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<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>16</Volume>
				<Issue>2</Issue>
				<PubDate PubStatus="epublish">
					<Year>2015</Year>
					<Month>02</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Exogenous p53 Upregulated Modulator of Apoptosis (PUMA) Decreases Growth of Lung Cancer A549 Cells</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>741</FirstPage>
			<LastPage>746</LastPage>
			<ELocationID EIdType="pii">30498</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>Purpose: To investigate the influence of exogenous p53 upregulated modulator of apoptosis (PUMA) expressionon cell proliferation and apoptosis in human non-small cell lung cancer A549 cells and transplanted tumor cellgrowth in nude mice. Materials and &lt;br/&gt;&lt;b&gt;Methods&lt;/b&gt;: A549 cells were divided into the following groups: control, noncarrier(NC), PUMA (transfected with pCEP4- (HA) 2-PUMA plasmid), DDP (10μg/mL cisplatin treatment)and PUMA+DDP (transfected with pCEP4-(HA)2-PUMA plasmid and 10μg/mL cisplatin treatment). The MTTmethod was used to detect the cell survival rate. Cell apoptosis rates were measured by flow cytometry, andPUMA, Bax and Bcl-2 protein expression levels were measured by Western blotting. &lt;br/&gt;&lt;b&gt;Results&lt;/b&gt;: Compared to thecontrol group, the PUMA, DDP and PUMA+DDP groups all had significantly decreased A549 cell proliferation(p&lt;0.01), with the largest reduction in the PUMA+DDP group. Conversely, the apoptosis rates of the three groupswere significantly increased (P &lt; 0.01), and the PUMA and DDP treatments were synergistic. Moreover, Baxprotein levels significantly increased (p&lt;0.01), while Bcl-2 protein levels significantly decreased (p&lt;0.01). Finally,both the volume and the weights of transplanted tumors were significantly reduced (p&lt;0.01), and the inhibitionratio of the PUMA+DDP group was significantly higher than in the single DDP or PUMA groups. &lt;br/&gt;&lt;b&gt;Conclusions&lt;/b&gt;:Exogenous PUMA effectively inhibited lung cancer A549 cell proliferation and transplanted tumor growth byincreasing Bax protein levels and reducing Bcl-2 protein levels.</Abstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">p53 upregulated modulator of apoptosis</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">non-small cell lung cancer</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Apoptosis</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">tumor transplant</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://journal.waocp.org/article_30498_af7d4b08c831ab305e7682619865e0dc.pdf</ArchiveCopySource>
</Article>
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