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Nuclear Receptor Small Heterodimer Partner in Apoptosis Signaling and Liver Cancer
Departments of Medicine and Oncological Sciences, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT 84132, USA
* Author to whom correspondence should be addressed.
Received: 30 November 2010; in revised form: 30 December 2010 / Accepted: 4 January 2011 / Published: 5 January 2011
Abstract: Small heterodimer partner (SHP, NR0B2) is a unique orphan nuclear receptor that contains the dimerization and a putative ligand-binding domain, but lacks the conserved DNA binding domain. SHP exerts its physiological function as an inhibitor of gene transcription through physical interaction with multiple nuclear receptors and transcriptional factors. SHP is a critical transcriptional regulator affecting diverse biological functions, including bile acid, cholesterol and lipid metabolism, glucose and energy homeostasis, and reproductive biology. Recently, we and others have demonstrated that SHP is an epigenetically regulated transcriptional repressor that suppresses the development of liver cancer. In this review, we summarize recent major findings regarding the role of SHP in cell proliferation, apoptosis, and DNA methylation, and discuss recent progress in understanding the function of SHP as a tumor suppressor in the development of liver cancer. Future study will be focused on identifying SHP associated novel pro-oncogenes and anti-oncogenes in liver cancer progression and applying the knowledge gained on SHP in liver cancer prevention, diagnosis and treatment.
Keywords: nuclear receptors; small heterodimer partner; apoptosis; cell cycle; liver cancer
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MDPI and ACS Style
Zhang, Y.; Wang, L. Nuclear Receptor Small Heterodimer Partner in Apoptosis Signaling and Liver Cancer. Cancers 2011, 3, 198-212.
Zhang Y, Wang L. Nuclear Receptor Small Heterodimer Partner in Apoptosis Signaling and Liver Cancer. Cancers. 2011; 3(1):198-212.
Zhang, Yuxia; Wang, Li. 2011. "Nuclear Receptor Small Heterodimer Partner in Apoptosis Signaling and Liver Cancer." Cancers 3, no. 1: 198-212.