en Molecular Genetics & Genomics Molecular Genetics & Genomics مقاله کوتاه Short Communication <div style="text-align: justify;"><span style="font-family:Times New Roman;"><span style="font-size:11pt"><span style="line-height:normal"><span calibri=""><b><span new="" roman="" times="">Background</span></b><em>: </em><span new="" roman="" times="">MiR-34a and miR-126 mainly act as tumor suppressors and are often downregulated in various cancers, including </span><span new="" roman="" times="">non-small cell lung cancer</span><span new="" roman="" times=""> (NSCLC). We aimed to determine the methylation status of miR-34a and miR-126 in NSCLC patients.</span></span></span></span><br> <span style="font-size:11pt"><span style="line-height:normal"><span calibri=""><b><span new="" roman="" times="">Methods: </span></b><span new="" roman="" times="">The current study included 63 paraffin-embedded NSCLC and paired adjacent normal tissues. After DNA extraction and bisulfite treatment, the methylation status of miR-34a and miR-126 were evaluated using the MSP method.</span></span></span></span><br> <span style="font-size:11pt"><span style="line-height:normal"><span calibri=""><b><span new="" roman="" times="">Results:</span></b><span new="" roman="" times=""> There was no statistically significant difference between tumor and normal tissues regarding the methylation status of miR-34a and miR-126<br> (<i>p</i> > 0.05). Moreover, we found no significant correlation between the methylation status of miR-34a and miR-126 with patients&rsquo; demographic parameters, including gender, age, and pathology subtype (<i>p</i> > 0.05).</span></span></span></span><br> <b><span style="font-size:11.0pt"><span style="line-height:115%"><span new="" roman="" times="">Conclusion: </span></span></span></b><span style="font-size:11.0pt"><span style="line-height:115%"><span new="" roman="" times="">Considering the low expression of mir-126 and mir-34 in NSCLC, more sensitive methods are recommended to be exploited for detecting the level of methylation or underlying mechanisms other than promoter hypermethylation in silencing these genes in NSCLC. </span></span></span></span></div> DNA methylation, miR-34a, miR-126, Non-small cell lung carcinoma 53 58 http://ibj.pasteur.ac.ir/browse.php?a_code=A-10-5168-1&slc_lang=en&sid=1 Nazanin Mehrzad nazy_mehrzad@yahoo.com 0000-0003-4881-0160 No Molecular Medicine Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran Mohammad Saber Zamani msaber.ir@gmail.com 0000-0002-4614-6254 No Molecular Medicine Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran Amir Abbass Rahimi amirabbas_rahimi@yahoo.com 0000-0002-1982-8081 No Molecular Medicine Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran Masoud Shamaei Dr_shamaei@yahoo.com 0000-0002-1991-0536 No Mesih Deneshvari Hospital Shahid Beheshti Medical Sciences University, Tehran, Iran Morteza Karimipoor mortezakarimi@yahoo.com 0000-0002-2406-5963 Yes Molecular Medicine Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran