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An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells
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MicroRNA-137 inhibits pituitary prolactinoma proliferation by targeting AKT2

Q Xu1, Z X Yu2, Y L Xie3,4

  • 1Department of Endocrinology, Xijing Hospital, Air Force Medical University, Xi'an, 710032, China.

Journal of Endocrinological Investigation
|November 25, 2022
PubMed
Abstract

Insights

MicroRNA-137 (miR-137) inhibits aggressive pituitary tumors by targeting AKT2. This finding offers a potential therapeutic strategy for aggressive prolactinomas, a common pituitary adenoma type.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Prolactinoma, the most common pituitary adenoma, often requires medical treatment, but aggressive forms necessitate surgery.
  • MicroRNAs (miRNAs) are implicated in tumorigenesis, invasion, and metastasis, acting as oncogenes or tumor suppressors.
  • Aberrant miRNA expression is linked to various cancers, including pituitary tumors.

Purpose of the Study:

  • To identify aggressiveness-associated microRNAs (miRNAs) in prolactinoma.
  • To elucidate the underlying molecular mechanisms of these miRNAs in pituitary tumor progression.
  • To explore potential therapeutic targets for aggressive prolactinoma.

Main Methods:

  • Bioinformatic analysis of miRNA expression profile (GSE46294) from the Gene Expression Omnibus (GEO) database.
  • Identification of differentially expressed miRNAs (DEMs) and analysis of their target genes using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment.
  • Experimental validation using RT-qPCR, western blot, CCK-8 assays, and double luciferase reporter assay to confirm the role of miR-137 targeting AKT2 in MMQ cell proliferation.

Main Results:

  • Twenty-four DEMs were identified, with fourteen upregulated and ten downregulated.
  • Target genes of downregulated DEMs were enriched in the PI3K-Akt pathway.
  • MiR-137 was confirmed to target AKT2, inhibiting MMQ cell proliferation.

Conclusions:

  • MiR-137 plays a suppressive role in the aggressive behavior of prolactinomas.
  • Targeting AKT2 by miR-137 represents a potential mechanism to inhibit prolactinoma cell proliferation.
  • MiR-137 may serve as a novel therapeutic target for aggressive prolactinoma.
Keywords:
Aggressive prolactinomasBioinformaticmicroRNAs

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