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LncRNA MCM3AP-AS1 promotes chemoresistance in triple-negative breast cancer through the miR-524-5p/RBM39 axis

Yueping Wang1,2, Xuedong Wang3, Haiyi Sun4

  • 1Department of Medical Laboratory Science, Anhui No. 2 Provincial People's Hospital, 1868 #Dangshan Road, North 2nd Ring, Hefei, 230041, Anhui, China.

Molecular and Cellular Biochemistry
|March 13, 2024
PubMed

Insights

Triple-negative breast cancer (TNBC) chemoresistance can be overcome by targeting MCM3AP-AS1. Silencing MCM3AP-AS1 enhances apoptosis and chemosensitivity in drug-resistant TNBC cells by upregulating miR-524-5p and downregulating RBM39.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with poor treatment outcomes.
  • Long non-coding RNA MCM3AP-AS1 has been implicated in breast cancer development.
  • Understanding mechanisms of chemoresistance in TNBC is crucial for improving patient survival.

Purpose of the Study:

  • To investigate the role of MCM3AP-AS1 in the chemoresistance of triple-negative breast cancer cells.
  • To elucidate the molecular mechanisms underlying MCM3AP-AS1's action in TNBC chemoresistance.

Main Methods:

  • Construction of doxorubicin/docetaxel-resistant TNBC cell lines (SUM159PTR, MDA-MB-231R).
  • Quantification of MCM3AP-AS1, miR-524-5p, and RBM39 expression using RT-qPCR and Western blot.
  • Assessment of cell viability and apoptosis via CCK-8 assay and flow cytometry.
  • Validation of molecular interactions using dual-luciferase assays and in vivo xenograft models.

Main Results:

  • MCM3AP-AS1 was significantly upregulated in drug-resistant TNBC cells.
  • Silencing MCM3AP-AS1 sensitized resistant cells to chemotherapy, promoting apoptosis.
  • MCM3AP-AS1 directly targets miR-524-5p, which in turn targets RBM39.
  • The MCM3AP-AS1/miR-524-5p/RBM39 axis was identified as a key regulator of chemoresistance and apoptosis in TNBC.

Conclusions:

  • MCM3AP-AS1 silencing enhances chemosensitivity in drug-resistant TNBC cells.
  • This effect is mediated by the upregulation of miR-524-5p and downregulation of RBM39, leading to increased apoptosis.
  • Targeting MCM3AP-AS1 represents a potential therapeutic strategy to overcome chemoresistance in TNBC.
Keywords:
ApoptosisChemoresistanceDoxorubicin/docetaxelMCM3AP-AS1RNA binding motif 39Triple-negative breast cancerceRNAmiR-524-5p

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