<?xml version="1.0"?>
<Articles JournalTitle="Iranian Journal of Allergy, Asthma and Immunology">
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>24</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="epublish">
        <Year>2025</Year>
        <Month>10</Month>
        <Day>29</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">MiR-425-5p Mediation of Malignant Behavior and Immune Escape of Cervical Cancer Cells by Targeting NCAM1</title>
    <FirstPage>834</FirstPage>
    <LastPage>850</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Mi</FirstName>
        <LastName>Xiang</LastName>
        <affiliation locale="en_US">Department of Obstetrics, Puren Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, China</affiliation>
      </Author>
      <Author>
        <FirstName>Yi</FirstName>
        <LastName>Yu</LastName>
        <affiliation locale="en_US">Department of Obstetrics, Puren Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, China</affiliation>
      </Author>
      <Author>
        <FirstName>Qin</FirstName>
        <LastName>Gao</LastName>
        <affiliation locale="en_US">Department of Obstetrics and Gynecology, Puren Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, China</affiliation>
      </Author>
      <Author>
        <FirstName>Jie</FirstName>
        <LastName>Xing</LastName>
        <affiliation locale="en_US">Department of Obstetrics, Puren Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, China</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2025</Year>
        <Month>01</Month>
        <Day>08</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2025</Year>
        <Month>04</Month>
        <Day>19</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">MicroRNA (miR)-425-5p is used as a molecular biomarker to identify cervical cancer (CxCa). However, few studies have examined the miR-425-5p-based modulation of the vital activities of CxCa cells.
The levels of neural cell adhesion molecule 1 (NCAM1) and miR-425-5p in CxCa tissues and cells were tested using western blot and reverse transcription quantitative polymerase chain reaction (RT-qPCR) tests. CxCa cells&#x2019; malignant phenotype was examined through clone formation tests, and transwell tests. CD8+T cells were co-cultured with CxCa cells and then analyzed for apoptosis rates and the expression of activation proteins (granzyme B (GZMB) and perforin) as well as immune factors (tumor necrosis factor-alpha (TNF-&#x3B1;) and interferon-gamma (IFN-&#x3B3;)) using flow cytometry, western blot, and enzyme-linked immunosorbent assay (ELISA) methods. Finally, in nude mouse experiments, the tumor size was measured for subcutaneous tumors, and the expression of CD8+T cell-related factors was detected.
The NCAM1 and miR-425-5p were down-regulated and up-regulated in CxCa tissue and cells, respectively. After silencing miR-425-5p, CxCa cells showed attenuation in vitality, clone formation rate, and their capacities to migrate, penetrate, and evade immune responses. NCAM1 was targeted and silenced by miR-425-5p. When NCAM1 was silenced, it partially counteracted miR-425-5p&#x2019;s inhibitory effects on the immune escape and proliferation. In nude mice, the tumor size and weight decreased after silencing miR-425-5p, and levels of CD8, IFN-&#x3B3;, TNF-&#x3B1;, perforin, and GZMB were elevated. However, these changes were reversed when NCAM1 was silenced.
In conclusion, miR-425-5p mediates the biological behavior and immune evasion of CxCa cells by regulating NCAM1.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/4302</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/4302/2250</pdf_url>
  </Article>
</Articles>
