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Given the direct control of translation by tRNA modifications, tRNA modifying enzymes may function as regulators of cancer progression. Here, we show that a tRNA methyltransferase 9\u2010like (\n                    <jats:italic>hTRM9L\/KIAA1456<\/jats:italic>\n                    ) mRNA is down\u2010regulated in breast, bladder, colorectal, cervix and testicular carcinomas. In the aggressive SW620 and HCT116 colon carcinoma cell lines,\n                    <jats:italic>hTRM9L<\/jats:italic>\n                    is silenced and its re\u2010expression and methyltransferase activity dramatically suppressed tumour growth\n                    <jats:italic>in vivo<\/jats:italic>\n                    . This growth inhibition was linked to decreased proliferation, senescence\u2010like G0\/G1\u2010arrest and up\u2010regulation of the RB interacting protein LIN9. Additionally, SW620 cells re\u2010expressing\n                    <jats:italic>hTRM9L<\/jats:italic>\n                    did not respond to hypoxia via HIF1\u2010\u03b1\u2010dependent induction of GLUT1. Importantly,\n                    <jats:italic>hTRM9L<\/jats:italic>\n                    \u2010negative tumours were highly sensitive to aminoglycoside antibiotics and this was associated with altered tRNA modification levels compared to antibiotic resistant\n                    <jats:italic>hTRM9L<\/jats:italic>\n                    \u2010expressing SW620 cells. Our study links hTRM9L and tRNA modifications to inhibition of tumour growth via LIN9 and HIF1\u2010\u03b1\u2010dependent mechanisms. It also suggests that aminoglycoside antibiotics may be useful to treat hTRM9L\u2010deficient tumours.\n                  <\/jats:p>","DOI":"10.1002\/emmm.201201161","type":"journal-article","created":{"date-parts":[[2013,2,4]],"date-time":"2013-02-04T11:09:26Z","timestamp":1359976166000},"page":"366-383","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":114,"title":["A human tRNA methyltransferase 9\u2010like protein prevents tumour growth by regulating LIN9 and HIF1\u2010\u03b1"],"prefix":"10.1038","volume":"5","author":[{"given":"Ulrike","family":"Begley","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria Soledad","family":"Sosa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alvaro","family":"Avivar\u2010Valderas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ashish","family":"Patil","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren","family":"Endres","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yeriel","family":"Estrada","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clement T.Y.","family":"Chan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dan","family":"Su","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter C.","family":"Dedon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julio A.","family":"Aguirre\u2010Ghiso","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Begley","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2013,2,4]]},"reference":[{"key":"BFEMMM201201161_CR1","doi-asserted-by":"crossref","first-page":"4212","DOI":"10.1093\/emboj\/cdg417","volume":"22","author":"CM Beausejour","year":"2003","unstructured":"Beausejour CM, Krtolica A, Galimi F, Narita M, Lowe SW, Yaswen P, Campisi J (2003) Reversal of human cellular senescence: roles of the p53 and p16 pathways. 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