Long non-coding RNA FGF14-AS2 represses proliferation, migration, invasion, and induces apoptosis in breast cancer by

Y Yang1, N Xun, J-G Wu

  • 1Department of Pathology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China. ftjaxh@163.com.

Abstract

Insights

Long noncoding RNA FGF14 antisense RNA 2 (FGF14-AS2) directly interacts with miR-205-5p. This interaction suppresses breast cancer cell proliferation, migration, and invasion, while promoting apoptosis, offering a potential therapeutic strategy.

Area of Science:

  • Molecular Oncology
  • Genetics
  • Biochemistry

Background:

  • Breast cancer exhibits significant heterogeneity, complicating patient stratification and treatment.
  • The role of long noncoding RNA FGF14 antisense RNA 2 (FGF14-AS2) in breast cancer progression and prognosis is recognized, but its molecular mechanisms remain largely unexplored.

Purpose of the Study:

  • To investigate the molecular mechanism of FGF14-AS2 in breast cancer.
  • To explore the interaction between FGF14-AS2 and miR-205-5p and its functional consequences.

Main Methods:

  • Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) to assess FGF14-AS2 and miR-205-5p expression.
  • Cellular assays (MTT, Transwell, flow cytometry) to evaluate proliferation, migration, invasion, and apoptosis.
  • Bioinformatic prediction (DIANA-LncBase v2) and Dual-Luciferase Reporter Assay to confirm the interaction between FGF14-AS2 and miR-205-5p.

Main Results:

  • FGF14-AS2 was found to be downregulated, while miR-205-5p was upregulated in breast cancer tissues and cells, correlating with tumor stage and size.
  • Overexpression of FGF14-AS2 or knockdown of miR-205-5p inhibited breast cancer cell proliferation, migration, and invasion, and induced apoptosis.
  • FGF14-AS2 directly binds to miR-205-5p, and this interaction antagonizes the effects of miR-205-5p on cancer cell behavior.

Conclusions:

  • FGF14-AS2 directly interacts with miR-205-5p to suppress breast cancer proliferation, migration, and invasion, while inducing apoptosis.
  • This regulatory axis presents a potential therapeutic target for breast cancer treatment.

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