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  <front>
    <journal-meta>
      <journal-id journal-id-type="publisher-id">82</journal-id>
      <journal-title-group>
        <journal-title>Journal of Advances in Basic Medicine</journal-title>
        <abbrev-journal-title>Electronic Communication Technology</abbrev-journal-title>
      </journal-title-group>
      <publisher>
        <publisher-name>睿核出版社有限公司</publisher-name>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id">14895</article-id>
      <title-group>
        <article-title>LINC01614 is involved in the regulation of myocardial ischemia by directly targeting miR-138-5p</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <string-name>Junliang Zhu</string-name>
        </contrib>
        <contrib contrib-type="author">
          <string-name>Jianhuang Chen</string-name>
        </contrib>
        <contrib contrib-type="author">
          <string-name>Kaixue Zhang</string-name>
        </contrib>
      </contrib-group>
      <pub-date pub-type="epub">
        <year>2025</year>
        <month>1</month>
      </pub-date>
      <issue>1</issue>
      <abstract>
        <p>Background
Long noncoding RNAs (lncRNAs) have been paid much attentions recently in the prevention of multiple diseases. As a currently investigated lncRNA, LINC01614 acts as a promoter in tumor progression. However, the function of LINC01614 in myocardial ischemia is elusive.
Materials and methods
In this study, to figure out the role of LINC01614 in myocardial ischemia, we explored the expression level of LINC01614 and miR-138-5p from the GEO database. SiRNA strategy was applied to knockdown LINC01614, qRT-PCR and western blot assays were performed to assess the mRNA and protein expression levels. After silenced LINC01614, cell proliferation assay and flow cytometry were conducted to determine the proliferative and apoptotic capabilities. In addition, dual luciferase reporter assay ascertained the correlation between LINC01614 and miR-138-5p.
Results
LINC01614 was found to be over-expressed whereas miR-138-5p was down-regulated in patients with heart related diseases. Reduction of LINC01614 promoted cell proliferation and repressed the apoptotic property in cardiomyocytes. Moreover, LINC01614 could directly target miR-138-5p and decline its expression level. Moreover, the overexpression of miR-138-5p could greatly reverse the function of LINC01614 in H/R groups.
Conclusion
In conclusion, our results illustrated the important function of LINC01614 in the acquisition of cell proliferations and apoptotic assay, which accelerates myocardial damage by inhibiting miR-138-5p.</p>
      </abstract>
    </article-meta>
  </front>
</article>
