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Review
. 2023 Apr;28(3-4):313-325.
doi: 10.1007/s10495-022-01802-4. Epub 2023 Jan 18.

A double-edged sword: role of apoptosis repressor with caspase recruitment domain (ARC) in tumorigenesis and ischaemia/reperfusion (I/R) injury

Affiliations
Review

A double-edged sword: role of apoptosis repressor with caspase recruitment domain (ARC) in tumorigenesis and ischaemia/reperfusion (I/R) injury

Kun Liu et al. Apoptosis. 2023 Apr.

Abstract

Apoptosis repressor with caspase recruitment domain (ARC) acts as a potent and multifunctional inhibitor of apoptosis, which is mainly expressed in postmitotic cells, including cardiomyocytes. ARC is special for its N-terminal caspase recruitment domain and caspase recruitment domain. Due to the powerful inhibition of apoptosis, ARC is mainly reported to act as a cardioprotective factor during ischaemia‒reperfusion (I/R) injury, preventing cardiomyocytes from being devastated by various catastrophes, including oxidative stress, calcium overload, and mitochondrial dysfunction in the circulatory system. However, recent studies have found that ARC also plays a potential regulatory role in tumorigenesis especially in colorectal cancer and renal cell carcinomas, through multiple apoptosis-associated pathways, which remains to be explored in further studies. Therefore, ARC regulates the body and maintains the balance of physiological activities with its interesting duplex. This review summarizes the current research progress of ARC in the field of tumorigenesis and ischaemia/reperfusion injury, to provide overall research status and new possibilities for researchers.

Keywords: Apoptosis; Apoptosis repressor with caspase recruitment domain (ARC); Ischaemia/reperfusion (I/R) injury; The nucleolar protein 3 (NOL3); Tumorigenesis.

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    1. Yaacoub K, Pedeux R, Tarte K, Guillaudeux T (2016) Role of the tumor microenvironment in regulating apoptosis and cancer progression. Cancer Lett 378:150–159. https://doi.org/10.1016/j.canlet.2016.05.012 - DOI - PubMed
    1. Chen Y, Lin JS (2017) The application of aptamer in apoptosis. Biochimie 132:1–8. https://doi.org/10.1016/j.biochi.2016.10.008 - DOI - PubMed
    1. Zhang YQ, Herman B (2006) ARC protects rat cardiomyocytes against oxidative stress through inhibition of caspase-2 mediated mitochondrial pathway. J Cell Biochem 99:575–588. https://doi.org/10.1002/jcb.20946 - DOI - PubMed
    1. Koseki T, Inohara N, Chen S, Núñez G (1998) ARC, an inhibitor of apoptosis expressed in skeletal muscle and heart that interacts selectively with caspases. Proc Natl Acad Sci U S A 95:5156–5160. https://doi.org/10.1073/pnas.95.9.5156 - DOI - PubMed - PMC
    1. Hunter AL, Zhang J, Chen SC et al (2007) Apoptosis repressor with caspase recruitment domain (ARC) inhibits myogenic differentiation. FEBS Lett 581:879–884. https://doi.org/10.1016/j.febslet.2007.01.050 - DOI - PubMed

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