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<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>14</Volume>
				<Issue>9</Issue>
				<PubDate PubStatus="epublish">
					<Year>2013</Year>
					<Month>09</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>CXCL12-CXCR4 Promotes Proliferation and Invasion of Pancreatic Cancer Cells</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>5403</FirstPage>
			<LastPage>5408</LastPage>
			<ELocationID EIdType="pii">28132</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>&lt;br/&gt;&lt;b&gt;Objective&lt;/b&gt;: CXCL12 exerts a wide variety of chemotactic effects on cells. Evidence indicates that CXCL12,in conjunction with its receptor, CXCR4, promotes invasion and metastasis of tumor cells. Our objective was toexplore whether the CXCL12-CXCR4 biological axis might influence biological behavior of pancreatic cancercells. &lt;br/&gt;&lt;b&gt;Methods&lt;/b&gt;: Miapaca-2 human pancreatic cancer cells were cultured under three different conditions:normal medium (control), medium + recombinant CXCL12 (CXCL12 group), or medium + CXCR4-inhibitorAMD3100 (AMD3100 group). RT-PCR was applied to detect mRNA expression levels of CXCL12, CXCR4, matrixmetalloproteinase 2 (MMP-2), MMP-9, and human urokinase plasminogen activator (uPA). Additionally, cellproliferation and invasion were performed using CCK-8 colorimetry and transwell invasion assays, respectively.&lt;br/&gt;&lt;b&gt;Results&lt;/b&gt;: CXCL12 was not expressed in Miapaca-2 cells, but CXCR4 was detected, indicating that these cells arecapable of receiving signals from CXCL12. Expression of extracellular matrix-degrading enzymes MMP-2, MMP-9, and uPA was upregulated in cells exposed to exogenous CXCL12 (P&lt;0.05). Additionally, both proliferationand invasion of pancreatic cancer cells were enhanced in the presence of exogenous CXCL12, but AMD3100intervention effectively inhibited these processes (P&lt;0.05). &lt;br/&gt;&lt;b&gt;Conclusions&lt;/b&gt;: The CXCL12-CXCR4 biological axisplays an important role in promoting proliferation and invasion of pancreatic cancer cells.</Abstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">CXCL12</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">CXCR4</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">AMD3100</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Pancreatic cancer</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Proliferation</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Invasion</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://journal.waocp.org/article_28132_782ce587b33d96c3692da563734b12f8.pdf</ArchiveCopySource>
</Article>
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