ETS1-activated SNHG10 exerts oncogenic functions in glioma via targeting miR-532-3p/FBXL19 axis

Lide Jin1, Shengquan Huang1, Congjin Guan2

  • 1The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, No.157 Jinbi Road, Kunming, 650032, Yunnan, China.

Cancer Cell International
|December 10, 2020
PubMed
Abstract

Insights

Long non-coding RNA SNHG10 promotes glioma progression by activating FBXL19 through sponging miR-532-3p. This oncogenic role is transcriptionally regulated by ETS1, highlighting a novel therapeutic target for glioma.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their regulatory roles in cancer progression.
  • LncRNA SNHG10 has been implicated in various cancers, but its specific function and mechanism in glioma remain unclear.

Purpose of the Study:

  • To elucidate the role and underlying mechanism of lncRNA SNHG10 in glioma.
  • To investigate the regulatory pathway involving SNHG10, miR-532-3p, and FBXL19 in glioma progression.

Main Methods:

  • Gene expression analysis using RT-qPCR.
  • Functional assays including EdU, TUNEL, sphere formation, wound healing, and Transwell assays.
  • Molecular interaction studies employing ChIP, RIP, RNA pull-down, and luciferase reporter assays.

Main Results:

  • SNHG10 expression is elevated in glioma cells and promotes proliferation, migration, invasion, and stemness.
  • SNHG10 sponges miR-532-3p, which normally inhibits glioma cell growth and stemness by targeting FBXL19.
  • ETS1 transcriptionally activates SNHG10, establishing the SNHG10/miR-532-3p/FBXL19 signaling axis in mediating glioma malignancy.

Conclusions:

  • SNHG10 acts as an oncogene in glioma, driven by ETS1-mediated transcriptional activation.
  • The SNHG10/miR-532-3p/FBXL19 pathway is crucial for glioma cell growth and stemness.
  • Targeting this pathway presents a potential therapeutic strategy for glioma.

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