Inhibition of Proliferation of Non-small Cell Lung Cancer Cells by a bFGF Antagonist Peptide
Inhibition of Proliferation of Non-small Cell Lung Cancer Cells by a bFGF Antagonist Peptide
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DOI：
10.1007/s10989-013-9372-x
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发表时间：
2014-03
影响因子：
2.5
通讯作者：
Rui-xue Wang;Wu Luo;D. He;Jianzhang Wu;G. Zhu;Xiangpeng Tan;Tao Huang;Yonglin Yu;Xiao-ping Wu
中科院分区：
文献类型：
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作者：
Rui-xue Wang;Wu Luo;D. He;Jianzhang Wu;G. Zhu;Xiangpeng Tan;Tao Huang;Yonglin Yu;Xiao-ping Wu
非小细胞肺癌（NSCLC）是全球癌症相关死亡的主要原因。碱性成纤维细胞生长因子（bFGF）在 NSCLC 患者中表达上调，在肿瘤生长中发挥重要作用。在本文中，我们试图通过探索bFGF结合肽（称为P7）作为有效bFGF拮抗剂对NSCLC细胞的抗增殖作用来评估其治疗潜力。我们的实验表明，P7 肽抑制 bFGF 刺激的 NSCLC 细胞系（包括 A549、H1299 和 H460）的增殖。 P7的抑制机制包括抑制细胞周期蛋白D1、阻断Erk1/2、P38、Akt的激活以及抑制bFGF内化，从而使细胞周期停滞在G0/G1期。使用具有有效抗增殖特性的 bFGF 拮抗剂肽的策略可能具有治疗 NSCLC 的潜力。
Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality worldwide. Basic fibroblast growth factor (bFGF) is up-regulated in NSCLC patients and plays an important role in tumor growth. In this paper, we attempt to evaluate the therapeutic potential of bFGF binding peptide (named as P7) using as a potent bFGF antagonist via exploration of its anti-proliferation effect on NSCLC cells. Our experiments showed that P7 peptide inhibited bFGF-stimulated proliferation of NSCLC cell lines including A549, H1299, and H460. The inhibitory mechanism of P7 involved cell cycle arrest at the G0/G1phase caused by suppression of cyclin D1, blockage of the activation of Erk1/2, P38, Akt, and inhibition of bFGF internalization. Strategies using bFGF antagonist peptides with potent anti-proliferation property may have therapeutic potential in NSCLC.