MiR-218-5p inhibits glioma progression by targeting CKLF-like MARVEL transmembrane domain-containing 3

BACKGROUND: This study aimed to investigate the role of miR-218-5p and CKLF-like marvel transmembrane domain-containing 3 (CMTM3) and the interaction between them in glioma. METHODS: The presence of CMTM3 in glioma cells and tissues was detected using immunohistochemical analysis, quantitative reverse transcription polymerase chain reaction, and western blotting. Public databases were used to examine the relationship between CMTM3 expression and patient survival. Transwell assay was performed to evaluate the invasive potential of glioma cells with downregulated CMTM3. Luciferase reporter assay was performed to validate the role of miR-218-5p in regulating CMTM3 expression. Intracranial xenograft models were established to investigate the role of CMTM3 in glioma in vivo. RESULTS: CMTM3 was upregulated in glioma cells and tissues. Higher CMTM3 expression was significantly associated with shorter overall survival and more advanced clinicopathological characteristics in patients with glioma. Functional assays demonstrated that downregulation of CMTM3 potently suppressed the proliferative and invasive abilities of glioma cells in vitro and reduced tumor growth by approximately 66% in an intracranial xenograft model. Transfection with a miR-218-5p mimic suppressed CMTM3 expression by approximately 68% at the mRNA level and 70% at the protein level in glioma cell lines, indicating that CMTM3 was directly regulated by miR-218-5p. Additionally, the miR-218-5p mimic significantly inhibited the proliferative and invasive abilities of glioma cells. CONCLUSION: MiR-218-5p regulates the oncogenic role of CMTM3 in glioma. Therefore, targeting the miR-218-5p/CMTM3 axis is a promising therapeutic strategy for glioma.