Regulatory Effect of Integrin α5 and β1 on Proliferation Inhibition of K562 Cells Induced by Interferon α-2b

BACKGROUND OBJECTIVE: Integrin β1 can inhibit the proliferation of chronic myelocytic leukemia (CML) ph+ cells. The dysfunction of integrin β1 might accelerate the growth of CML ph+ cells. This study was to explore the effects of integrin α5 and β1 on the proliferation inhibition of K562 cells induced by IFNα-2b. METHODS: The expression indexes of integrin α5 and β1 on K562 cells, the binding capability of K562 cells to fibronectin (FN), and K562 cell-FN binding blocking induced by integrin α5 and β1 antibodies were evaluated by flow cytometry (FCM). The viability of K562 cells, treated with IFNα-2b (10 000 u/ml), was observed by MTT assay. The mRNA level of focal adhesion kinase (FAK) in K562 cells was detected by reverse transcription-polymerase chain reaction (RT-PCR) 48 h after treatment of interferon α-2b (IFNα-2b). RESULTS: The positive rates of integrin α5 and β1 were significantly higher on K562 cells than on bone marrow mononuclear cells from healthy donors [(97.59±1.04)% vs. (64.05±2.38)%, (99.24±0.52)% vs. (72.40±3.56)%, P0.05]. IFNα-2b could not change the expression of integrin α5 and β1 on K562 cells, but improved the binding capability of K562 cells to FN, which could be blocked by anti-α5 and/or anti-β1 antibodies. IFNα-2b enhanced the expression of FAK gene, and inhibited the proliferation of K562 cells. The anti-α5 and anti-β1 antibodies improved the inhibitory effect of IFNα-2b on the proliferation of K562 cells, and blocked IFNα-2b-induced increase of FAK gene expression. CONCLUSION: IFNα-2b could inhibit the proliferation of K562 cells through restoring the function of integrin α5 and β1, enhancing binding capability of integrin α5 and β1 to FN, and up-regulating FAK gene expression.