<?xml version="1.0" encoding="utf-8"?>
<journal>
<title>Iranian Biomedical Journal</title>
<title_fa>مجله بیومدیکال ایران</title_fa>
<short_title>IBJ</short_title>
<subject>Basic Sciences</subject>
<web_url>http://ibj.pasteur.ac.ir</web_url>
<journal_hbi_system_id>1</journal_hbi_system_id>
<journal_hbi_system_user>admin</journal_hbi_system_user>
<journal_id_issn>1028-852X</journal_id_issn>
<journal_id_issn_online>2008-823X</journal_id_issn_online>
<journal_id_pii>-</journal_id_pii>
<journal_id_doi>10.61882/ibj</journal_id_doi>
<journal_id_iranmedex></journal_id_iranmedex>
<journal_id_magiran></journal_id_magiran>
<journal_id_sid>-</journal_id_sid>
<journal_id_nlai>8888</journal_id_nlai>
<journal_id_science>-</journal_id_science>
<language>en</language>
<pubdate>
	<type>jalali</type>
	<year>1398</year>
	<month>8</month>
	<day>1</day>
</pubdate>
<pubdate>
	<type>gregorian</type>
	<year>2019</year>
	<month>11</month>
	<day>1</day>
</pubdate>
<volume>23</volume>
<number>6</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>BIRC5 Gene Disruption via CRISPR/Cas9n Platform Suppress Acute Myelocytic Leukemia Progression</title>
	<subject_fa>Medical Biotechnology</subject_fa>
	<subject>Medical Biotechnology</subject>
	<content_type_fa>مقاله کامل</content_type_fa>
	<content_type>Full Length/Original Article</content_type>
	<abstract_fa></abstract_fa>
	<abstract>&lt;strong&gt;Background:&lt;/strong&gt; Acute myelocytic leukemia (AML) is a clonal malignancy resulting from the accumulation of genetic abnormalities in the cells. Human baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC5), encodes survivin, is one of only a handful of genes that is differentially over-expressed in numerous malignant diseases including AML. &lt;strong&gt;Methods: &lt;/strong&gt;The &lt;em&gt;BIRC5 &lt;/em&gt;was silenced permanently in two AML cell lines, HL‑60 and KG-1, via the CRISPR/Cas9n system. After transfection of CRISPR constructs, genomic DNA was extracted and amplified to assess mutation detection. To evaluate &lt;em&gt;BIRC5&lt;/em&gt; gene expression, quantitative real-time PCR was performed. Also, MTT cell viability and Annexin‑V/propidium iodide flowcytometric staining were performed, and the data were analyzed using the Kolmogorov-Smirnov, Levene&amp;#39;s, and ANOVA tests. &lt;strong&gt;Results:&lt;/strong&gt; The results indicated that Cas9n and its sgRNAs successfully triggered site-specific cleavage and mutation in the &lt;em&gt;BIRC5&lt;/em&gt; gene locus. Moreover, suppression of &lt;em&gt;BIRC5&lt;/em&gt; resulted in the reduction of cell viability, and induction of apoptosis and necrosis in HL60 and KG1 suggested that the permanent suppression of &lt;em&gt;BIRC5&lt;/em&gt; remarkably dropped the gene expression and cells viability. &lt;strong&gt;Conclusion:&lt;/strong&gt; This study reinforces the idea that &lt;em&gt;BIRC5&lt;/em&gt; disruption via Cas9n:sgRNAs has favorable effects&lt;br&gt;
on the AML clinical outcome. It thereby can be a promising candidate in a variety of leukemia treatments.</abstract>
	<keyword_fa></keyword_fa>
	<keyword>Acute myelocytic leukemia (AML), CRISPR, Gene editing, Survivin</keyword>
	<start_page>369</start_page>
	<end_page>378</end_page>
	<web_url>http://ibj.pasteur.ac.ir/browse.php?a_code=A-10-1-786&amp;slc_lang=en&amp;sid=1</web_url>


<author_list>
	<author>
	<first_name>Manizheh </first_name>
	<middle_name></middle_name>
	<last_name>Narimani</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></email>
	<code></code>
	<orcid>0000-0002-7848-0986</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Cancer and Immunology Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Mohammadreza</first_name>
	<middle_name></middle_name>
	<last_name>Sharifi</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></email>
	<code></code>
	<orcid>0000-0002-1538-9034</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences,  Isfahan, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Mohammad Saeed</first_name>
	<middle_name></middle_name>
	<last_name>Hakhamaneshi</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></email>
	<code></code>
	<orcid>0000-0002-5481-1031</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Cancer and Immunology Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Daem</first_name>
	<middle_name></middle_name>
	<last_name>Roshani</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></email>
	<code></code>
	<orcid>0000-0003-4746-1114</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Cancer and Immunology Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Mohammad </first_name>
	<middle_name></middle_name>
	<last_name>Kazemi</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></email>
	<code></code>
	<orcid>0000-0002-6794-6891</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences,  Isfahan, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Seyed Hossein</first_name>
	<middle_name></middle_name>
	<last_name>Hejazi</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></email>
	<code></code>
	<orcid>0000-0002-3733-1220</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Skin Diseases and Leishmaniasis Research Center, Department of Parasitology &amp; Mycology,  School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Ali</first_name>
	<middle_name></middle_name>
	<last_name>Jalili</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></email>
	<code></code>
	<orcid>0000-0002-1833-4928</orcid>
	<coreauthor>Yes
</coreauthor>
	<affiliation>Cancer and Immunology Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


</author_list>


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