Abstract
AbstractThe tumor suppressor prostate apoptosis response-4 (Par-4) has recently turned ‘twenty-five’. Beyond its indisputable role as an apoptosis inducer, an increasing and sometimes bewildering, new roles for Par-4 are being reported. These roles include its ability to regulate autophagy, senescence, and metastasis. This growing range of responses to Par-4 is reflected by our increasing understanding of the various mechanisms through which Par-4 can function. In this review, we summarize the existing knowledge on Par-4 tumor suppressive mechanisms, and discuss how the interaction of Par-4 with different regulators influence cell fate. This review also highlights the new secretory pathway that has emerged and the likely discussion on its clinical implications.
Funder
New York University Abu Dhabi
Publisher
Springer Science and Business Media LLC
Subject
Cancer Research,Cell Biology,Cellular and Molecular Neuroscience,Immunology
Reference138 articles.
1. Sells, S. F. et al. Commonality of the gene programs induced by effectors of apoptosis in androgen-dependent and -independent prostate cells. Cell Growth Differ. 5, 457–466 (1994).
2. El-Guendy, N., Zhao, Y., Gurumurthy, S., Burikhanov, R. & Rangnekar, V. M. Identification of a unique core domain of par-4 sufficient for selective apoptosis induction in cancer cells. Mol. Cell Biol. 23, 5516–5525 (2003).
3. Hebbar, N., Wang, C. & Rangnekar, V. M. Mechanisms of apoptosis by the tumor suppressor Par-4. J. Cell Physiol. 227, 3715–3721 (2012).
4. El-Guendy, N. & Rangnekar, V. M. Apoptosis by Par-4 in cancer and neurodegenerative diseases. Exp. Cell Res. 283, 51–66 (2003).
5. Boehrer, S. et al. In lymphatic cells par-4 sensitizes to apoptosis by down-regulating bcl-2 and promoting disruption of mitochondrial membrane potential and caspase activation. Cancer Res 62, 1768–1775 (2002).
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