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<!DOCTYPE ArticleSet PUBLIC "-//NLM//DTD PubMed 2.7//EN" "https://dtd.nlm.nih.gov/ncbi/pubmed/in/PubMed.dtd">
<ArticleSet>
<Article>
<Journal>
				<PublisherName>West Asia Organization for Cancer Prevention (WAOCP), APOCP's West Asia Chapter.</PublisherName>
				<JournalTitle>Asian Pacific Journal of Cancer Prevention</JournalTitle>
				<Issn>1513-7368</Issn>
				<Volume>13</Volume>
				<Issue>8</Issue>
				<PubDate PubStatus="epublish">
					<Year>2012</Year>
					<Month>08</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>SENP2 Regulates Hepatocellular Carcinoma Cell Growth by Modulating the Stability of β-catenin</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>3583</FirstPage>
			<LastPage>3587</LastPage>
			<ELocationID EIdType="pii">26725</ELocationID>
			
			
			<Language>EN</Language>
<AuthorList>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>1970</Year>
					<Month>01</Month>
					<Day>01</Day>
				</PubDate>
			</History>
		<Abstract>SUMOylation has emerged as an important post-translational modification that modulates the localization,stability and activity of a broad spectrum of proteins. A dynamic process, it can be reversed by a family of SUMOspecificproteases (SENPs). However, the biological roles of SENPs in mammalian development and pathogenesisremain largely elusive. Here, we demonstrated that SENP2 plays a critical role in the control of hepatocellularcarcinoma cell growth. SENP2 was found to be down-regulated in hepatocellular carcinoma (HCC) tissues andover-expression suppressed the growth and colony formation of HCC cells. In contrast, silencing of SENP2 bysiRNAs promoted cancer cell growth. We further found that stability of β-catenin was markedly decreasedwhen SENP2 was over-expressed. Interestingly, the decrease was dependent on the de-SUMOylation activity ofSENP2, because over-expression of a SENP2 catalytic mutant form had no obviously effects on β-catenin. Ourresults suggest that SENP2 might play a role in hepatocellular carcinoma cell growth control by modulating thestability of β-catenin.</Abstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">SENP2</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">β-catenin</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Hepatocellular carcinoma</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">HepG2 cells</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://journal.waocp.org/article_26725_7634aad083ab4161f7d3b5ec11bade67.pdf</ArchiveCopySource>
</Article>
</ArticleSet>
