English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

OBJECTIVE  To date, long noncoding RNAs (lncRNAs) have proven to function as key regulators in tumorigenesis. Among these lncRNAs,  MEG3  displays low levels in various neoplasms and tumor cell lines. However, the regulatory mechanism of  MEG3  and  MIR-376B-3P , one of the microRNAs from downstream gene clusters of the  DLK1-MEG3  locus, remains insufficiently defined.    METHODS  The authors used quantitative real-time polymerase chain reaction analysis to analyze whether decreased  MEG3  and  MIR-376B-3P  expression levels were associated with the invasiveness of clinical nonfunctioning pituitary adenomas (CNFPAs) in 30 patients. Furthermore, functional experiments unveiled the pathophysiological role of  MEG3 ,  MIR-376B-3P , and  HMGA2  in pituitary-derived folliculostellate (PDFS) cell lines. Moreover, dual-luciferase reporter assay, Western blot analysis, and immunofluorescence were applied to reveal the correlations among  MEG3 ,  MIR-376B-3P , and  HMGA2 .    RESULTS   MEG3  and  MIR-376B-3P  were decreased in patients with CNFPA, and their transcriptional levels were highly associated with invasive CNFPAs. Moreover, excessive expression of  MEG3  and  MIR-376B-3P  inhibited tumorigenesis and promoted apoptosis in PDFS cells. Importantly, the authors found that  MEG3  acted as an enhancer of  MIR-376B-3P  expression. Furthermore, as a target gene of  MIR-376B-3P ,  HMGA2  served as an oncogene in pituitary adenoma and could be negatively regulated by  MEG3  via enriching  MIR-376B-3P .    CONCLUSIONS  This study offers a novel mechanism of an  MEG3/MIR-376B-3P/HMGA2  regulatory network in CNFPAs, which may become a breakthrough for anticancer treatments.

MEG3/MIR-376B-3P/HMGA2 axis is involved in pituitary tumor invasiveness