<?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>1401</year>
	<month>10</month>
	<day>1</day>
</pubdate>
<pubdate>
	<type>gregorian</type>
	<year>2023</year>
	<month>1</month>
	<day>1</day>
</pubdate>
<volume>12</volume>
<number>1</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>Effects of hsa-piR-32877 Suppression with Antisense LNA GapmeRs on the Proliferation and Apoptosis of Human Acute Myeloid Leukemia Cells</title>
	<subject_fa>Hematology</subject_fa>
	<subject>Hematology</subject>
	<content_type_fa>Original Article</content_type_fa>
	<content_type>Original Article</content_type>
	<abstract_fa></abstract_fa>
	<abstract>&lt;span style=&quot;font-size:12px;&quot;&gt;&lt;span style=&quot;font-family:Tahoma;&quot;&gt;&lt;span style=&quot;unicode-bidi:embed&quot;&gt;&lt;span style=&quot;line-height:107%&quot;&gt;Acute myeloid leukemia (AML) is an invasive form of hematologic malignancies which results in the overproduction of myeloid cells in the bone marrow. Aberrant expression of piwi-interacting RNAs (piRNAs) which belong to small non-coding RNAs, play important roles in different cancer cells&amp;#39; progress. hsa- piR- 32877 is up-regulated in AML. Down regulation of hsa-piR-32877 by antisense LNA GapmeRs could be potential for suppression of myeloid cell proliferation and induce myeloid cell apoptosis. We have blocked the expression of hsa-piR-32877 by antisense LNA GapmeRs in human bone marrow blast cells, and the M-07e cell line. Samples were transfected with antisense LNA GapmeRs at 24, 48, and 72 hours. The Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was performed to investigate the expression of hsa-piR-32877, CASP3, and CASP9. Both CASP3 and CASP9 play important roles in apoptosis. Cell proliferation was studied via CFSE (carboxyfluorescein diacetate succinimidyl ester) assay. Results showed that hsa-piR-32877 was down-regulated by antisense LNA GapmeRs in the patient and cell line samples. Also, after transfection, cell proliferation and apoptosis decreased and increased, respectively. Our data suggested that hsa-piR-32877 suppression may act as a novel therapeutic method for the inhibition of human leukemic cells proliferation in AML&lt;span dir=&quot;RTL&quot; lang=&quot;FA&quot;&gt;.&lt;/span&gt;&lt;/span&gt;&lt;/span&gt;&lt;/span&gt;&lt;/span&gt;</abstract>
	<keyword_fa></keyword_fa>
	<keyword>Acute myeloid leukemia, Antisense LNA GapmeRs, hsa-piR-32877, CASP3, CASP9</keyword>
	<start_page>18</start_page>
	<end_page>29</end_page>
	<web_url>http://ijmcmed.org/browse.php?a_code=A-10-1083-3&amp;slc_lang=en&amp;sid=1</web_url>


<author_list>
	<author>
	<first_name>Sepideh</first_name>
	<middle_name></middle_name>
	<last_name>Naseri</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>sepideh1374nasseri@gmail.com</email>
	<code>100319475328460032670</code>
	<orcid>100319475328460032670</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>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>mo_sharifi@med.mui.ac.ir</email>
	<code>100319475328460032671</code>
	<orcid>100319475328460032671</orcid>
	<coreauthor>Yes
</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>Valiollah</first_name>
	<middle_name></middle_name>
	<last_name>Mehrzad</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>v_mehrzad@med.mui.ac.ir</email>
	<code>100319475328460032672</code>
	<orcid>100319475328460032672</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Department of Internal Medicine, Division of Hematology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


</author_list>


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