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Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
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MicroRNA-223 Targeting STIM1 Inhibits the Biological Behavior of Breast Cancer.

Yanfang Yang1, Zhansheng Jiang2, Ning Ma1

  • 1Second Department of Breast Cancer, Tianjin, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|February 8, 2018
PubMed
Summary
This summary is machine-generated.

MicroRNA-223 (miR-223) inhibits breast cancer cell proliferation and invasion by targeting stromal interaction molecule 1 (STIM1). The miR-223/STIM1 pathway presents a potential therapeutic target for breast cancer treatment.

Keywords:
Breast cancerInvasionMiR-223MicrornaProliferationStromal interaction molecule1

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Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • MicroRNA-223 (miR-223) dysregulation is implicated in various cancers.
  • Stromal interaction molecule 1 (STIM1) is a key regulator of calcium signaling, with roles in cancer progression.
  • The specific interaction and clinical significance of miR-223 targeting STIM1 in breast cancer remain to be fully elucidated.

Purpose of the Study:

  • To investigate the cellular effects of microRNA-223 (miR-223) in breast cancer.
  • To determine the clinical significance of the miR-223/STIM1 axis in breast cancer.
  • To explore STIM1 as a direct target of miR-223 in breast cancer cells.

Main Methods:

  • Utilized breast cancer cell lines and normal breast epithelial cells.
  • Employed miR-223 mimics, anti-miR-223, and STIM1 overexpression vectors for transfection.
  • Assessed gene and protein expression via RT-qPCR, Western blotting, and dual-luciferase reporter assays.
  • Evaluated cell proliferation and invasion using MTT and Trans-well assays.
  • Correlated miR-223 and STIM1 expression with clinical outcomes using in situ hybridization (ISH) and immunohistochemistry (IHC).

Main Results:

  • Breast cancer tissues and cells showed significantly lower miR-223 and higher STIM1 expression compared to normal counterparts.
  • miR-223 inhibited breast cancer cell proliferation and invasion by negatively regulating STIM1 expression.
  • Overexpression of STIM1 partially rescued the inhibitory effects of miR-223.
  • High STIM1 expression was detrimental, while high miR-223 expression was beneficial for disease-free survival (DFS).
  • STIM1 expression was inversely correlated with miR-223 expression in breast cancer specimens.

Conclusions:

  • miR-223 suppresses breast cancer cell proliferation and invasion through targeting STIM1.
  • The miR-223/STIM1 axis represents a potential therapeutic target for breast cancer.
  • This molecular axis holds promise for improving patient outcomes in breast cancer treatment.