<?xml version="1.0" encoding="UTF-8"?>
<!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>15</Volume>
				<Issue>18</Issue>
				<PubDate PubStatus="epublish">
					<Year>2014</Year>
					<Month>12</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Over-Expression of Beclin-1 Facilitates Acquired Resistance to Histone Deacetylase Inhibitor-Induced Apoptosis</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>7913</FirstPage>
			<LastPage>7917</LastPage>
			<ELocationID EIdType="pii">29857</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>Apoptotic cell death plays a predominant role in histone deacetylase (HDAC) inhibitor-induced cytotoxicity.Nuclear morphological changes and activation of apoptotic executors are involved in CTS203-induced cell death.However, emerging issues of HDAC inhibitor-resistance have been observed in patients. Herein, MCF-7 cellswere continuously exposed to CTS203 until the derived cells could proliferate normally in its presence. Thenewly obtained CTS203-resistant cells were nominated as MCF-7/203R. Compared to MCF-7 original cells, theMCF-7/203R cells were less sensitive to CTS203-induced apoptosis, with a minimal 6-fold higher IC50 value. Incontrast, the expression of Beclin-1 was dramatically up-regulated, positively correlated to the acquisition ofCTS203-resistance. Our results revealed the participation of autophagy in acquired HDAC inhibitor-resistanceand further identified Beclin-1 as a promising target for anti-drug resistance.</Abstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">HDAC inhibitor</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Drug resistance</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Beclin-1</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Autophagy</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Apoptosis</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://journal.waocp.org/article_29857_b159257fa26820837507030643f3b298.pdf</ArchiveCopySource>
</Article>
</ArticleSet>
