenin and related flavonoids through cytochrome c release and activation of caspase-9 and caspase-3 in leukaemia HL-60 cells |
| - | in-vitro, | AML, | HL-60 |
| - | in-vitro, | AML, | HL-60 |
| 1526- | Ba, | Baicalein induces apoptosis through ROS-mediated mitochondrial dysfunction pathway in HL-60 cells |
| - | in-vitro, | AML, | HL-60 |
| 2718- | BetA, | The anti-cancer effect of betulinic acid in u937 human leukemia cells is mediated through ROS-dependent cell cycle arrest and apoptosis |
| - | in-vitro, | AML, | U937 |
| 5692- | BJ, | Seed oil of Brucea javanica induces apoptosis through the PI3K/Akt signaling pathway in acute lymphocytic leukemia Jurkat cells |
| - | vitro+vivo, | AML, | NA |
| 5914- | Cats, | Induction of apoptosis by Uncaria tomentosa through reactive oxygen species production, cytochrome c release, and caspases activation in human leukemia cells |
| - | in-vitro, | AML, | HL-60 |
| 1086- | GA, | Anti-leukemic effects of gallic acid on human leukemia K562 cells: downregulation of COX-2, inhibition of BCR/ABL kinase and NF-κB inactivation |
| - | in-vitro, | AML, | K562 |
| 831- | GAR, | CUR, | Induction of apoptosis by garcinol and curcumin through cytochrome c release and activation of caspases in human leukemia HL-60 cells |
| - | in-vitro, | AML, | HL-60 |
| 5114- | JG, | Juglone, from Juglans mandshruica Maxim, inhibits growth and induces apoptosis in human leukemia cell HL-60 through a reactive oxygen species-dependent mechanism |
| - | in-vitro, | AML, | HL-60 |
| 5184- | PEITC, | Phenethyl isothiocyanate exhibits antileukemic activity in vitro and in vivo by inactivation of Akt and activation of JNK pathways |
| - | vitro+vivo, | AML, | U937 |
| 5217- | PG, | Role of redox signaling regulation in propyl gallate-induced apoptosis of human leukemia cells |
| - | in-vitro, | AML, | THP1 | - | in-vitro, | AML, | Jurkat | - | in-vitro, | AML, | HL-60 |
| 2970- | PL, | Piperlongumine induces apoptosis and autophagy in leukemic cells through targeting the PI3K/Akt/mTOR and p38 signaling pathways |
| - | in-vitro, | AML, | NA |
| 2005- | PLB, | Plumbagin induces apoptosis in lymphoma cells via oxidative stress mediated glutathionylation and inhibition of mitogen-activated protein kinase phosphatases (MKP1/2) |
| - | in-vivo, | Nor, | EL4 | - | in-vitro, | AML, | Jurkat |
| 41- | QC, | Quercetin induces mitochondrial-derived apoptosis via reactive oxygen species-mediated ERK activation in HL-60 leukemia cells and xenograft |
| - | vitro+vivo, | AML, | HL-60 |
| 42- | QC, | Quercetin induces apoptosis by activating caspase-3 and regulating Bcl-2 and cyclooxygenase-2 pathways in human HL-60 cells |
| - | in-vitro, | AML, | HL-60 |
| 1315- | SFN, | Sulforaphane Induces Apoptosis of Acute Human Leukemia Cells Through Modulation of Bax, Bcl-2 and Caspase-3 |
| - | in-vitro, | AML, | K562 |
| 1467- | SFN, | Sulforaphane generates reactive oxygen species leading to mitochondrial perturbation for apoptosis in human leukemia U937 cells |
| - | in-vitro, | AML, | U937 |
| 2109- | TQ, | Thymoquinone Induces Mitochondria-Mediated Apoptosis in Acute Lymphoblastic Leukaemia in Vitro |
| - | in-vitro, | AML, | CEM |
| 1832- | VitK3, | VitC, | Vitamin K3 and vitamin C alone or in combination induced apoptosis in leukemia cells by a similar oxidative stress signalling mechanism |
| - | in-vitro, | AML, | K562 |
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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:2 Cells:% prod#:% Target#:42 State#:% Dir#:2
wNotes=0 sortOrder:rid,rpid