Role of uL3 in the Crosstalk between Nucleolar Stress and Autophagy in Colon Cancer Cells
Open accessAbstract
The nucleolus is the site of ribosome biogenesis and has been recently described as important sensor for a variety of cellular stressors. In the last two decades, it has been largely demonstrated that many chemotherapeutics act by inhibiting early or late rRNA processing steps with consequent alteration of ribosome biogenesis and activation of nucleolar stress response. The overall result is cell cycle arrest and/or apoptotic cell death of cancer cells. Our previously data demonstrated that ribosomal protein uL3 is a key sensor of nucleolar stress activated by common chemotherapeutic agents in cancer cells lacking p53. We have also demonstrated that uL3 status is associated to chemoresistance; down-regulation of uL3 makes some chemotherapeutic drugs ineffective. Here, we demonstrate that in colon cancer cells, the uL3 status affects rRNA synthesis and processing with consequent activation of uL3-mediated nucleolar stress pathway. Transcriptome analysis of HCT 116p53−/− cells expressing uL3 and of a cell sub line stably depleted of uL3 treated with Actinomycin D suggests a new extra-ribosomal role of uL3 in the regulation of autophagic process. By using confocal microscopy and Western blotting experiments, we demonstrated that uL3 acts as inhibitory factor of autophagic process; the absence of uL3 is associated to increase of autophagic flux and to chemoresistance. Furthermore, experiments conducted in presence of chloroquine, a known inhibitor of autophagy, indicate a role of uL3 in chloroquine-mediated inhibition of autophagy. On the basis of these results and our previous findings, we hypothesize that the absence of uL3 in cancer cells might inhibit cancer cell response to drug treatment through the activation of cytoprotective autophagy. The restoration of uL3 could enhance the activity of many drugs thanks to its pro-apoptotic and anti-autophagic activity.
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Whole transcriptome analysis via RNA-seq followed by biological pathway enrichment analysis has been widely used for prediction of a specific autophagy status and/or step.
“In the last few years, whole transcriptome analysis via RNA-seq technology followed by biological pathway enrichment analysis [12] has been widely used to this end [13, 14].”
From A gene toolbox for monitoring autophagy transcription (2021) · cites this paper as [14]
The Methods (§§4.3–4.4) describe RNA-seq followed by gene-set enrichment analysis, and the Discussion (§3) uses those results to suggest a role for uL3 in inhibiting autophagy. This supports the paper as an example of the approach for inferring autophagy status, but it does not establish that the approach has been widely used or that it predicts a specific autophagy step. (LLM, conf=0.82)
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The EHMT2-MBLAC2 axis suppresses ribosomal DNA transcription in response to nucleolar DNA damage
Wang, C., Lu, Q., Cao, L., Zeng, S., Gao, Z., Yang, Y., Liu, X., Gao, S., & Dong, C. (2026) · Cell Death and Disease · doi:10.1038/s41419-026-08616-1 · Cited by 1 · see citing works
- Authors
- Pecoraro, A., Carotenuto, P., Franco, B., De Cegli, R., Russo, G., & Russo, A.
- Affiliations
- University of Naples Federico II (IT)
- Institute of Cancer Research (GB)
- Telethon Institute Of Genetics And Medicine (IT)
- Telethon Institute of Genetics and Medicine (TIGEM), Via Campi Flegrei, 34, 80078 Pozzuoli, Naples, Italy
- Corresponding author
- Russo, Giulia
- Russo, Annapina
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2020-03-20
- Volume
- 21
- Issue
- 6
- Pages
- 2143
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC7139652
- OpenAlex
- W3011545323
- Cited by
- 35
- References
- 50
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 9 · 2023: 3 · 2022: 5 · 2021: 7 · 2020: 6 · 2019: 1
- FWCI
- 4.48
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Regione Campania-POR FERS 2014/2020 (PROJECT N: B61G180004700007;)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA and protein synthesis mechanisms
- Keywords
- nucleolar stress, autophagy, colon cancer, ribosome biogenesis, rRNA processing, chemoresistance, p53-deficient cells, actinomycin D, chloroquine, autophagic flux, cytoprotective autophagy, HCT116 cells
- MeSH terms
- Ribosomal Protein L3, Autophagy, Cell Cycle, Cell Nucleolus, Colonic Neoplasms, Humans, Microtubule-Associated Proteins, Ribosomal Proteins, RNA Processing, Post-Transcriptional, RNA, Ribosomal, Stress, Physiological, Signal Transduction, Gene Expression Regulation, Neoplastic, Apoptosis, RNA Stability, Intracellular Space, Cell Line, Tumor
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