Effects of integrin beta1 on phycocyanin inhibiting proliferation of K562 cells

This study was purposed to investigate the effect of phycocyamin at different concentration on proliferation of K562 cells, to detect the changes of integrin β1 expression and intracellular focal adhesion kinase (FAK) gene expression on the surface K562 cells treated with phycocyanin, and to explore the possible machanism of integrin β1 effect on phycocyanin inhibiting proliferation of K562 cells. The expression level of integrin β1 on the surface of K562 cells was evaluated by flow cytometry (FCM); the growth of K562 cells treated with phycocyanin was measured by MTT assay; the expression level of FAK mRNA was analyzed by relatively quantitative RT-PCR after four-day culture of K562 cells with phycocyanin of 40 μg/ml, 80 μg/ml and 160 μg/ml, respectively. The results showed that integrin β1 expression on the surface of K562 cells was significantly higher than that in bone marrow mononuclear cells (BMMNC) from normal subjects. Phycocyanin could not change the level of integin β1 expression. Phycocyanin could increase the expression of FAK gene on K562 cells and inhibit the proliferation of K562 cells. It is concluded that phycocyanin can inhibit the proliferation of K562 cells through enhancing the conjunction of cell stroma with integrin β1 on K562 cell surface, up-regulating the expression level of FAK gene in K562 cells, restoring the signaling pathway of proliferation inhibition mediated by integrin β1. The possible mechanism of phycocyanin in the proliferation inhibition of K562 cells is to increase the expression of FAK gene. The phcocyanin may be considered as a potential agent for inhibition of cancer cell proliferation.