Long non-coding RNA SNHG8 enhances triple-negative breast cancer cell proliferation and migration by regulating the

Jintao Qian1, Xinhan Lei1, Yue Sun1

  • 1Department of General Surgery, the Second Affiliated Hospital of Anhui Medical University, Hefei, 230601, Anhui, China.

Biology Direct
|August 7, 2021
PubMed
Abstract

Insights

Long non-coding RNA SNHG8 promotes triple-negative breast cancer (TNBC) cell proliferation and migration. It does so by interacting with miR-335-5p and PYGO2, highlighting a potential therapeutic target for TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) are increasingly recognized as critical regulators in cancer development.
  • Triple-negative breast cancer (TNBC) is an aggressive subtype with limited targeted therapies.
  • The specific role of lncRNA small nucleolar RNA host gene 8 (SNHG8) in TNBC remains largely unexplored.

Purpose of the Study:

  • To investigate the functional role of SNHG8 in the proliferation and migration of TNBC cells.
  • To elucidate the molecular mechanism underlying SNHG8's function in TNBC.

Main Methods:

  • Quantitative reverse transcription PCR (RT-qPCR) to assess SNHG8 expression.
  • Cell proliferation assays (EdU, colony formation) and migration assays (Transwell).
  • Western blot for epithelial-mesenchymal transition (EMT) markers, and molecular interaction studies (RIP, RNA pull down, luciferase reporter assays).

Main Results:

  • SNHG8 expression was significantly upregulated in TNBC cells.
  • SNHG8 knockdown inhibited TNBC cell proliferation, migration, and EMT.
  • SNHG8 functioned as a molecular sponge for miR-335-5p, and PYGO2 was identified as a target of miR-335-5p.

Conclusions:

  • SNHG8 promotes TNBC cell proliferation, migration, and EMT.
  • The SNHG8/miR-335-5p/PYGO2 axis is a key pathway driving TNBC progression.
  • Targeting the SNHG8/miR-335-5p/PYGO2 axis may offer a novel therapeutic strategy for TNBC.

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