Research Paper Volume 13, Issue 16 pp 20808—20819
LINC01087 inhibits glioma cell proliferation and migration, and increases cell apoptosis via miR-384/Bcl-2 axis
- 1 Department of Neurosurgery, Cangzhou Central Hospital, Cangzhou, Hebei Province, China
Received: March 16, 2021 Accepted: August 2, 2021 Published: August 30, 2021https://doi.org/10.18632/aging.203478
How to Cite
Copyright: © 2021 Tian et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Long non-coding RNA (LncRNA) is associated with disease progression. It is reported that LINC01087 is highly expressed in cancer and participates in tumorigenesis. However, whether it regulates the development of glioma has not been studied. So, the goal of this research is to determine the role of LINC01087 in gliomas and to provide potential targets for clinical treatment.
Methods: The gene expression was detected by quantitative reverse transcriptase polymerase chain reaction (QRT-PCR) and Western blotting (WB). Cell proliferation was analyzed by CCK8 and colony formation test, and apoptosis was detected by flow cytometry. Luciferase report experiment and RNA Binding Protein Immunoprecipitation confirmed the interaction between LINC01087, miR-384 and Bcl-2. The effect of regulating LINC01087 on the growth of glioma was confirmed in vitro.
Results: The LINC01087 expression was up-regulated in clinical glioma samples (n = 35). Furthermore, LINC01087 silencing can obviously suppress the proliferation of glioma cells and induce apoptosis. Mechanically, we found that LINC01087 was the molecular sponge of miR-384. LINC01087 could inhibit the miR-384 expression and boost the Bcl-2 expression through sponge expression of miR-384. The repair of Bcl-2 effectively saved the proliferation and apoptosis of glioma cells lacking LINC01087.
Conclusion: LINC01087 is highly expressed in glioma and can participate in the growth of glioma through miR-384/Bcl-2 axis. So, it is a potential therapeutic target.