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Long non-coding RNA XIST exerts oncogenic functions in human glioma by targeting miR-137

Zong Wang1, Jiangwei Yuan2, Li Li1

  • 1Department of Neurosurgery, Zhumadian Central HospitalZhumadian 463000, P. R. China.

American Journal of Translational Research
|May 5, 2017
PubMed

Insights

Long non-coding RNA XIST is upregulated in glioma, promoting cell proliferation. It sponges miR-137, leading to increased Rac1 expression, suggesting XIST as a therapeutic target for glioma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long non-coding RNA XIST (X-inactive specific transcript) is implicated in tumor progression.
  • The role and regulatory mechanisms of XIST in glioma remain largely uncharacterized.

Purpose of the Study:

  • To investigate the expression and function of XIST in glioma.
  • To elucidate the molecular mechanism underlying XIST's role in glioma pathogenesis.

Main Methods:

  • Analysis of XIST and miR-137 expression in glioma tissues.
  • Cell proliferation assays.
  • Bioinformatics prediction and luciferase reporter assays to confirm direct binding.
  • Western blotting to assess protein expression.

Main Results:

  • XIST expression was significantly upregulated in glioma tissues and promoted glioma cell proliferation.
  • miR-137 expression was significantly decreased in glioma tissues.
  • XIST directly bound to and negatively regulated miR-137, acting as an endogenous sponge.
  • XIST upregulated Rac1 expression by sponging miR-137.
  • Rac1 inhibition or miR-137 overexpression suppressed XIST-induced glioma cell proliferation.

Conclusions:

  • A novel regulatory axis involving XIST, miR-137, and Rac1 in glioma pathogenesis was identified.
  • XIST acts as an oncogenic lncRNA in glioma by modulating the miR-137-Rac1 pathway.
  • XIST represents a potential therapeutic target for glioma treatment.
Keywords:
GliomaRac1XISTlong non-coding RNAmiR-137

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