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. 2022 Jun 29;23(8):e54265. doi: 10.15252/embr.202154265

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© 2022 The Authors. Published under the terms of the CC BY 4.0 license.

This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Our invasion cell‐based model demonstrated that in high MTAP‐expressing low metastatic cancer cells, MTA level is relatively low, facilitating PRMT5 to dimethylate vimentin, leading to vimentin degradation. Conversely, in highly metastatic cancer cells with MTAP loss, accumulated MTA inhibits PRMT5 activity so that low dimethylated vimentin is stabilized and responsible for lung cancer metastasis.