Prefoldin subunit MM1 promotes cell migration via facilitating filopodia formation

Prefoldin subunit MM1 promotes cell migration via facilitating filopodia formation
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前折叠蛋白亚基 MM1 通过促进丝状伪足形成促进细胞迁移

DOI:
10.1016/j.bbrc.2020.09.063
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发表时间:
2020-12-10
影响因子:
3.1
通讯作者:
Li, Chenghua
Li, Chenghua
中科院分区:
生物学4区
文献类型:
--
作者:
Fan, Shijie;Chen, Yonglong;Li, Chenghua

文献摘要

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c-Myc调节剂1 (MM1),也称为PFDN5,是前折叠蛋白的第五个亚基。先前有报道称,基于mm1的前折叠蛋白在细胞骨架组装过程中促进肌动蛋白的折叠,这在细胞迁移中起关键作用。然而,没有证据支持MM1影响细胞迁移。在本研究中,我们发现MM1促进多种细胞系的细胞迁移。进一步的研究表明,MM1促进β -肌动蛋白聚合成丝状,并增加丝状足的密度和长度。MM1对丝状足形成和细胞迁移的影响取决于其前折叠蛋白活性。虽然c-Myc被MM1抑制,但同时敲除c-Myc并不能挽救MM1消融引起的迁移抑制。综上所述,我们首次报道了折叠蛋白前亚基MM1参与细胞迁移;MM1参与细胞迁移是由于其在丝状足形成过程中促进β -肌动蛋白聚合的前折叠蛋白活性。我们的发现可能有助于阐明细胞迁移和肿瘤转移的机制。(C) 2020爱思唯尔公司版权所有。
c-Myc modulator 1 (MM1), also known as PFDN5, is the fifth subunit of prefoldin. It was previously reported that MM1-based prefoldin promotes folding of actin during assembly of cytoskeleton, which plays key roles in cell migration. However, no evidence supports that MM1 affects cell migration. In the present study, we found that MM1 promotes cell migration in multiple cell lines. Further study revealed that MM1 promotes polymerization of beta-actin into filamentous form and increases both density and length of filopodia. Effects of MM1 on filopodia formation and cell migration depend on its prefoldin activity. Though c-Myc is repressed by MM1, simultaneous knock-down of c-Myc fails to rescue migration inhibition induced by MM1 ablation. Taken together, we here, for the first time, report that prefoldin subunit MM1 is involved in cell migration; this involvement of MM1 in cell migration is due to its prefoldin activity to boost polymerization of beta-actin during filopodia formation. Our findings may be helpful to elucidate the mechanism of cell migration and cancer metastasis. (C) 2020 Elsevier Inc. All rights reserved.