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Long non-coding RNA AGAP2-AS1 exerts oncogenic properties in glioblastoma by epigenetically silencing TFPI2 through

Wenzheng Luo1, Xueyuan Li1, Zhenyu Song1

  • 1Department of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, P.R. China.

Aging
|June 13, 2019
PubMed

Insights

Long non-coding RNA AGAP2-AS1 promotes glioblastoma (GBM) growth by silencing TFPI2. Targeting AGAP2-AS1 offers a potential therapeutic strategy for GBM patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Long non-coding RNAs (LncRNAs) play critical roles in cancer development.
  • AGAP2-AS1 is implicated as an oncogene in various cancers, including glioblastoma (GBM).
  • The precise mechanisms of AGAP2-AS1 in GBM progression remain largely unknown.

Purpose of the Study:

  • To investigate the role and underlying mechanisms of AGAP2-AS1 in glioblastoma.
  • To explore the relationship between AGAP2-AS1, TFPI2, and GBM progression.
  • To evaluate AGAP2-AS1 as a potential therapeutic target for GBM.

Main Methods:

  • Analysis of AGAP2-AS1 expression in GBM tissues and cells.
  • Functional assays (proliferation, invasion, apoptosis) upon AGAP2-AS1 manipulation.
  • Investigation of molecular interactions involving AGAP2-AS1, EZH2, and LSD1.
  • Assessment of TFPI2's role in GBM and its regulation by AGAP2-AS1.
  • In vivo tumor growth experiments in a GBM model.

Main Results:

  • AGAP2-AS1 expression is upregulated in GBM and correlates with poor prognosis.
  • Silencing AGAP2-AS1 inhibits GBM cell proliferation and invasion while promoting apoptosis.
  • AGAP2-AS1 recruits EZH2 and LSD1 to suppress TFPI2 transcription.
  • TFPI2 overexpression exhibits tumor-suppressive effects in GBM.
  • AGAP2-AS1 knockdown inhibits GBM tumor growth in vivo.

Conclusions:

  • AGAP2-AS1 functions as an oncogene in GBM by epigenetically silencing TFPI2 via EZH2 and LSD1.
  • This study elucidates a novel mechanism for AGAP2-AS1 in GBM pathogenesis.
  • AGAP2-AS1 represents a promising therapeutic target for glioblastoma treatment.
Keywords:
AGAP2-AS1EZH2TFPI2glioblastomalncRNA

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