MicroRNA‑25 promotes cell proliferation, migration and invasion in glioma by directly targeting cell adhesion molecule 2
- Gang Peng
- Yi Liu
- Chenxing Yang
- Chenfu Shen
Affiliations: Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China
- Published online on: October 30, 2021 https://doi.org/10.3892/etm.2021.10938
Copyright: © Peng
et al. This is an open access article distributed under the
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Commons Attribution License.
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Numerous microRNAs (miRNAs/miRs) have been demonstrated to serve oncogenic or suppressive roles in glioma. Exploration of the underlying molecular mechanism of miRNAs in the development and progression of glioma is beneficial for the identification of novel therapeutic targets. In the present study, the function of miR‑25 in glioma progression, as well as its underlying mechanism, were investigated. It was determined that miR‑25 was significantly upregulated in glioma tissues and cell lines compared with normal brain tissues and cells, respectively. Furthermore, high expression levels of miR‑25 were associated with an advanced clinical stage. The knockdown of miR‑25 expression significantly reduced glioma cell proliferation, migration and invasion. Cell adhesion molecule 2 (CADM2) was identified as a direct target of miR‑25 in glioma cells. Moreover, CADM2 expression level was significantly downregulated and inversely correlated with miR‑25 expression level in glioma tissues, indicating that the expression of CADM2 was negatively regulated by miR‑25. The inhibition of CADM2 expression counteracted the effects on glioma cell proliferation, migration and invasion caused by miR‑25 downregulation. Furthermore, CADM2 knockdown considerably promoted the proliferation and migration of glioma cells. In summary, the present study demonstrated that miR‑25 was significantly upregulated in glioma and that it promoted glioma cell proliferation, migration and invasion, at least partially, by directly targeting CADM2. These findings expanded the understanding of the molecular mechanism that underlies glioma progression.