Abstract
Breast tumours are heterogeneous, including cells with cancer stem cell properties and more differentiated tumour cells. As breast cancer stem cells are often resistant to chemotherapy, recent efforts have been focusing on treatments that may shift them towards a more differentiated phenotype, making them more susceptible to treatment. Here, we examined whether t cisplatin induces cell differentiation in four breast cancer cell lines that represent different types of breast tumours (BT549, MDA‐MB‐468, MDA‐MB‐231, MCF7). Cisplatin treatment of 20 μM reduced cell viability from 100% to 50–80%, depending on the cell line. Flow cytometric quantification showed that treatment with cisplatin induced a 18–65% decrease of stem cell marker expression (CD49f, SSEA4) and a 4–97% increase in expression of differentiation markers (CK18, Tubulin). It is concluded that in addition to its effects on cell survival, cisplatin shifts breast cancer cell lines towards a more differentiated phenotype.Research Support: Malaysian Ministry of Higher Education Postgraduate Scholarship
Highlights
Breast cancer is one of the most frequent cancers among women worldwide (Jemal et al, 2010)
To give insight into the mechanisms through which cisplatin sensitizes breast cancer cells to chemotherapy, we examined the effects of cisplatin on cell phenotype and survival using four human cancer cell lines representing different molecular and differentiation subtypes of breast cancer
At lower doses (2.5–5 μM), cisplatin enhanced cell viability and proliferation in BT-549 and MDA-MB-231 cells, whilst a small decline in viability and proliferation was observed in MDA-MB468 and MCF-7 cells
Summary
Breast cancer is one of the most frequent cancers among women worldwide (Jemal et al, 2010). Breast cancer heterogeneity and cellular hierarchy has led to the identification of five molecular subtypes, which are distinguished based on their molecular and clinical characteristics, and pathogenesis (Sotiriou and Pusztai, 2009; Bosch et al, 2010; Hastak et al, 2010; Al-Ejeh et al, 2011). These include the poorly characterized claudin-low tumors, the basal-like, human epidermal growth factor receptor 2 (HER2) positive, luminal A, and luminal B tumors
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