Bcl-2 promotes metastasis through the epithelial-to-mesenchymal transition in the BCap37 medullary breast cancer cell line.

Metastatic breast cancer is one of the major types of cancer in women. However, despite being the focus of considerable research efforts, its molecular mechanism remains to be fully elucidated. The B-cell lymphoma/leukemia gene-2 (Bcl-2) protein is well known for its role in inhibiting programmed cell death/apoptosis. However, little is known concerning its function in cell invasion and migration. In the present study, cell migration and invasion assays revealed that anti-apoptotic Bcl-2 protein induced migration and invasion without affecting cell proliferation in the BCap37 breast cancer cell line. In addition, it was found that the overexpression of Bcl-2 in BCap37 cells increased metastasis to the lung in a mouse model. Using western blotting and RT q-PCR analysis, it was demonstrated that the overexpression of Bcl-2 inhibited the expression of E-cadherin, an epithelial marker, whereas it increased the levels of mesenchymal markers N-cadherin and vimentin. Therefore, the results suggested that Bcl-2 may induce cellular metastasis in breast cancer via the epithelial-to-mesenchymal transition.