miR-378a-3p modulates tamoxifen sensitivity in breast cancer MCF-7 cells through targeting GOLT1A

Kazuhiro Ikeda1, Kuniko Horie-Inoue1, Toshihide Ueno2

  • 1Division of Gene Regulation and Signal Transduction, Research Center for Genomic Medicine, Saitama Medical University, Saitama, Japan.

Scientific Reports
|August 11, 2015
PubMed

Insights

MicroRNAs like miR-378a-3p are crucial in breast cancer endocrine therapy resistance. Downregulation of miR-378a-3p and its target GOLT1A may drive resistance to tamoxifen, impacting patient prognosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Breast cancer is often hormone-dependent, treated with endocrine therapy.
  • Many breast cancers develop resistance to endocrine therapies like tamoxifen.
  • Understanding resistance mechanisms is vital for improving treatment outcomes.

Purpose of the Study:

  • To investigate microRNAs (miRNAs) associated with endocrine therapy resistance in breast cancer.
  • To identify specific miRNAs and their target genes involved in tamoxifen resistance.

Main Methods:

  • High-throughput miRNA sequencing on MCF-7 cells and resistant models (tamoxifen-resistant and long-term estrogen-deprived).
  • In silico analysis to predict miRNA targets.
  • Validation in clinical breast cancer tissues and cell growth assays.

Main Results:

  • miR-21 was highly expressed in all tested breast cancer cells.
  • miR-378a-3p was downregulated in resistant cells and tissues, correlating with poor tamoxifen treatment prognosis.
  • GOLT1A, a target of miR-378a-3p, was overexpressed and its inhibition slowed resistant cell growth.
  • Low GOLT1A levels predicted better patient survival.

Conclusions:

  • miR-378a-3p downregulation contributes to endocrine therapy resistance in breast cancer.
  • The miR-378a-3p/GOLT1A axis plays a role in tamoxifen resistance mechanisms.
  • Targeting the miR-378a-3p/GOLT1A pathway may offer new therapeutic strategies for resistant breast cancer.

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