CASP3 Target Analysis Report Summary
About the Target
Based on the given context information, the following key viewpoints can be extracted regarding the role and regulation of caspase-3 (CASP3):
In corals, CASP3 is activated by an unknown sensor and pathway during invasive infection, leading to the cleavage of gasdermin E (GSDME) and subsequent induction of pyroptosis [1A].
In cancer cells, increased levels of prostate cancer antigen 3 (PC-3) can perturb zinc regulation, potentially altering basal caspase-3 activity within the cell [2].
During apoptosis, activated caspase-3 cleaves a small percentage of p65, generating a p65 fragment that interferes with the activation-induced nuclear translocation of RPS3. This selective inhibition of NF-kappaB anti-apoptotic transcription shifts the cellular balance towards apoptosis [3].
The expression of pUL138 in gastric cancer cells can inhibit caspase-3 cleavage and block the function of heat shock protein 70 (HSP70), thereby promoting apoptotic cancer cell death [4].
Caspase-3 activation is involved in the Phoenix Rising pathway, where it promotes programmed cell death by apoptosis and leads to the production of prostaglandin E2 (PGE2), which accelerates tumor repopulation [5A].
Caspase-3 activation is also linked to the DNA damage response (DDR) pathway, where it plays a role in determining cell fate in response to DNA damage caused by radiation [5B].
These viewpoints provide insights into the diverse roles and regulatory mechanisms of caspase-3 in various biological contexts, including coral infection, cancer progression, apoptosis, and DNA damage response.
Caspase-3, also known as caspase-3/-7, is a key protein involved in the apoptotic signaling pathway in different cell types. In Jurkat T cells, MST1 acts as a regulator of the extrinsic apoptotic pathway, and its proteolytic activation is stimulated by active ERK1/2 signaling. Caspase-8 may potentially activate MST1 in these cells, and MST1, in turn, potentiates the activation of caspase-3, -7, and -8, forming a positive feed-back loop to amplify the apoptotic signal [6].
In gastric cancer (GC) cells, MeCP2 inhibits apoptosis by suppressing the MYOD1/Caspase-3 signaling pathway. Knockdown of MeCP2 leads to increased expression of MYOD1 and results in the up-regulation of active Caspase-3, inducing apoptosis and inhibiting GC cell proliferation [7].
TFF3, when overexpressed, activates the PI3K/AKT pathway to block the mitochondria-induced apoptotic pathway in prostate tumorigenesis. Silencing TFF3 has the opposite effect, promoting the release of proapoptotic proteins from the mitochondria, activating caspase-9 and caspase-3, and inducing apoptotic cell death [8].
During Newcastle disease virus (NDV) infection in a chicken fibroblast cell line, knockdown of 2'-5'-oligoadenylate synthetase-like (OASL) leads to lower expression of CASP3 gene and other caspase genes. This reduction in caspase expression results in a higher level of NDV viral RNA [9].
Overall, caspase-3 plays a crucial role in apoptosis regulation in different cellular contexts, either as a positive regulator in the apoptotic pathway or as a target for inhibition by specific proteins. Its involvement is observed in T cells, gastric cancer cells, prostate tumorigenesis, and NDV infection.
Figure [1]
Figure [2]
Figure [3]
Figure [4]
Figure [5]
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Figure [9]
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