LINC01232 regulates miR-516a-5p/BCL9 axis to promote triple-negative breast cancer progression

Wei Liu1, Yunfeng Niu2, Jie An3

  • 1Department of General Surgery, Bethune International Peace Hospital, No. 398 Zhongshan West Road, Qiaoxi District, Shijiazhuang, Hebei, China. liuweihpyy2023@163.com.

Insights

Triple-negative breast cancer (TNBC) involves high LINC01232 levels. Inhibiting this long non-coding RNA (lncRNA) reduces TNBC cell growth and spread by affecting the miR-516a-5p/BCL9 pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Triple-negative breast cancer (TNBC) lacks targeted therapies and has a poor prognosis.
  • The role of long non-coding RNAs (lncRNAs) in TNBC pathogenesis is an area of active investigation.
  • Identifying novel molecular pathways is crucial for developing effective TNBC treatments.

Purpose of the Study:

  • To investigate the function of the lncRNA LINC01232 in TNBC.
  • To elucidate the regulatory mechanism of LINC01232 involving the miR-516a-5p/BCL9 pathway.
  • To assess LINC01232 as a potential therapeutic target for TNBC.

Main Methods:

  • Quantitative reverse transcription polymerase chain reaction (qRT-PCR) to measure LINC01232 expression in TNBC tissues.
  • Luciferase reporter assays and cellular function tests to analyze the interaction between LINC01232, miR-516a-5p, and BCL9.
  • In vitro experiments evaluating the impact of LINC01232 silencing on TNBC cell proliferation, migration, and invasion.

Main Results:

  • LINC01232 expression was significantly upregulated in TNBC tissues compared to normal tissues.
  • Silencing LINC01232 inhibited proliferation, colony formation, migration, and invasion of breast cancer cells.
  • LINC01232 acts as a competing endogenous RNA (ceRNA) for miR-516a-5p, leading to increased BCL9 expression.

Conclusions:

  • LINC01232 promotes TNBC malignant progression via the miR-516a-5p/BCL9 pathway.
  • LINC01232 represents a potential diagnostic biomarker and therapeutic target for TNBC.
  • This study offers new insights into the molecular mechanisms underlying TNBC development.

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