<?xml version="1.0" encoding="utf-8"?>
<journal>
<title>International Journal of Molecular and Cellular Medicine</title>
<title_fa>مجله بین المللی سلولی و مولکولی</title_fa>
<short_title>Int J Mol Cell Med</short_title>
<subject>Medical Sciences</subject>
<web_url>http://ijmcmed.org</web_url>
<journal_hbi_system_id>1</journal_hbi_system_id>
<journal_hbi_system_user>admin</journal_hbi_system_user>
<journal_id_issn>2251-9637</journal_id_issn>
<journal_id_issn_online>2251-9645</journal_id_issn_online>
<journal_id_pii></journal_id_pii>
<journal_id_doi>10.22088/IJMCM.BUMS</journal_id_doi>
<journal_id_iranmedex></journal_id_iranmedex>
<journal_id_magiran></journal_id_magiran>
<journal_id_sid></journal_id_sid>
<journal_id_nlai></journal_id_nlai>
<journal_id_science></journal_id_science>
<language>en</language>
<pubdate>
	<type>jalali</type>
	<year>1395</year>
	<month>1</month>
	<day>1</day>
</pubdate>
<pubdate>
	<type>gregorian</type>
	<year>2016</year>
	<month>4</month>
	<day>1</day>
</pubdate>
<volume>5</volume>
<number>2</number>
<publish_type>online</publish_type>
<publish_edition>1</publish_edition>
<article_type>fulltext</article_type>
<articleset>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>Carcinoembryonic Antigen Expression and Resistance to Radiation-and 5-Fluorouracil-Induced Apoptosis and Autophagy</title>
	<subject_fa>Biomarkers (diagnosis &amp; treatment)</subject_fa>
	<subject>Biomarkers (diagnosis &amp; treatment)</subject>
	<content_type_fa>Original Article</content_type_fa>
	<content_type>Original Article</content_type>
	<abstract_fa></abstract_fa>
	<abstract>&lt;p dir=&quot;ltr&quot;&gt;Understanding the mechanism of tumor resistance is critical for cancer therapy. In this study, we investigated the effect of carcinoembryonic antigen (CEA) overexpression on UV-and 5-fluorouracil (5-FU)-induced apoptosis and autophagy in colorectal cancer cells. We used histone deacetylase (HDAC) inhibitor, NaB and DNA demethylating agent, 5- azacytidine (5-AZA) to induce CEA expression in HT29/219 and SW742 colorectal cancer cell lines. MTT assay was used to measure IC&lt;sub&gt;50&lt;/sub&gt; value of the cells exposed to graded concentrations of 5- FU with either 0.1 mM NaB or 1 &amp;mu;M 5-AZA for 72 h . Using CHO- and SW742-CEA transfectants, we also investigated the effect of CEA expression on UV- and 5-FU-induced apoptosis and autophagy. Treatment of HT29/219 cell line with NaB and 5-AZA increased CEA expression by 29% and 31%, respectively. Compared with control cells, the IC&lt;sub&gt;50&lt;/sub&gt; value for 5-FU of NaB and 5-AZA-treated cells increased by 40% and 57%, respectively. Treatment of SW742 cells with NaB or 5-AZA increased neither CEA expression nor the IC&lt;sub&gt;50&lt;/sub&gt; value for 5-FU. In comparison to parental cells, CEA expression also significantly protected transfected cells against UV-induced apoptosis. Decreased proportions of autophagy and apoptosis were also observed in 5-FU treated SW742- and CHO-CEA transfectants. We conclude that CEA expression can effectively protect colorectal cancer cells against radiation and drug-induced apoptosis and autophagy.&lt;/p&gt;
</abstract>
	<keyword_fa></keyword_fa>
	<keyword>Carcinoembryonic antigen (CEA), colorectal cancer, 5-fluorouracil, apoptosis, autophagy</keyword>
	<start_page>80</start_page>
	<end_page>89</end_page>
	<web_url>http://ijmcmed.org/browse.php?a_code=A-10-398-2&amp;slc_lang=en&amp;sid=1</web_url>


<author_list>
	<author>
	<first_name>Ebrahim</first_name>
	<middle_name></middle_name>
	<last_name>Eftekhar</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>eftekhar_msc@yahoo.com</email>
	<code>10031947532846007347</code>
	<orcid>10031947532846007347</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Department of Biochemistry, Shiraz University of Medical Sciences, School of Medicine, Shiraz, Iran.</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Hajar</first_name>
	<middle_name></middle_name>
	<last_name>Jaberi</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>jaberiehajar@yahoo.com</email>
	<code>10031947532846007348</code>
	<orcid>10031947532846007348</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Department of Biochemistry, Shiraz University of Medical Sciences, School of Medicine, Shiraz, Iran.</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Fakhraddin</first_name>
	<middle_name></middle_name>
	<last_name>Naghibalhossaini</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>fakhraddin.naghibalhossaini@mail.mcgill.ca</email>
	<code>10031947532846007349</code>
	<orcid>10031947532846007349</orcid>
	<coreauthor>Yes
</coreauthor>
	<affiliation>Autoimmune Research Center, Shiraz University of Medical Sciences, School of Medicine, Shiraz, Iran.</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


</author_list>


	</article>
</articleset>
</journal>
