prikaz prve stranice dokumenta Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival
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Scientific paper - Original scientific paper
Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival
Proceedings of the National Academy of Sciences of the United States of America, 114 (2016), 4; 496-505. https://doi.org/10.1073/pnas.1614876114
Bublik, Débora R.; Bursać, Slađana; Sheffer, Michal; Oršolić, Ines; Shalit, Tali; Tarcic, Ohad; Kotler, Eran; Mouhadeb, Odelia; Hoffman, Yonit; Fuchs, Gilad; Levin, Yishai; Volarević, Siniša; Oren, Moshe

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Bublik, D. R., Bursać, S., Sheffer, M., Oršolić, I., Shalit, T., Tarcic, O. ... Oren, M.. Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival. Proceedings of the National Academy of Sciences of the United States of America, 114. (4), 496-505. doi: 10.1073/pnas.1614876114

Bublik, Débora R., et al. "Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival." Proceedings of the National Academy of Sciences of the United States of America, vol. 114, no. 4, pp. 496-505. https://doi.org/10.1073/pnas.1614876114

Bublik, Débora R., Slađana Bursać, Michal Sheffer, Ines Oršolić, Tali Shalit, Ohad Tarcic, Eran Kotler, et al. "Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival." Proceedings of the National Academy of Sciences of the United States of America 114, no. 4 496-505. https://doi.org/10.1073/pnas.1614876114

Bublik, D. R., et al. 'Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival', Proceedings of the National Academy of Sciences of the United States of America, 114(4), pp. 496-505. doi: 10.1073/pnas.1614876114

Bublik DR, Bursać S, Sheffer M, Oršolić I, Shalit T, Tarcic O, and sur.. Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival. Proceedings of the National Academy of Sciences of the United States of America [Internet]. [cited 2024 April 25];114(4):496-505. doi: 10.1073/pnas.1614876114

D. R. Bublik, et al., "Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival", Proceedings of the National Academy of Sciences of the United States of America, vol. 114, no. 4, pp. 496-505. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:675871. [Accessed: 25 April 2024]

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Metadata
Title (english)Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival
AuthorDébora R. Bublik
AuthorSlađana Bursać
AuthorMichal Sheffer
AuthorInes Oršolić
AuthorTali Shalit
AuthorOhad Tarcic
AuthorEran Kotler
AuthorOdelia Mouhadeb
AuthorYonit Hoffman
AuthorGilad Fuchs
AuthorYishai Levin
AuthorSiniša Volarević
AuthorMoshe Oren
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Molecular Medicine and Biotechnology)
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
The microRNA miR-504 targets TP53 mRNA encoding the p53 tumor suppressor. miR-504 resides within the fibroblast growth factor 13 (FGF13) gene, which is overexpressed in various cancers. We report that the FGF13 locus, comprising FGF13 and miR-504, is transcriptionally repressed by p53, defining an additional negative feedback loop in the p53 network. Furthermore, we show that FGF13 1A is a nucleolar protein that represses ribosomal RNA transcription and attenuates protein synthesis. Importantly, in cancer cells expressing high levels of FGF13, the depletion of FGF13 elicits increased proteostasis stress, associated with the accumulation of reactive oxygen species and apoptosis. Notably, stepwise neoplastic transformation is accompanied by a gradual increase in FGF13 expression and increased dependence on FGF13 for survival ("nononcogene addiction"). Moreover, FGF13 overexpression enables cells to cope more effectively with the stress elicited by oncogenic Ras protein. We propose that, in cells in which activated oncogenes drive excessive protein synthesis, FGF13 may favor survival by maintaining translation rates at a level compatible with the protein quality- control capacity of the cell. Thus, FGF13 may serve as an enabler, allowing cancer cells to evade proteostasis stress triggered by oncogene activation.
Keywords (english)
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review - international
Publication versionPublished version
Journal titleProceedings of the National Academy of Sciences of the United States of America
Numberingvol. 114, no. 4, pp. 496-505
p-ISSN0027-8424
DOIhttps://doi.org/10.1073/pnas.1614876114
URN:NBNurn:nbn:hr:184:675871
Accepted2016-12-19
Document URLhttp://www.pnas.org/content/114/4/E496.long
Type of resourceText
Access conditionsInstitutional access
Terms of useLicence In copyright icon
Created on2018-05-08 16:37:18