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LINC01096 knockdown inhibits progression of triple-negative breast cancer by increasing miR-3130-3p

G-P Wang1, Z-L Mou, Y-Y Xu

  • 1Department of Central Laboratory, the Rizhao People's Hospital Affiliated to Jining Medical University, Rizhao, Shandong, China. wgprzph93@126.com.

European Review for Medical and Pharmacological Sciences
|September 21, 2019
PubMed
Abstract

Insights

Reducing LINC01096 levels inhibits triple-negative breast cancer (TNBC) progression and promotes apoptosis. This suggests LINC01096 is a potential therapeutic target for TNBC by modulating miR-3130-3p.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with limited targeted therapies.
  • Long noncoding RNAs (lncRNAs) play emerging roles in TNBC development and progression.
  • The specific function and mechanism of LINC01096 in TNBC remain largely uncharacterized.

Purpose of the Study:

  • To investigate the role of LINC01096 in TNBC cell behavior, including viability, apoptosis, migration, and invasion.
  • To elucidate the underlying mechanism of LINC01096 action in TNBC.
  • To explore the interaction between LINC01096 and microRNA (miR)-3130-3p in TNBC.

Main Methods:

  • Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) to assess LINC01096 and miR-3130-3p expression in 60 TNBC patients and cell lines (T47-D, BT-549).
  • In vitro assays including MTT, flow cytometry, and trans-well assays to evaluate cell viability, apoptosis, migration, and invasion.
  • Luciferase reporter assay to confirm the direct targeting relationship between LINC01096 and miR-3130-3p.

Main Results:

  • LINC01096 expression was significantly upregulated in TNBC tissues and cells, correlating with poor patient outcomes.
  • Silencing LINC01096 suppressed TNBC cell viability, migration, and invasion, while inducing apoptosis.
  • LINC01096 directly targets and downregulates miR-3130-3p, which itself exhibits tumor-suppressive functions in TNBC.

Conclusions:

  • LINC01096 knockdown inhibits TNBC cell viability, migration, and invasion by upregulating miR-3130-3p.
  • This study identifies a novel regulatory axis (LINC01096/miR-3130-3p) with therapeutic implications for TNBC.
  • LINC01096 represents a potential novel therapeutic target for the treatment of triple-negative breast cancer.

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