Bovine dialyzable leukocyte extract modulates AP-1 DNA-binding activity and nuclear transcription factor expression in MCF-7 breast cancer cells.

Abstract

BACKGROUND:

We have previously demonstrated that bovine dialyzable leukocyte extract (bDLE) induces death through an apoptosis mechanism in MCF-7 breast cancer cells. Depending on the cell type and stimulus, activating protein-1 (AP-1) has been shown to regulate cell proliferation and differentiation, the stress response, apoptosis and survival. It remains unknown whether AP-1 and other transcription factors are mechanisms by which bDLE induces cell death.

METHODS:

To determine whether bDLE modulates the AP-1 DNA binding and gene expression, MCF-7 breast cancer cells were treated with bDLE (0, 1, 5, 10 U) for 72 h and evaluated by electrophoretic mobility shift assay, reverse transcriptase-polymerase chain reaction and Western blot assays.

RESULTS:

bDLE induced inhibition of cell growth, suppressed the AP-1 DNA-binding activity, decreased c-Jun protein expression and modulated NFATx, NFATc, NFkappaB, c-Jun and c-Fos transcription factor gene expression in MCF-7 breast cancer cells.

DISCUSSION:

The present data indicate that bDLE can block the AP-1 DNA-binding activity and expression of several transcriptions factors in breast cancer cells, which will have great potential in improving cancer therapy.

• Authors: E Mendoza-Gamboa, M A Franco-Molina, P Zapata-Benavides, P Castillo-Tello, M E Vera-García, R S Tamez-Guerra, C Rodríguez-Padilla
• Journal: Cytotherapy (Cytotherapy) Vol. 10 Issue 2 Pg. 212-9 ( 2008) ISSN: 1477-2566 [Electronic] England
• PMID: 18368600 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• DNA, Neoplasm
• Proto-Oncogene Proteins c-fos
• Transcription Factor AP-1
• Transfer Factor

Topics

• Animals
• Breast Neoplasms (genetics, pathology)
• Cattle
• Cell Line, Tumor
• Cell Nucleus (drug effects, metabolism)
• Cell Proliferation (drug effects)
• DNA, Neoplasm (metabolism)
• Female
• Gene Expression Regulation, Neoplastic (drug effects)
• Humans
• Protein Binding (drug effects)
• Proto-Oncogene Proteins c-fos (genetics, metabolism)
• Transcription Factor AP-1 (genetics, metabolism)
• Transfer Factor (pharmacology)