Abstract
BackgroundPreviously, we reported that polyploid giant cancer cells (PGCCs) induced by cobalt chloride (CoCl2) could have generated daughter cells with strong invasiveness and migration capabilities via asymmetric divisions. This study compared the expression of epithelial-mesenchymal transition (EMT)-related proteins, including E-cadherin, N-cadherin, and vimentin, between PGCCs and their daughter cells, and control breast cancer cell lines MCF-7 and MDA-MB-231. The clinicopathological significance of EMT-related protein expression in human breast cancer was analyzed.MethodsWestern blot was used to compare the expression levels of E-cadherin, N-cadherin, and vimentin in breast cancer lines MCF-7 and MDA-MB-231, between PGCCs with budding daughter cells and control breast cancer cells. Furthermore, 167 paraffin-embedded breast tumor tissue samples were analyzed, including samples obtained from 52 patients with primary breast cancer with lymph node metastasis (group I) and their corresponding lymph node metastatic tumors (group II), 52 patients with primary breast cancer without metastasis (group III), and 11 patients with benign breast lesions (group IV). The number of PGCCs was compared among these four groups.ResultsThe number of PGCCs increased with the malignant grade of breast tumor. Group IIhad the highest number of PGCCs and the differences among group I, II, III and IV had statistically significance (P =0.000). In addition, the expression of E-cadherin (P = 0.000), N-cadherin (P = 0.000), and vimentin (P = 0.000) was significantly different among the four groups. Group II exhibited the highest expression levels of N-cadherin and vimentin and the lowest expression levels of E-cadherin.ConclusionsThese data suggest that the number of PGCCs and the EMT-related proteins E-cadherin, N-cadherin, and vimentin may be valuable biomarkers to assess metastasis in patients with breast cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-015-0277-8) contains supplementary material, which is available to authorized users.
Highlights
We reported that polyploid giant cancer cells (PGCCs) induced by cobalt chloride (CoCl2) could have generated daughter cells with strong invasiveness and migration capabilities via asymmetric divisions
CoCl2-induced PGCC formation in breast cancer cells When the breast cancer cell lines MCF-7 and MDAMB-231 were treated with high concentrations of CoCl2 over a long period, normal-sized diploid cancer cells were selectively killed while some large cells with giant nuclei (PGCCs) survived
After a high concentration CoCl2 treatment (450 μM) of MCF-7 cells for 72 h killed most diploid cells, PGCCs could be observed after removal of floating dead cells, in contrast to the control MCF-7 cells (Fig. 1A-a and A-b)
Summary
We reported that polyploid giant cancer cells (PGCCs) induced by cobalt chloride (CoCl2) could have generated daughter cells with strong invasiveness and migration capabilities via asymmetric divisions. This study compared the expression of epithelial-mesenchymal transition (EMT)-related proteins, including E-cadherin, N-cadherin, and vimentin, between PGCCs and their daughter cells, and control breast cancer cell lines MCF-7 and MDA-MB-231. PGCCs express normal and cancer stem cell markers, and can be induced to differentiate into other tissues, such as adipose, cartilage, erythrocytes, fibroblasts, and bone [3, 4, 9, 10]. They generate daughter cells (regular-sized diploid cancer cells) via asymmetric cell divisions, a process of reductive division known as depolyploidization [11, 12]. Compared to diploid cancer cells, PGCCs with budding daughter cells and PGCCs alone express lower levels of cytokeratin and higher levels of vimentin, indicating that PGCCs and their budding daughter cells have undergone epithelial-mesenchymal transition (EMT) [10]
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