Ribosomal proteins: functions beyond the ribosome

Zhou, Xiang; Liao, Wenjuan; Liao, Jingling; Liao, Peng; Lu, Hua

doi:10.1093/jmcb/mjv014

Cited by 576 publications

(530 citation statements)

References 196 publications

(217 reference statements)

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“…29 Although low doses of Act D have been studied in p53 cell system, it has been demonstrated that the selective inhibition of rRNA synthesis by Act D was able to cause a perturbation of cell cycle progression also in cells silenced of p53, but the molecular pathways by which this occurs has not been determined. 9 Here we show that low doses of Act D (5 nM) induce the expression of rpL3 and its release from the ribosome in p53 mutated and p53 negative cells (Fig. 1).…”

Section: Discussionmentioning

confidence: 51%

“…Perturbations in processes such as rRNA synthesis, rRNA modification as well as ribosomal protein (r-protein) imbalance produce alterations in ribosome biogenesis and resulting in nucleolar stress, causing an accumulation of ribosome-free form of r-proteins. [9][10][11] In response to this event some r-proteins translocate from the nucleolus to the nucleoplasm where bind to (mouse double minute-2 homolog) MDM2 thus promoting p53 stabilization and subsequent p53 mediated cell cycle arrest or apoptosis. 12 Recent findings revealed novel stress response pathways, which function independently of p53 and still lead to cell cycle arrest and/or apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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Regulatory role of rpL3 in cell response to nucleolar stress induced by Act D in tumor cells lacking functional p53

et al. 2016

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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.

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Section: Discussionmentioning

confidence: 51%

Section: Introductionmentioning

confidence: 99%

Regulatory role of rpL3 in cell response to nucleolar stress induced by Act D in tumor cells lacking functional p53

et al. 2016

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“…In addition to their primary function in ribosome biogenesis, many RPs have extraribosomal functions (Warner and McIntosh, 2009;Zhou et al, 2015). As suggested by Warner and McIntosh (Warner and McIntosh, 2009), the following criteria must be met to define extraribosomal functions of RPs: (i) interaction with some nonribosomal components of the cell; (ii) the interaction has physiological effects on cellular functions; (iii) the effects occur away from ribosomes; (iv) the effects do not influence protein synthesis.…”

Section: The Extraribosomal Functions Of Rpsmentioning

confidence: 99%

The role of ribosomal proteins in the regulation of cell proliferation, tumorigenesis, and genomic integrity

Xiong

Sun

2016

Sci. China Life Sci.

109

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Ribosomal proteins (RPs), the essential components of the ribosome, are a family of RNA-binding proteins, which play prime roles in ribosome biogenesis and protein translation. Recent studies revealed that RPs have additional extra-ribosomal functions, independent of protein biosynthesis, in regulation of diverse cellular processes. Here, we review recent advances in our understanding of how RPs regulate apoptosis, cell cycle arrest, cell proliferation, neoplastic transformation, cell migration and invasion, and tumorigenesis through both MDM2/p53-dependent and p53-independent mechanisms. We also discuss the roles of RPs in the maintenance of genome integrity via modulating DNA damage response and repair. We further discuss mutations or deletions at the somatic or germline levels of some RPs in human cancers as well as in patients of Diamond-Blackfan anemia and 5q-syndrome with high susceptibility to cancer development. Moreover, we discuss the potential clinical application, based upon abnormal levels of RPs, in biomarker development for early diagnosis and/or prognosis of certain human cancers. Finally, we discuss the pressing issues in the field as future perspectives for better understanding the roles of RPs in human cancers to eventually benefit human health. ribosomal protein, tumorigenesis, genomic integrity, ribosomal stress, p53, MDM2 Citation:Xu, X., Xiong, X., and Sun, Y. (2016). The role of ribosomal proteins in the regulation of cell proliferation, tumorigenesis, and genomic integrity. Sci China Life Sci 59, 656 -672.

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“…Another critical determinant of proper gene expression and cell survival is the presence and proper function of all 79 RPs that are found within eukaryotic ribosome (Zhou et al, 2015). Ribosome is a complex molecular machine that is primarily responsible for 6 translation and protein synthesis from messenger RNA (mRNA).…”

Section: Figure 1 Nuclear Envelope Budding In Drosophila Muscle Cellsmentioning

confidence: 99%

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2016

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About the ProgramThe Portland State University (PSU) Ronald E. McNair Scholars Program at Portland State University works with motivated and talented undergraduates who want to pursue PhDs. It introduces juniors and seniors who are first-generation and lowincome, and/or members of under-represented groups to academic research and to effective strategies for getting into and graduating from PhD programs.The McNair Scholars Program has academic-year activities and a full-time summer research internship. Scholars take academic and skills-building seminars and workshops during the year, and each scholar works closely with a faculty mentor on original research in the summer. Scholars present their research findings at the McNair Summer Symposium and at other conferences, and are encouraged to publish their papers in the McNair Journal and other scholarly publications. AbstractWhat explains support for democracy among Russian youth? Studies in political socialization conducted in the early 1990s, incorporating generational change, suggest that Russia's main obstacle to the consolidation of democracy was nostalgia for the Soviet Union. The passing of time now allows for the inclusion of the post-Soviet generational cohort, also referred to as the Putin Generation. The post-Soviet youth are a byproduct of political instability and economic turmoil with little or no direct personal experience of the Soviet period. These developments allow for new theoretical mechanisms related to government legitimacy to be included in the analysis. Drawing upon 2011 survey data conducted by the World Values Surveys, this article seeks to advance our understanding of why generational change affects attitudes toward democracy. It extends the literature in two ways: firstly, by adding a new political generation; and secondly, by incorporating government legitimacy into the analysis explaining support for democracy.

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Ribosomal proteins: functions beyond the ribosome

Cited by 576 publications

References 196 publications

Regulatory role of rpL3 in cell response to nucleolar stress induced by Act D in tumor cells lacking functional p53

Regulatory role of rpL3 in cell response to nucleolar stress induced by Act D in tumor cells lacking functional p53

The role of ribosomal proteins in the regulation of cell proliferation, tumorigenesis, and genomic integrity

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