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P7 peptides suppress the proliferation of K562 cells induced by basic fibroblast growth factor.

机译:P7肽抑制碱性成纤维细胞生长因子诱导的K562细胞增殖。

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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.
机译:尽管已知碱性成纤维细胞生长因子(bFGF)参与肿瘤进展,但很少有研究针对bFGF在包括慢性粒细胞白血病(CML)的造血系统恶性肿瘤中的作用。最近在CML患者中发现bFGF水平升高,并且bFGF被认为在刺激白血病细胞的生长中起重要作用。 bFGF有丝分裂活性的抑制可能有助于CML治疗。我们以前已经获得了一种新型的bFGF结合肽(命名为P7),对bFGF诱导的细胞增殖具有很强的抑制活性。在这项研究中,我们研究了P7对CML衍生的K562细胞增殖的影响。结果表明,P7抑制bFGF刺激的增殖,在G0 / G1期阻滞细胞周期,抑制MAP激酶的激活,逆转bFGF对细胞膜超微结构的作用,并引起与增殖。我们的结果表明,从靶向bFGF的角度来看,bFGF结合肽可能对CML具有潜在的抗肿瘤作用。

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