Response of CD44+/CD24-/low breast cancer stem/progenitor cells to tamoxifen-and doxorubicin-induced autophagy

Vildan Betul Yenigun, Bulent Ozpolat, Gamze Torun Kose

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

The cancer stem cell hypothesis emphasizes that cancers are driven by cells having stem cell properties, and it is believed that cancer stem cells (CSCs) may be responsible for resistance against therapeutic approaches and for recurrent tumors. Since the biology of the normal breast requires large numbers of stem cells, it has been thought that breast stem cells play an important role in initiating breast cancer. A better characterization of breast CSCs appears to be an essential step to improve the understanding of the biology of breast cancer and its management. The scope of this study was to isolate breast CSCs from a breast cancer cell line (MCF-7) using cell surface markers, and to test whether these cells have any resistance to autophagic cell death mechanisms mediated by commonly used chemotherapies and hormonal therapies such as doxorubicin (adriamycin) and tamoxifen (anti-estrogen), respectively. For this purpose, the CD44+/CD24-/lowMCF-7 breast cancer stem/progenitor cell population was isolated and treated with doxorubicin or tamoxifen and evaluated for their response to growth, autophagy and apoptosis. Our findings suggest that CD44+/CD24-/lowcells were less sensitive to doxorubicin, but did not demonstrate a significant difference towards tamoxifen in regards to the induction of autophagy.

Original languageEnglish (US)
Pages (from-to)1477-1483
Number of pages7
JournalInternational Journal of Molecular Medicine
Volume31
Issue number6
DOIs
StatePublished - Jun 2013

Keywords

  • Apoptosis
  • Autophagy
  • Breast cancer stem cells
  • Doxorubicin
  • Tamoxifen

ASJC Scopus subject areas

  • Genetics

Fingerprint

Dive into the research topics of 'Response of CD44+/CD24-/low breast cancer stem/progenitor cells to tamoxifen-and doxorubicin-induced autophagy'. Together they form a unique fingerprint.

Cite this