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Our previous study revealed substantial upregulation of N-terminal (Nt)-fMet-containing proteins in the cytosol of SW480 colorectal cancer cells. However, the functional and pathophysiological implications remain unclear. Here, we demonstrated that removal of the Nt-formyl moiety of Nt-fMet-containing proteins (via expressing <jats:italic>Escherichia coli<\/jats:italic> PDF peptide deformylase) resulted in a dramatic increase in the proliferation of SW480 colorectal cancer cells. This proliferation coincided with the acquisition of cancer stem cell features, including reduced cell size, enhanced self-renewal capacity, and elevated levels of the cancer stem cell surface marker CD24 and pluripotent transcription factor SOX2. Furthermore, deformylation of Nt-fMet-containing proteins promoted the tumorigenicity of SW480 colorectal cancer cells in an in vivo xenograft mouse model. Taken together, these findings suggest that cytosolic deformylation has a tumor-enhancing effect, highlighting its therapeutic potential for cancer treatment.<\/jats:p>","DOI":"10.1038\/s41598-024-65701-1","type":"journal-article","created":{"date-parts":[[2024,6,28]],"date-time":"2024-06-28T06:02:19Z","timestamp":1719554539000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Cytosolic N-terminal formyl-methionine deformylation derives cancer stem cell features and tumor progression"],"prefix":"10.1038","volume":"14","author":[{"given":"Dasom","family":"Kim","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jongeun","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ok-Hee","family":"Seok","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoontae","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cheol-Sang","family":"Hwang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,6,28]]},"reference":[{"issue":"2","key":"65701_CR1","doi-asserted-by":"publisher","first-page":"338","DOI":"10.1136\/gutjnl-2022-327736","volume":"72","author":"E Morgan","year":"2023","unstructured":"Morgan, E. et al. Global burden of colorectal cancer in 2020 and 2040: Incidence and mortality estimates from GLOBOCAN. Gut 72(2), 338\u2013344 (2023).","journal-title":"Gut"},{"key":"65701_CR2","doi-asserted-by":"publisher","first-page":"467","DOI":"10.1146\/annurev-pathmechdis-031521-041113","volume":"18","author":"JC Sedlak","year":"2023","unstructured":"Sedlak, J. C., Yilmaz, \u00d6. H. & Roper, J. Metabolism and colorectal cancer. Annu. Rev. Pathol. Mech. Dis. 18, 467\u2013492 (2023).","journal-title":"Annu. Rev. Pathol. Mech. Dis."},{"key":"65701_CR3","doi-asserted-by":"publisher","first-page":"103920","DOI":"10.1016\/j.critrevonc.2023.103920","volume":"182","author":"N Ebrahimi","year":"2023","unstructured":"Ebrahimi, N. et al. Cancer stem cells in colorectal cancer: Signaling pathways involved in stemness and therapy resistance. Crit. Rev. Oncol. Hematol. 182, 103920 (2023).","journal-title":"Crit. Rev. Oncol. 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