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Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples
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miR-200c suppresses stemness and increases cellular sensitivity to trastuzumab in HER2+ breast cancer

Hailin Tang1, Cailu Song1, Feng Ye1

  • 1State Key Laboratory of Oncology in South China, Department of Breast Oncology, Collaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.

Journal of Cellular and Molecular Medicine
|October 11, 2019
PubMed

Insights

MicroRNA-200c (miR-200c) can overcome trastuzumab resistance in HER2-positive breast cancer. Enhancing miR-200c levels reduces cancer stem cell traits and improves drug sensitivity.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Trastuzumab resistance is a significant challenge in treating HER2-overexpressing breast cancer.
  • MicroRNA-200c (miR-200c) is implicated in cancer stem cell (CSC) functions, including tumor recurrence, metastasis, and drug resistance.

Purpose of the Study:

  • To investigate the role of miR-200c in trastuzumab resistance and cancer stemness maintenance in HER2-overexpressing breast cancer.
  • To evaluate the therapeutic potential of miR-200c in combination with trastuzumab.

Main Methods:

  • Utilized HER2-positive (SKBR3) and HER2-negative (MCF-7) breast cancer cell lines and their CD44+ CD24- mammosphere-derived stem cells (SKBR3-S, MCF-7-S).
  • Assessed miR-200c expression, tumor sphere formation, CSC population, proliferation, apoptosis, and in vivo tumor progression.
  • Investigated the effect of miR-200c overexpression alone and in combination with trastuzumab.

Main Results:

  • miR-200c expression was low in breast cancer cell lines and their stem cell populations.
  • Overexpression of miR-200c significantly reduced tumor sphere formation and CSC populations in SKBR3-S cells.
  • Combined miR-200c and trastuzumab treatment decreased proliferation and increased apoptosis in SKBR3 and SKBR3-S cells.
  • miR-200c overexpression improved malignant progression in vivo and reduced downstream target genes associated with breast cancer progression.

Conclusions:

  • miR-200c plays a crucial role in maintaining the cancer stem cell-like phenotype.
  • Overexpression of miR-200c enhances drug sensitivity to trastuzumab in HER2-positive breast cancer cells and stem cells.
  • miR-200c represents a potential therapeutic target for overcoming trastuzumab resistance in HER2+ breast cancer.
Keywords:
CD44+CD24− phenotypeHER2breast cancermiR-200cstem celltrastuzumab

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