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Crosstalk between Meg3 and miR-1297 regulates growth of testicular germ cell tumor through PTEN/PI3K/AKT pathway

Nian-Qin Yang1, Xiao-Jin Luo2, Jian Zhang1

  • 1Department of Urology, Zhongshan Hospital, Fudan University Shanghai 200032, China.

American Journal of Translational Research
|May 10, 2016
PubMed

Insights

Maternally Expressed Gene 3 (Meg3) long non-coding RNA and miR-1297 crosstalk regulates testicular germ cell tumor (TGCT) growth via the PTEN/PI3K/AKT pathway. Meg3 re-expression offers a potential TGCT therapeutic strategy.

Area of Science:

  • Molecular Biology
  • Oncology
  • Gene Regulation

Background:

  • Maternally Expressed Gene 3 (Meg3) long non-coding RNA (lncRNA) is implicated in tumorigenesis.
  • MicroRNA-1297 (miR-1297) may regulate the PTEN/PI3K/Akt pathway in testicular germ cell tumors (TGCT).
  • The interaction between Meg3 and miR-1297 in TGCT remains unexplored.

Purpose of the Study:

  • To investigate the crosstalk between Meg3 and miR-1297 in TGCT.
  • To elucidate the regulatory mechanism of Meg3 and miR-1297 on the PTEN/PI3K/Akt pathway in TGCT.
  • To assess the therapeutic potential of Meg3 re-expression in TGCT.

Main Methods:

  • Quantitative analysis of Meg3, miR-1297, and PTEN levels in TGCT and adjacent non-tumor tissues.
  • Bioinformatic prediction of binding sites between miR-1297, Meg3, and PTEN mRNA.
  • Luciferase reporter assays and double fluorescent in situ hybridization to confirm interactions.
  • Assessment of cell growth and signaling pathway activation following Meg3 overexpression.

Main Results:

  • Meg3 levels were significantly decreased in TGCT, while miR-1297 levels were unchanged.
  • PTEN protein levels were significantly reduced in TGCT, correlating with decreased Meg3.
  • Meg3 overexpression abolished miR-1297's effects on PTEN and inhibited TGCT cell growth by deactivating the Akt pathway, suggesting competitive binding.
  • Co-localization of Meg3 and miR-1297 was observed in TGCT cells.

Conclusions:

  • A novel pathway involving Meg3 and miR-1297 crosstalk regulating TGCT growth through the PTEN/PI3K/AKT signaling pathway has been identified.
  • Meg3 acts as a tumor suppressor by competitively binding with miR-1297, thereby preventing miR-1297-mediated PTEN downregulation.
  • Re-expression of Meg3 presents a promising therapeutic strategy for TGCT.
Keywords:
Maternally Expressed Gene 3 (Meg3)PTEN/PI3K/AKTTesticular germ cell tumor (TGCT)miR-1297

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