HOXD Antisense Growth-Associated Long Noncoding RNA Promotes Triple-Negative Breast Cancer Progression by Activating

Chenguang Zhang1, Ying Yang2, Lina Yi3

  • 1Department of Breast Surgery, The Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.

Abstract

Insights

HOXD antisense growth-associated long noncoding RNA (HAGLR) promotes triple-negative breast cancer (TNBC) progression by activating the Wnt pathway. Inhibiting HAGLR suppressed TNBC cell growth and invasion, offering a potential therapeutic target.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with limited therapeutic options.
  • Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.
  • HOXD antisense growth-associated long noncoding RNA (HAGLR) has been implicated in various cancers.

Purpose of the Study:

  • To investigate the role and mechanism of HAGLR in triple-negative breast cancer (TNBC).
  • To explore the potential of HAGLR as a therapeutic target for TNBC.

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) for RNA expression analysis.
  • In vitro functional assays to assess TNBC cell proliferation, migration, invasion, and apoptosis.
  • Molecular assays including MS2-RNA immunoprecipitation, luciferase reporter assays, and RNA pull-down assays to determine molecular interactions.

Main Results:

  • HAGLR expression is significantly upregulated in TNBC tissues and cells.
  • Inhibition of HAGLR suppresses TNBC cell proliferation, migration, and invasion, while promoting apoptosis.
  • HAGLR acts as a molecular sponge for miR-93-5p, leading to the upregulation of serine- and arginine-rich splicing factor 1 (SRSF1).
  • The HAGLR/miR-93-5p/SRSF1 axis activates the Wnt signaling pathway, thereby promoting TNBC progression.

Conclusions:

  • HAGLR promotes TNBC progression via the miR-93-5p/SRSF1 axis by activating the Wnt signaling pathway.
  • Targeting HAGLR represents a potential therapeutic strategy for triple-negative breast cancer.

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