Tumour-initiating capacity is independent of epithelial-mesenchymal transition status in breast cancer cell lines.

Abstract

BACKGROUND:

Epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs) are considered to be crucial for cancer biology. The purpose of this study was to determine whether EMT directly led to the acquisition of tumour-initiating capacity in breast cancer cell lines.

METHODS:

Epithelial-mesenchymal transition was induced in five breast cancer cell lines and one normal breast cell line by EMT-related cytokine stimulation. Mesenchymal-epithelial transition (MET) was induced by stably overexpressing miR-200c in three mesenchymal-like breast cancer cell lines. Molecular expression and cell function analysis were performed to evaluate the effect of EMT or MET on tumour-initiating capacity and other biological characteristics.

RESULTS:

The induction of EMT did not enhance tumour-initiating capacity but, instead, conferred a CD44(+)/CD24(-/low) phenotype as well as cell proliferation, migration, and resistance to doxorubicin and radiation on breast cancer cell lines. Furthermore, MET did not lead to inhibition or loss of the tumour-initiating capacity in mesenchymal-like breast cancer cell lines, but it markedly attenuated other malignant properties, including proliferation, invasion, and resistance to therapy.

CONCLUSIONS:

Epithelial-mesenchymal transition does not alter tumour-initiating capacity of breast cancer cells but some other biological characteristics. Therefore, EMT and tumour-initiating capacity may not be directly linked in breast cancer cell lines.

• Authors: G Xie, A Ji, Q Yuan, Z Jin, Y Yuan, C Ren, Z Guo, Q Yao, K Yang, X Lin, L Chen
• Journal: British journal of cancer (Br J Cancer) Vol. 110 Issue 10 Pg. 2514-23 (May 13 2014) ISSN: 1532-1827 [Electronic] England
• PMID: 24755887 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antibiotics, Antineoplastic
• Antigens, Neoplasm
• CD44 protein, human
• Cytokines
• Hyaluronan Receptors
• Insulin
• MIRN200 microRNA, human
• MicroRNAs
• Doxorubicin
• Cholera Toxin
• Hydrocortisone

Topics

• Animals
• Antibiotics, Antineoplastic (pharmacology)
• Antigens, Neoplasm (analysis)
• Breast Neoplasms (pathology)
• Cell Division
• Cell Line, Tumor
• Cell Movement
• Cholera Toxin (pharmacology)
• Cytokines (pharmacology)
• Doxorubicin (pharmacology)
• Drug Resistance, Neoplasm
• Epithelial-Mesenchymal Transition (drug effects, physiology)
• Female
• Humans
• Hyaluronan Receptors (analysis)
• Hydrocortisone (pharmacology)
• Immunophenotyping
• Insulin (pharmacology)
• Mice
• Mice, Inbred NOD
• Mice, SCID
• MicroRNAs (biosynthesis, genetics, physiology)
• Neoplasm Transplantation
• Neoplastic Stem Cells (drug effects, physiology, radiation effects)
• Radiation Tolerance