lncRNA MEG3 inhibits pituitary tumor development by participating in cell proliferation, apoptosis and EMT processes
Open accessAbstract
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.
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In melanoma and pituitary tumors, miR-23a binds to lncRNA Malat1 and MEG3.
“in melanoma and pituitary tumors, miR-23a binds to lncRNA Malat1 and MEG3.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [101]
The Results section identifies miR-23b-3p—not miR-23a—as the molecule that binds MEG3 in the pituitary-tumor study, citing a luciferase reporter assay and RNA pull-down assay. The passages do not address binding to MALAT1 in melanoma. (LLM, conf=0.86)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredDownregulation of Malat1 or MEG3 leads to an increase in miR-23a levels, consequently promoting tumor cell proliferation, migration, and invasion.
“A downregulation of Malat1 or MEG3 leads to an increase in miR-23a levels, consequently promoting tumor cell proliferation, migration, and invasion [100,101].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [101]
The Results (page not provided) report that MEG3 knockdown increased proliferation, migration and invasion in pituitary tumor cells, and that inhibiting miR-23b-3p rescued those effects. The paper identifies the regulated microRNA as miR-23b-3p, not the claimed miR-23a; it does not study MALAT1. (LLM, conf=0.90)
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- Authors
- Wang, X., Li, X., & Wang, Z.
- Affiliations
- Soochow University (CN)
- Nantong University (CN)
- Corresponding author
- Li, Xiangdong
- Venue
- Oncology Reports
- Publisher
- Spandidos Publications
- Published
- 2021-02-23
- Volume
- 45
- Issue
- 4
- ISSN
- 1021-335X (ISSN-L)
- 1791-2431
- PMC
- PMC7934213
- OpenAlex
- W3133384705
- Cited by
- 24
- References
- 46
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 6 · 2023: 3 · 2022: 5 · 2021: 2
- FWCI
- 1.59
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- Oncology Reports (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pituitary Gland Disorders and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Keywords
- MEG3, long non-coding RNA, miR-23b-3p, FOXO4, epithelial-mesenchymal transition, cell proliferation, apoptosis, tumor cell migration and invasion, lncRNA-miRNA interaction, tumor suppressor, therapeutic target, GH3 cells, MMQ cells
- MeSH terms
- Adult, Aged, Female, Humans, Male, Middle Aged, Pituitary Gland, Pituitary Neoplasms, Gene Expression Regulation, Neoplastic, Apoptosis, Cell Cycle Proteins, MicroRNAs, Cell Line, Tumor, Cell Proliferation, Forkhead Transcription Factors, Epithelial-Mesenchymal Transition, RNA, Long Noncoding, Carcinogenesis
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