| Aim: To explore the effect and mechanism of macrophage colony stimulating factor(M-CSF) on HIF-1α/BNIP3/Bax signaling in human breast cancer MCF-7 cells.Methods: MCF-7 cells, MCF-7-C cells and MCF-7-M cells were maintained in RPMI 1640 supplemented with 10% NBCS. Western blot was explored to analyze the expression of HIF-1α, BNIP3, Bax, Caspase 3 and Caspase 9 in three cells treated with or without ADM. Immunoprecipitation combination with Western blot was used to detect the interaction between bcl-2 and BNIP3 or Bax protein. Hoechst33342 staining and flow cytometry were utilized to evaluate the effect of M-CSF on the apoptosis in MCF-7 cells treated with ADM.Results: MCF-7-M cell had a higher HIF-1α expression than MCF-7 cell or MCF-7-C cell(p<0.01), and there was little difference for expression level of Bax, Caspase 3 and Caspase 9 protein(p>0.05) in three kind of cells, after cells treated with ADM, MCF-7-M cell had a lower expression of HIF-1α, BNIP3, Bax, Caspase 3 and Caspase 9 than MCF-7 cell or MCF-7-C cell(p<0.01), and there was little for expression level of HIF-1α, BNIP3, Bax, Caspase 3 and Caspase 9 protein(p>0.05) between MCF-7 cell and MCF-7-C cell. MCF-7-M cell had a higher Bax amount binding to Bcl-2 than MCF-7 cell or MCF-7-C cell(p<0.05)and there was little difference for BNIP3 amount binding to Bcl-2 in three kind of cells(p>0.05), after cells treated with ADM, MCF-7-M cell had a higher Bax amount(p<0.05)and a lower BNIP3 amount binding to Bcl-2(p<0.01)than MCF-7 cell or MCF-7-C cell. The apoptotic rate of MCF-7-M cell was significantly decreased(p<0.01), compared with MCF-7 cell treated with ADM, which is dependent on the ADM concentration.Conclusions: Cytoplasmic M-CSF facilitates the capability of antiapoptosis by inhibiting IF-1α/BNIP3/Bax signaling, which accentuates the Bcl-2 dissociation from Bcl-2- BNIP3 compounds and the formation of Bcl-2-Bax compounds. |
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