A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Diverse oncogenes use common mechanisms to drive growth of major forms of human cancer
Tekijät: Kauko, Otto; Turunen, Mikko; Pihlajamaa, Päivi; Häkkinen, Antti; Queiroz, Rayner M. L.; Pääkkönen, Mirva; Ventelä, Sami; Gaetani, Massimiliano; Lundström, Susanna L.; Murgia, Antonio; Sahu, Biswajyoti; Routila, Johannes; Wei, Gong-Hong; Irjala, Heikki; Griffin, Julian L.; Lilley, Kathryn S.; Kivioja, Teemu; Hautaniemi, Sampsa; Taipale, Jussi
Kustantaja: American Association for the Advancement of Science
Kustannuspaikka: WASHINGTON
Julkaisuvuosi: 2025
Journal: Science Advances
Tietokannassa oleva lehden nimi: SCIENCE ADVANCES
Lehden akronyymi: SCI ADV
Artikkelin numero: eadt1798
Vuosikerta: 11
Numero: 34
Sivujen määrä: 20
eISSN: 2375-2548
DOI: https://doi.org/10.1126/sciadv.adt1798
Verkko-osoite: https://doi.org/10.1126/sciadv.adt1798
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/499837445
Mutations in numerous genes contribute to human cancer, with different oncogenic lesions prevalent in different cancer types. However, the malignant phenotype is simple, characterized by unrestricted cell growth, invasion, and often metastasis. One possible hypothesis explaining this dichotomy is that cancer genes regulate common targets, which then function as master regulators of essential cancer phenotypes. To identify mechanisms that drive the most fundamental feature shared by all tumors-unrestricted cell proliferation-we used a multiomic approach, which identified translation and ribosome biogenesis as common targets of major oncogenic pathways across cancer types. Proteomic analysis of tumors and functional studies of cell cultures established nucleolar and coiled-body phosphoprotein 1 as a key node, whose convergent regulation, both transcriptionally and posttranslationally, is critical for tumor cell proliferation. Our results indicate that lineage-specific oncogenic pathways regulate the same set of targets for growth control, revealing key downstream nodes that could be targeted for therapy or chemoprevention.
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This work was supported by following grants: Academy of Finland, Finnish Center of Excellence program: 2012–2017 (250345) and 2018–2025 (312042) (J.T.); Cancer Foundation Finland (J.T.); Cancer Research UK grant C55958/A28801/RG99643 (J.T.); Swedish Research Council D0815201 (J.T.); Finnish medical foundation grant 3977 (O.K.); Cancer Foundation Finland 61-5961 (O.K.); Academy of Finland 288836 (P.P.); European Union’s Horizon 2020 Research and Innovation Programme under grant agreement no. 965193 (DECIDER) (S.H.); and Academy of Finland projects 325956 and 322927 (S.H. and A.H.)
