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2019-09-04

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cc-by (c) Oliveira-Mateos, Cristina et al., 2019
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/155231

The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent inhibition of let-7 miRNAs

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https://doi.org/10.1038/s41467-019-11910-6

Resum

One largely unknown question in cell biology is the discrimination between inconsequential and functional transcriptional events with relevant regulatory functions. Here, we find that the oncofetal HMGA2 gene is aberrantly reexpressed in many tumor types together with its antisense transcribed pseudogene RPSAP52. RPSAP52 is abundantly present in the cytoplasm, where it interacts with the RNA binding protein IGF2BP2/IMP2, facilitating its binding to mRNA targets, promoting their translation by mediating their recruitment on polysomes and enhancing proliferative and self-renewal pathways. Notably, downregulation of RPSAP52 impairs the balance between the oncogene LIN28B and the tumor suppressor let-7 family of miRNAs, inhibits cellular proliferation and migration in vitro and slows down tumor growth in vivo. In addition, high levels of RPSAP52 in patient samples associate with a worse prognosis in sarcomas. Overall, we reveal the roles of a transcribed pseudogene that may display properties of an oncofetal master regulator in human cancers.

Matèries

Expressió gènica, Micro RNAs, Genètica, Transducció de senyal cel·lular, Proteïnes

Matèries (anglès)

Gene expression, MicroRNAs, Genetics, Cellular signal transduction, Proteins

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Articles publicats en revistes (Ciències Fisiològiques)
Articles publicats en revistes (Bioquímica i Fisiologia)
Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))

Citació

OLIVEIRA-MATEOS, Cristina, et al. The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent inhibition of let-7 miRNAs. Nature Communications. 2019. Vol. 10, num. 1, pags. 3979. ISSN 2041-1723. [consulted: 5 of June of 2026]. Available at: https://hdl.handle.net/2445/155231

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