Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2023 Oct 30;13(11):1593.
doi: 10.3390/biom13111593.

The Effects of Deregulated Ribosomal Biogenesis in Cancer

Affiliations
Review

The Effects of Deregulated Ribosomal Biogenesis in Cancer

Yiwei Lu et al. Biomolecules. .

Abstract

Ribosomes are macromolecular ribonucleoprotein complexes assembled from RNA and proteins. Functional ribosomes arise from the nucleolus, require ribosomal RNA processing and the coordinated assembly of ribosomal proteins (RPs), and are frequently hyperactivated to support the requirement for protein synthesis during the self-biosynthetic and metabolic activities of cancer cells. Studies have provided relevant information on targeted anticancer molecules involved in ribosome biogenesis (RiBi), as increased RiBi is characteristic of many types of cancer. The association between unlimited cell proliferation and alterations in specific steps of RiBi has been highlighted as a possible critical driver of tumorigenesis and metastasis. Thus, alterations in numerous regulators and actors involved in RiBi, particularly in cancer, significantly affect the rate and quality of protein synthesis and, ultimately, the transcriptome to generate the associated proteome. Alterations in RiBi in cancer cells activate nucleolar stress response-related pathways that play important roles in cancer-targeted interventions and immunotherapies. In this review, we focus on the association between alterations in RiBi and cancer. Emphasis is placed on RiBi deregulation and its secondary consequences, including changes in protein synthesis, loss of RPs, adaptive transcription and translation, nucleolar stress regulation, metabolic changes, and the impaired ribosome biogenesis checkpoint.

Keywords: cell signaling pathways; metastasis; nucleolar stress regulation; ribosomal biogenesis; ribosomes; tumorigenesis.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Ribosome protein modulates RiBi’s controllable target.
Figure 2
Figure 2
Stimulation of and involvement with the p53 pathway by ribosomal proteins. Abbreviations: ARF, ADP ribose ribosylation factor; MDM2, murine double minute 2; RPL5, ribosomal protein L5; RPL11, ribosomal protein L11.
Figure 3
Figure 3
Factors involved in mTOR-directed regulation of ribosomal biogenesis. Abbreviations: elF-, elongation factor; GTP, guanosine triphosphate; mTOR, mammalian target of rapamycin; Pol, (RNA) polymerase.

Similar articles

Cited by

References

    1. Norris K., Hopes T., Aspden J.L. Ribosome heterogeneity and specialization in development. Wiley Interdiscip. Rev. RNA. 2021;12:e1644. doi: 10.1002/wrna.1644. - DOI - PMC - PubMed
    1. Zolotenkova E.A., Gopanenko A.V., Tupikin A.E., Kabilov M.R., Malygin A.A. Mutation at the Site of Hydroxylation in the Ribosomal Protein uL15 (RPL27a) Causes Specific Changes in the Repertoire of mRNAs Translated in Mammalian Cells. Int. J. Mol. Sci. 2023;24:6173. doi: 10.3390/ijms24076173. - DOI - PMC - PubMed
    1. Lafita-Navarro M., Conacci-Sorrell M. Nucleolar stress: From development to cancer. Semin. Cell Dev. Biol. 2023;136:64–74. doi: 10.1016/j.semcdb.2022.04.001. - DOI - PMC - PubMed
    1. Elhamamsy A.R., Metge B.J., Alsheikh H.A., Shevde L.A., Samant R.S. Ribosome Biogenesis: A Central Player in Cancer Metastasis and Therapeutic Resistance. Cancer Res. 2022;82:2344–2353. doi: 10.1158/0008-5472.CAN-21-4087. - DOI - PMC - PubMed
    1. Baßler J., Hurt E. Eukaryotic Ribosome Assembly. Annu. Rev. Biochem. 2019;88:281–306. doi: 10.1146/annurev-biochem-013118-110817. - DOI - PubMed

Publication types

Grants and funding

This study was supported by the National Natural Science Foundation of China (Grant Numbers: 81372878, 81272873 and 82072887) and Joint Project for Key Research and Development Programme of Liaoning province (Grant Numbers: 2020JH2/10300143).

LinkOut - more resources