BECN1/Beclin1 is one of the key proteins in autophagy regulation. However, the biological functions of BECN1 in non-small cell lung cancer (NSCLC) were obscure. Here, we found that neither BECN1 knockdown nor overexpression affected the proliferation of NSCLC cells. Surprisingly, BECN1 overexpression increased cell migration and knocking down BECN1 significantly reduced the migratory ability of NSCLC cells. We further demonstrated that BECN1 could interact with Vimentin and affected its K48-linked ubiquitination. What's more, BECN1 could also interact with ubiquitin-specific peptidase 14 (USP14), the key de-ubiquitinase of Vimentin, and regulated USP14 mediated de-ubiquitination of Vimentin. Thus, our studies revealed an oncosupportive role of BECN1 in the migration of NSCLC cells through regulating the ubiquitination of Vimentin.

中文翻译：

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BECN1通过调节波形蛋白的泛素化促进NSCLC细胞的迁移。

BECN1 / Beclin1是自噬调节的关键蛋白之一。但是，BECN1在非小细胞肺癌（NSCLC）中的生物学功能尚不清楚。在这里，我们发现BECN1敲低和过表达都不会影响NSCLC细胞的增殖。出人意料的是，BECN1过表达增加了细胞迁移，而敲低BECN1则大大降低了NSCLC细胞的迁移能力。我们进一步证明BECN1可以与波形蛋白相互作用，并影响其与K48连接的泛素化。更重要的是，BECN1还可以与波形蛋白的关键去泛素酶泛素特异性肽酶14（USP14）相互作用，并调节USP14介导的波形蛋白去泛素作用。因此，我们的研究揭示了BECN1在通过调节波形蛋白的泛素化作用在NSCLC细胞迁移中的辅助支持作用。