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Here we show how two NOP2\/Sun RNA methyltransferase 3 (NSUN3)-dependent RNA modifications\u20145-methylcytosine (m\n                    <jats:sup>5<\/jats:sup>\n                    C) and its derivative 5-formylcytosine (f\n                    <jats:sup>5<\/jats:sup>\n                    C) (refs.\n                    <jats:sup>2\u20134<\/jats:sup>\n                    )\u2014drive the translation of mitochondrial mRNA to power metastasis. Translation of mitochondrially encoded subunits of the oxidative phosphorylation complex depends on the formation of m\n                    <jats:sup>5<\/jats:sup>\n                    C at position 34 in mitochondrial tRNA\n                    <jats:sup>Met<\/jats:sup>\n                    . m\n                    <jats:sup>5<\/jats:sup>\n                    C-deficient human oral cancer cells exhibit increased levels of glycolysis and changes in their mitochondrial function that do not affect cell viability or primary tumour growth in vivo; however, metabolic plasticity is severely impaired as mitochondrial m\n                    <jats:sup>5<\/jats:sup>\n                    C-deficient tumours do not metastasize efficiently. We discovered that CD36-dependent non-dividing, metastasis-initiating tumour cells require mitochondrial m\n                    <jats:sup>5<\/jats:sup>\n                    C to activate invasion and dissemination. Moreover, a mitochondria-driven gene signature in patients with head and neck cancer is predictive for metastasis and disease progression. Finally, we confirm that this metabolic switch that allows the metastasis of tumour cells can be pharmacologically targeted through the inhibition of mitochondrial mRNA translation in vivo. Together, our results reveal that site-specific mitochondrial RNA modifications could be therapeutic targets to combat metastasis.\n                  <\/jats:p>","DOI":"10.1038\/s41586-022-04898-5","type":"journal-article","created":{"date-parts":[[2022,6,29]],"date-time":"2022-06-29T11:09:31Z","timestamp":1656500971000},"page":"593-603","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":317,"title":["Mitochondrial RNA modifications shape metabolic plasticity in metastasis"],"prefix":"10.1038","volume":"607","author":[{"given":"Sylvain","family":"Delaunay","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3810-6647","authenticated-orcid":false,"given":"Gloria","family":"Pascual","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bohai","family":"Feng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2276-8128","authenticated-orcid":false,"given":"Kevin","family":"Klann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mikaela","family":"Behm","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1523-2093","authenticated-orcid":false,"given":"Agnes","family":"Hotz-Wagenblatt","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karsten","family":"Richter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karim","family":"Zaoui","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Esther","family":"Herpel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3832-090X","authenticated-orcid":false,"given":"Christian","family":"M\u00fcnch","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabine","family":"Dietmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jochen","family":"Hess","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9059-5049","authenticated-orcid":false,"given":"Salvador Aznar","family":"Benitah","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5636-6840","authenticated-orcid":false,"given":"Michaela","family":"Frye","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,6,29]]},"reference":[{"key":"4898_CR1","doi-asserted-by":"publisher","first-page":"1797","DOI":"10.1158\/2159-8290.CD-20-0844","volume":"10","author":"SM Fendt","year":"2020","unstructured":"Fendt, S. 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J.H. receives commercial funding from CureVac AG and acts as a consultant and advisory board member for Bristol-Myers Squibb and MSD Sharp & Dohme. M.F. receives commercial funding from Merck. The other authors declare no competing interests.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}]}}