lncRNA MEG3 inhibits pituitary tumor development by participating in cell proliferation, apoptosis and EMT processes
- Xuejian Wang
- Xiangdong Li
- Zhifeng Wang
Affiliations: Department of Neurosurgery, First Affiliated Hospital of Soochow University, Soochow University, Soochow, Jiangsu 225000, P.R. China, Department of Neurosurgery, Affiliated Hospital 2 of Nantong University, Nantong University, Nantong, Jiangsu 226000, P.R. China
- Published online on: February 23, 2021 https://doi.org/10.3892/or.2021.7991
Copyright: © Wang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Pituitary tumors do not pose a threat to life but can cause visual disturbances and serious clinical syndromes, such as infertility and metabolic syndrome. Therefore, screening of key genes involved in the occurrence and development of pituitary tumors can provide new targets for the treatment of pituitary tumors. The aim of the present study was to investigate the molecular mechanism of long non‑coding (lnc.) RNA maternally expressed 3 (MEG3) in cell proliferation, apoptosis and epithelial‑mesenchymal transition (EMT) processes of pituitary tumor. Tissue samples were obtained from 34 patients who underwent surgical treatment of pituitary tumors. Pituitary tumor cells (GH3 and MMQ) were transfected with pcDNA3.1(+)‑MEG3, short hairpin (sh)MEG3, microRNA (miR)‑23‑3p inhibitor or their controls using Lipofectamine® 2000. Reverse transcription‑quantitative PCR and western blot analyses were used to detect the levels of MEG3, miR‑23b‑3p and FOXO4, as well as proliferation‑, apoptosis‑ and EMT‑associated genes and proteins. Cell Counting Kit‑8 and flow cytometry assays were performed to detect proliferation and apoptosis, and Transwell assay was undertaken to assess invasion and migration. Luciferase reporter and RNA pulldown assays were performed to verify the binding between lncRNA MEG3, miR‑23b‑3p and FOXO4. Pearson's correlation analysis was used to analyze the correlation between expression levels of MEG3, miR‑23b‑3p and FOXO4. lncRNA MEG3 was expressed at lower levels in pituitary tumor tissues and cells. Overexpression of lncRNA MEG3 inhibited proliferation, invasion and migration and accelerated apoptosis of pituitary tumor cells. lncRNA MEG3 negatively regulated miR‑23b‑3p expression levels, while miR‑23b‑3p negatively regulated FOXO4 expression levels. Overexpression of lncRNA MEG3 inhibited the EMT process in pituitary tumor cells. miR‑23‑3p inhibitor rescued the effect of shMEG3 on proliferation, invasion, migration, apoptosis and the EMT process in pituitary tumor cells. lncRNA MEG3 inhibited pituitary tumor development by participating in cell proliferation, apoptosis and the EMT process, which may present a novel target for pituitary tumor treatment.