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microRNA-155 regulates cell proliferation and invasion by targeting FOXO3a in glioma

Nan Ling1, Junyi Gu, Zhe Lei

  • 1Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou 215006, P.R. China.

Oncology Reports
|August 24, 2013
PubMed

Insights

MicroRNA-155 (miR-155) acts as an oncogene in glioma by inhibiting FOXO3a, promoting cell proliferation, migration, and invasiveness. This study elucidates miR-155's role in glioma tumorigenesis.

Area of Science:

  • Molecular Biology
  • Oncology
  • Gene Regulation

Background:

  • MicroRNAs (miRNAs) are key regulators of gene expression implicated in various cancers.
  • MicroRNA-155 (miR-155) has a dual role as an oncogene or tumor suppressor, with its function in glioma remaining unclear.
  • FOXO3a is a known negative regulator of Akt signaling, potentially interacting with miR-155.

Purpose of the Study:

  • To investigate the role of miR-155 in glioma tumorigenesis.
  • To determine the association between miR-155 and FOXO3a in glioma.
  • To elucidate the mechanism by which miR-155 influences glioma cell behavior.

Main Methods:

  • Analysis of miR-155 and FOXO3a expression in glioma cell lines and tissues.
  • Gain-of-function and loss-of-function experiments to assess miR-155's impact on cell proliferation, apoptosis, migration, and invasion.
  • Luciferase reporter assays to confirm direct targeting of FOXO3a by miR-155 at the 3'-UTR.

Main Results:

  • miR-155 was significantly upregulated, while FOXO3a was downregulated in glioma samples.
  • Overexpression of miR-155 promoted glioma cell proliferation, inhibited apoptosis, and enhanced migration and invasion.
  • miR-155 directly targets the 3'-UTR of FOXO3a, leading to its downregulation.

Conclusions:

  • miR-155 functions as an oncogene in glioma development and progression.
  • The oncogenic role of miR-155 in glioma is mediated through the downregulation of its target gene, FOXO3a.
  • Targeting miR-155 may represent a potential therapeutic strategy for glioma.

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