Diverse oncogenes use common mechanisms to drive growth of major forms of human cancer - UTU Research Portal

A1 Refereed original research article in a scientific journal

Diverse oncogenes use common mechanisms to drive growth of major forms of human cancer

Authors: 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

Publisher: American Association for the Advancement of Science

Publishing place: WASHINGTON

Publication year: 2025

Journal: Science Advances

Journal name in source: SCIENCE ADVANCES

Journal acronym: SCI ADV

Article number: eadt1798

Volume: 11

Issue: 34

Number of pages: 20

eISSN: 2375-2548

DOI: https://doi.org/10.1126/sciadv.adt1798

Web address : https://doi.org/10.1126/sciadv.adt1798

Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/499837445

Abstract

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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Funding information in the publication:
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.)