prikaz prve stranice dokumenta Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival
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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, br. 4, str. 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, br. 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), str. 496-505. doi: 10.1073/pnas.1614876114

Bublik DR, Bursać S, Sheffer M, Oršolić I, Shalit T, Tarcic O, i 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]. [pristupljeno 25.04.2024.];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, br. 4, str. 496-505. [Online]. Dostupno na: https://urn.nsk.hr/urn:nbn:hr:184:675871. [Citirano: 25.04.2024.]

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Podaci o radu
Naslov (engleski)Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival
AutorDébora R. Bublik
AutorSlađana Bursać
AutorMichal Sheffer
AutorInes Oršolić
AutorTali Shalit
AutorOhad Tarcic
AutorEran Kotler
AutorOdelia Mouhadeb
AutorYonit Hoffman
AutorGilad Fuchs
AutorYishai Levin
AutorSiniša Volarević
AutorMoshe Oren
Autorova ustanovaSveučilište u Rijeci
Medicinski fakultet
(Katedra za molekularnu medicinu i biotehnologiju)
Znanstveno / umjetničko
područje, polje i grana		BIOMEDICINA I ZDRAVSTVO
Temeljne medicinske znanosti
Sažetak (engleski)
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.
Ključne riječi (engleski)
Jezikengleski
Vrsta publikacijeZnanstveni rad - Izvorni znanstveni rad
Status objaveObjavljen
Vrsta recenzijeRecenziran - međunarodna recenzija
Verzija publikacijeObjavljena verzija rada (izdavačev PDF)
Naslov časopisaProceedings of the National Academy of Sciences of the United States of America
Brojčani podacivol. 114, br. 4, str. 496-505
p-ISSN0027-8424
DOIhttps://doi.org/10.1073/pnas.1614876114
URN:NBNurn:nbn:hr:184:675871
Datum prihvaćanja za tisak2016-12-19
URL dokumentahttp://www.pnas.org/content/114/4/E496.long
Vrsta resursaTekst
Prava pristupaInstitucijski pristup
Uvjeti korištenjaIkona licence Zaštićeno autorskim pravom.
Datum i vrijeme pohrane2018-05-08 16:37:18