P7 peptides suppress the proliferation of K562 cells induced by basic fibroblast growth factor
P7 peptides suppress the proliferation of K562 cells induced by basic fibroblast growth factor
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DOI：
10.1007/s13277-012-0348-9
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发表时间：
2012-02
期刊：
影响因子：
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通讯作者：
Cong Wang;Yonglin Yu;Quchou Li;Susu Gao;Xinglong Jia;Xilei Chen;Rui-xue Wang;Tao Li;Wenhui Wang;Xiaokun Li;Xiao-ping Wu
中科院分区：
文献类型：
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作者：
Cong Wang;Yonglin Yu;Quchou Li;Susu Gao;Xinglong Jia;Xilei Chen;Rui-xue Wang;Tao Li;Wenhui Wang;Xiaokun Li;Xiao-ping Wu
尽管已经知道碱性成纤维细胞生长因子（bFGF）参与肿瘤进展，但很少有研究涉及bFGF在造血系统恶性肿瘤（包括慢性粒细胞白血病（CML））中的作用。近年来发现慢性粒细胞白血病（CML）患者体内bFGF水平升高，认为bFGF在促进白血病细胞生长中起重要作用。抑制bFGF的促有丝分裂活性可能有助于CML的治疗。我们先前已经获得了一种新的bFGF结合肽（命名为P7），对bFGF诱导的细胞增殖具有强抑制活性。本研究探讨了P7对慢性粒细胞白血病K562细胞增殖的影响。结果表明，P7抑制bFGF刺激的细胞增殖，使细胞周期阻滞于G 0/G1期，抑制MAP激酶的激活，逆转bFGF对细胞膜超微结构的影响，并引起与增殖相关蛋白表达的显著变化。我们的研究结果表明，bFGF结合肽可能有潜在的抗肿瘤作用的角度来看，碱性成纤维细胞生长因子的慢性粒细胞白血病。
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.