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miR-221/222 overexpession in human glioblastoma increases invasiveness by targeting the protein phosphate PTPμ

C Quintavalle1, M Garofalo, C Zanca

  • 1Department of Cellular and Molecular Biology and Pathology, Federico II University of Naples, Naples, Italy.

Oncogene
|July 12, 2011
PubMed

Insights

MicroRNAs miR-221 and miR-222 promote glioma growth by downregulating PTPμ. Restoring PTPμ expression reverses these effects, suggesting a therapeutic target for glioblastoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Glioblastoma is a highly lethal adult brain cancer with poor patient survival.
  • MicroRNAs (miRs) are implicated in cancer development, but their specific roles in glioblastoma are not fully understood.

Purpose of the Study:

  • To identify microRNAs involved in glioma tumorigenesis.
  • To investigate the role of miR-221 and miR-222 in regulating glioblastoma cell behavior through their target, PTPμ.

Main Methods:

  • Differential microRNA expression profiling using miRarray in glioma and non-tumorigenic cells.
  • Validation of miR-221 and miR-222 targets using Western blot and real-time PCR.
  • Assessment of cell migration and growth in soft agar assays.
  • Analysis of miR-221, miR-222, and PTPμ expression in human glioma samples.

Main Results:

  • miR-221 and miR-222 were found to be differentially expressed in glioma cells.
  • Overexpression of miR-221 and miR-222 led to decreased PTPμ expression.
  • miR-221 and miR-222 promoted glioma cell migration and growth.
  • Re-expression of PTPμ reversed the pro-tumorigenic effects of miR-221 and miR-222.
  • An inverse correlation was observed between miR-221/miR-222 and PTPμ in human glioma tissues.

Conclusions:

  • miR-221 and miR-222 are key regulators of glioma tumorigenesis.
  • These miRs exert their effects, at least in part, by controlling PTPμ expression.
  • Targeting miR-221/miR-222 or PTPμ may offer a therapeutic strategy for glioblastoma.

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