Long Non-Coding RNA MEG3 Modifies Cell-Cycle, Migration, Invasion, and Proliferation Through AKAP12 by Sponging miR-29c in Meningioma Cells

Abstract

Meningioma (MEN) is a common central nervous system disease. Accumulating evidence indicated that long non-coding RNA maternally expressed gene 3 (MEG3) participated in the progression of MEN. However, the potential mechanisms of MEG3 in altering the aggressive phenotypes of MEN need further exploration. Levels of MEG3, microRNA (miR)-29c, and A-kinase anchor protein 12 (AKAP12) were determined using quantitative real-time Polymerase Chain Reaction (qRT-PCR) assay. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to verify the relationship between miR-29c and MEG3 or AKAP12. The protein level of AKAP12 was detected by western blot. Moreover, cell-cycle arrest, migration, invasion, and proliferation were assessed by flow cytometry, wound healing, transwell assays, and CCK-8 assay, respectively. Levels of MEG3 and AKAP12 were downregulated, while miR-29c was effectively increased in MEN tissues and cell line. Mechanically, MEG3 was a sponge of miR-29c to regulate the expression of AKAP12. Functionally, increase of MEG3 diminished cell-cycle, migration, invasion, and proliferation in MEN cells, and reintroduction of miR-29c could eliminate these effects. In addition, AKAP12 depletion overturned the inhibitory effects of miR-29c absence on cell-cycle, migration, invasion, and proliferation in vitro . Also, AKAP12 was co-regulated by MEG3/miR-29c axis. MEG3 mediated the aggressive behaviors of MEN cells via miR-29c/AKAP12 axis, supporting that MEG3 served as a promising biomarker for the diagnosis and treatment of human MEN.

Evolving Landscape of Long Non-coding RNAs in Cerebrospinal Fluid: A Key Role From Diagnosis to Therapy in Brain Tumors

“…MEG3, an imprinted gene located at 14q32, can encode non-coding RNAs with antiproliferative functions ( Ghafouri-Fard and Taheri, 2019 ). Ding et al (2020) confirmed that lncRNA MEG3 mediated the invasive behavior of meningioma cells through the miR-29c/AKAP12 axis. The upregulation in miR-29c levels can eliminate the adverse effects caused by MEG3 expression on the cell cycle, migration, invasion, and proliferation of meningioma cells ( Ding et al, 2020 ).…”

“… Ding et al (2020) confirmed that lncRNA MEG3 mediated the invasive behavior of meningioma cells through the miR-29c/AKAP12 axis. The upregulation in miR-29c levels can eliminate the adverse effects caused by MEG3 expression on the cell cycle, migration, invasion, and proliferation of meningioma cells ( Ding et al, 2020 ). Zhang et al (2010) also demonstrated that MEG3 mRNA was highly expressed in normal arachnoid cells but was lost in human meningioma cells, and there was a strong association between the loss of MEG3 expression and tumor grade.…”

Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism

“…In the aspects of the regulatory mechanism of MEG3, miR-29 c was a sponge of MEG3. A previous investigation indicates MEG3 modulates cell proliferation by sponging miR-29 c in meningioma, pinpointing the regulatory relationship between MEG3 and miR-29 c again [ 38 ]. Lessened miR-29 c was found in the patients with severe pneumonia and LPS-steered cell models.…”

LncRNA H19: A novel oncogene in multiple cancers

“…LncRNAs can function as oncogenes or tumor suppressor genes, and thus are involved in the occurrence and development of many different tumor types. Several lncRNAs are potential diagnostic and/or prognostic biomarkers including lncRNA HOTAIR 174 , lncRNA MALAT1 175 , lncRNA MEG3 176 , lncRNA PVT1 177 , lncRNA XIST 178 , and H19 27 . Although H19 is one of the most studied lncRNAs, many molecular mechanisms remain unelucidated.…”