LncPTEN1 overexpression led to the increase of Vimentin ubiquitination, whereas this effect disappeared in Trim16 knockdown cells demonstrating that Trim16 is essential for LncPTEN1 mediated Vimentin degradation (Fig. L,M) Collectively, these findings elucidate a molecular mechanism whereby LncPTEN1 functions as a critical scaffold to promoteTrim16-mediated Vimentin ubiquitination and subsequent proteasomal degradation, thereby attenuating EMT progression and ultimately suppressing lung cancer metastasis (Fig. S7). Here, VIM is linked to lung cancer.