P7 peptides suppress the proliferation of K562 cells induced by basic fibroblast growth factor
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Although it has been known that basic fibroblast growth factor (bFGF) is involved in tumor progression, few studies addressed the role of bFGF in hematopoietic system malignancies including chronic myeloid leukemia (CML). An elevated level of bFGF was recently found in CML patients, and bFGF was considered to play an important role in stimulating the growth of leukemia cells. Suppression of the mitogenic activity of bFGF may contribute to CML therapy. We have previously obtained a novel bFGF-binding peptide (named P7) with strong inhibitory activity against bFGF-induced cell proliferation. In this study, we investigated the effects of P7 on the proliferation of K562 cells derived from CML. The results demonstrated that P7 inhibited bFGF-stimulated proliferation, arrested the cell cycle at the G0/G1 phase, repressed the activation of MAP kinase, reversed the effects of bFGF on cell membrane ultrastructure, and caused significant changes in the expression of proteins related to proliferation. Our results suggested that the bFGF-binding peptide may have a potential antitumor effect on CML from the point of view of targeting bFGF.
KeywordsbFGF-binding peptide Proliferation Proteome Chronic myeloid leukemia
This work was supported by grants from the National Natural Science Foundation of China (30973671, 81071800), the Natural Science Foundation of Zhejiang Province of China (Y2090292), the Natural Science Foundation of Guangdong Province of China (9151064001000031), the Science and Technology Planning Project of Wenzhou (Y20090244), the Fundamental Research Funds for the Central Universities (X.P. Wu), Guangdong Provincial “Thousand-Hundred-Ten Talent Project” (X.P. Wu), and Guangdong Provincial Key Discipline in Biochemistry and Molecular Biology.
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