MiR-31 inhibits migration and invasion by targeting SATB2 in triple negative breast cancer

Long-Ji Luo1, Fan Yang1, Jia-Ji Ding1

  • 1Xuzhou Medical University, Xuzhou 221004, China; Department of General Surgery, Nanjing Medical University Affiliated Cancer Hospital Cancer Institute of Jiangsu Province, Baiziting 42, Nanjing 210009, China.

Gene
|September 6, 2016
PubMed

Insights

MicroRNA-31 (miR-31) suppresses triple-negative breast cancer (TNBC) metastasis by targeting SATB2. Restoring miR-31 inhibits cancer cell migration and invasion, highlighting its therapeutic potential.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Metastasis is the primary cause of breast cancer mortality.
  • Triple-negative breast cancer (TNBC) exhibits aggressive behavior and poor prognosis.
  • MicroRNAs (miRNAs) play crucial roles in tumor invasion and metastasis.

Purpose of the Study:

  • Investigate the mechanism by which miR-31 suppresses metastasis in breast cancer.
  • Determine the relationship between miR-31 and Special AT-rich sequence-binding protein-2 (SATB2) in breast cancer.

Main Methods:

  • Assessed miR-31 expression in TNBC tissues and cell lines.
  • Utilized 5-aza-2'-deoxycytidine (5-AZA-CdR) to modulate miR-31 expression.
  • Performed cell migration, invasion, and proliferation assays.
  • Conducted SATB2 silencing experiments.
  • Employed luciferase reporter assays to confirm direct targeting.

Main Results:

  • miR-31 was downregulated in TNBC.
  • Upregulating miR-31 inhibited MDA-MB-231 cell migration and invasion.
  • Downregulating miR-31 promoted MCF-7 cell migration and invasion.
  • SATB2 expression was negatively correlated with miR-31 and upregulated in breast cancer cells.
  • Silencing SATB2 reduced breast cancer cell proliferation, migration, and invasion.
  • SATB2 was identified as a direct target of miR-31.

Conclusions:

  • miR-31 acts as a metastasis suppressor in breast cancer.
  • miR-31 inhibits TNBC cell migration and invasion by downregulating SATB2 expression.
  • Targeting the miR-31/SATB2 axis presents a potential therapeutic strategy for TNBC.