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- W2192367718 abstract "Many chemotherapeutic drugs cause nucleolar stress and p53-independent pathways mediating the nucleolar stress response are emerging. Here, we demonstrate that ribosomal stress induced by Actinomycin D (Act D) is associated to the up-regulation of ribosomal protein L3 (rpL3) and its accumulation as ribosome-free form in lung and colon cancer cell lines devoid of p53. Free rpL3 regulates p21 expression at transcriptional and post-translational levels through a molecular mechanism involving extracellular-signal-regulated kinases1/2 (ERK1/2) and mouse double minute-2 homolog (MDM2). Our data reveal that rpL3 participates to cell response acting as a critical regulator of apoptosis and cell migration. It is noteworthy that silencing of rpL3 abolishes the cytotoxic effects of Act D suggesting that the loss of rpL3 makes chemotherapy drugs ineffective while rpL3 overexpression associates to a strong increase of Act D-mediated inhibition of cell migration. Taking together our results show that the efficacy of Act D chemotherapy depends on rpL3 status revealing new specific targets involved in the molecular pathways activated by Act D in cancers lacking of p53. Hence, the development of treatments aimed at upregulating rpL3 may be beneficial for the treatment of these cancers." @default.
- W2192367718 created "2016-06-24" @default.
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- W2192367718 date "2016-01-02" @default.
- W2192367718 modified "2023-10-18" @default.
- W2192367718 title "Regulatory role of rpL3 in cell response to nucleolar stress induced by Act D in tumor cells lacking functional p53" @default.
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- W2192367718 doi "https://doi.org/10.1080/15384101.2015.1120926" @default.
- W2192367718 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4825706" @default.
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