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Updated: Jan 19, 2026

Clinicopathological Analysis of miRNA Expression in Breast Cancer Tissues by Using miRNA In Situ Hybridization
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Clinicopathological Analysis of miRNA Expression in Breast Cancer Tissues by Using miRNA In Situ Hybridization

Published on: June 7, 2016

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Long noncoding RNA LINC00511 involves in breast cancer recurrence and radioresistance by regulating STXBP4 expression

L Liu1, Y Zhu, A-M Liu

  • 1Department of Nuclear Medicine, Affiliated Hospital of Southwest Medical University, Luzhou, China. chenyuebio@126.com.

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

Insights

Long intergenic noncoding RNA 00511 (LINC00511) is elevated in recurrent breast cancer, promoting tumor growth and reducing radiation sensitivity. Inhibiting LINC00511 enhances radiosensitivity by modulating the miR-185/STXBP4 axis, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Recurrent breast cancer after breast-conserving surgery and radiotherapy poses a significant clinical challenge.
  • Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in cancer progression and treatment response.

Purpose of the Study:

  • To investigate the molecular function of long intergenic noncoding RNA 00511 (LINC00511) in recurrent breast cancer.
  • To identify LINC00511's target proteins and its role in radiosensitivity after breast-conserving surgery and radiotherapy.

Main Methods:

  • Quantitative polymerase chain reaction (qPCR) to measure LINC00511 expression.
  • In vitro and in vivo experiments using short hairpin RNA (shRNA) to silence LINC00511 in breast cancer cell lines.
  • Bioinformatics analysis, dual luciferase reporter assays, qPCR, and Western blot to identify and validate microRNA (miRNA) targets.

Main Results:

  • LINC00511 expression was significantly higher in recurrent breast cancer tissues and correlated with poor survival.
  • LINC00511 knockdown suppressed tumor cell proliferation, induced apoptosis, and enhanced radiosensitivity in vitro and in vivo.
  • LINC00511 competitively binds to miR-185, upregulating syntaxin-binding protein 4 (STXBP4) expression and decreasing radiosensitivity.

Conclusions:

  • The LINC00511/miR-185/STXBP4 axis plays a crucial role in breast cancer progression and response to radiotherapy.
  • Inhibiting LINC00511 can improve radiosensitivity by restoring miR-185 function and reducing STXBP4 levels.
  • Targeting the LINC00511/miR-185/STXBP4 pathway represents a promising therapeutic strategy for enhancing breast cancer treatment outcomes.

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